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One of the primary goals that researchers look to achieve through customer base analysis is to leverage historical records of individual customer transactions and related context factors to forecast future behavior, and to link these forecasts with actionable characteristics of individuals, managerially significant customer sub-groups, and entire cohorts. This paper presents a new approach that helps firms leverage the automatic feature extraction capabilities of a specific type of deep learning models when applied to customer transaction histories in non-contractual business settings (i.e., when the time at which a customer becomes inactive is unobserved by the firm). We show how the proposed deep learning model improves on established models both in terms of individual-level accuracy and overall cohort-level bias. It also helps managers in capturing seasonal trends and other forms of purchase dynamics that are important to detect in a timely manner for the purpose of proactive customer-base management. We demonstrate the model performance in eight empirical real-life settings which vary broadly in transaction frequency, purchase (ir)regularity, customer attrition, availability of contextual information, seasonal variance, and cohort size. We showcase the flexibility of the approach and how the model further benefits from taking into account static (e.g., socio-economic variables, demographics) and dynamic context factors (e.g., weather, holiday seasons, marketing appeals)
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[unknown IMAGE 7100438023436] #has-images #recurrent-neural-networks #rnn
Based on our initial discussion, an ideal model for customer base analysis in data-rich environments would combine a robust forecasting capability both in the short and in the long-term with limited engineering requirements at low computational cost and providing a direct link toward managerial decision-making. Recognizing that traditional statistical forecasting models often suffer from poor efficiency when increasing model complexity and heavily rely on manual feature engineering and data labeling, Table 1 picks up these issues and compares some of the key differences between stochastic BTYD models and the deep learning approach we present in this section
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Yehud was a province of the Neo-Babylonian Empire established in the former territories of the Kingdom of Judah, which was destroyed by the Babylonians in the aftermath of the Jewish-Babylonian War, in 587/6 BCE.
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Yehud (Babylonian province) - Wikipedia
ical maps Historical population Historical literature Judaism Jerusalem Zionism Jewish leaders Jewish warfare show Related Jewish history Hebrew calendar Archaeology Museums Israel portal v t e <span>Yehud was a province of the Neo-Babylonian Empire established in the former territories of the Kingdom of Judah, which was destroyed by the Babylonians in the aftermath of the Jewish-Babylonian War, in 587/6 BCE. It first existed as a Jewish administrative division of the Neo-Babylonian Empire under Gedaliah. After the collapse of the Neo-Babylonian Empire in 539 BCE, the province was absorbed i




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Yehud was a province of the [...]stablished in the former territories of the Kingdom of Judah, which was destroyed by the Babylonians in the aftermath of the Jewish-Babylonian War, in 587/6 BCE.
Answer
Neo-Babylonian Empire

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Yehud was a province of the Neo-Babylonian Empire established in the former territories of the Kingdom of Judah, which was destroyed by the Babylonians in the aftermath of the Jewish-Babylonian War, in 587/6 BCE.

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Yehud (Babylonian province) - Wikipedia
ical maps Historical population Historical literature Judaism Jerusalem Zionism Jewish leaders Jewish warfare show Related Jewish history Hebrew calendar Archaeology Museums Israel portal v t e <span>Yehud was a province of the Neo-Babylonian Empire established in the former territories of the Kingdom of Judah, which was destroyed by the Babylonians in the aftermath of the Jewish-Babylonian War, in 587/6 BCE. It first existed as a Jewish administrative division of the Neo-Babylonian Empire under Gedaliah. After the collapse of the Neo-Babylonian Empire in 539 BCE, the province was absorbed i







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Yehud was a province of the Neo-Babylonian Empire established in the former territories of the [...], which was destroyed by the Babylonians in the aftermath of the Jewish-Babylonian War, in 587/6 BCE.
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Kingdom of Judah

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Yehud was a province of the Neo-Babylonian Empire established in the former territories of the Kingdom of Judah, which was destroyed by the Babylonians in the aftermath of the Jewish-Babylonian War, in 587/6 BCE.

Original toplevel document

Yehud (Babylonian province) - Wikipedia
ical maps Historical population Historical literature Judaism Jerusalem Zionism Jewish leaders Jewish warfare show Related Jewish history Hebrew calendar Archaeology Museums Israel portal v t e <span>Yehud was a province of the Neo-Babylonian Empire established in the former territories of the Kingdom of Judah, which was destroyed by the Babylonians in the aftermath of the Jewish-Babylonian War, in 587/6 BCE. It first existed as a Jewish administrative division of the Neo-Babylonian Empire under Gedaliah. After the collapse of the Neo-Babylonian Empire in 539 BCE, the province was absorbed i







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Yehud was a province of the Neo-Babylonian Empire established in the former territories of the Kingdom of Judah, which was destroyed by the Babylonians in the aftermath of the Jewish-Babylonian War, in [...] BCE.
Answer
587/6

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s a province of the Neo-Babylonian Empire established in the former territories of the Kingdom of Judah, which was destroyed by the Babylonians in the aftermath of the Jewish-Babylonian War, in <span>587/6 BCE. <span>

Original toplevel document

Yehud (Babylonian province) - Wikipedia
ical maps Historical population Historical literature Judaism Jerusalem Zionism Jewish leaders Jewish warfare show Related Jewish history Hebrew calendar Archaeology Museums Israel portal v t e <span>Yehud was a province of the Neo-Babylonian Empire established in the former territories of the Kingdom of Judah, which was destroyed by the Babylonians in the aftermath of the Jewish-Babylonian War, in 587/6 BCE. It first existed as a Jewish administrative division of the Neo-Babylonian Empire under Gedaliah. After the collapse of the Neo-Babylonian Empire in 539 BCE, the province was absorbed i







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Yehud was a province of the Neo-Babylonian Empire established in the former territories of the Kingdom of Judah, which was destroyed by the Babylonians in the aftermath of the [...] War, in 587/6 BCE.
Answer
Jewish-Babylonian

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Yehud was a province of the Neo-Babylonian Empire established in the former territories of the Kingdom of Judah, which was destroyed by the Babylonians in the aftermath of the Jewish-Babylonian War, in 587/6 BCE.

Original toplevel document

Yehud (Babylonian province) - Wikipedia
ical maps Historical population Historical literature Judaism Jerusalem Zionism Jewish leaders Jewish warfare show Related Jewish history Hebrew calendar Archaeology Museums Israel portal v t e <span>Yehud was a province of the Neo-Babylonian Empire established in the former territories of the Kingdom of Judah, which was destroyed by the Babylonians in the aftermath of the Jewish-Babylonian War, in 587/6 BCE. It first existed as a Jewish administrative division of the Neo-Babylonian Empire under Gedaliah. After the collapse of the Neo-Babylonian Empire in 539 BCE, the province was absorbed i







#Diagnosis #Diagnostic #Emergency #Infarction #Infarctus #Myocarde #Myocardial #SAU #U2D

Diagnostic evaluation emphasizes distinguishing between the following potential, life-threatening causes of chest pain:

● Acute coronary syndrome (ACS; myocardial infarction or unstable angina)

● Nonischemic chest pain, including potentially life-threatening conditions such as aortic dissection, pulmonary embolism, and esophageal rupture (table 1 and table 2A-B)

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r other related symptoms (eg, dyspnea, weakness) and to initiate appropriate therapy promptly. It is essential that initial assessment and management be rapid but methodical and evidence based. <span>Diagnostic evaluation emphasizes distinguishing between the following potential, life-threatening causes of chest pain: ●Acute coronary syndrome (ACS; myocardial infarction or unstable angina) ●Nonischemic chest pain, including potentially life-threatening conditions such as aortic dissection, pulmonary embolism, and esophageal rupture (table 1 and table 2A-B) The diagnosis of acute coronary-related ischemia depends upon the characteristics of the chest pain (if present), specific associated symptoms, abnormalities on electrocardiogram (ECG),




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Clinicians should consider the possibility of ACS in any adult who presents to the emergency department complaining of chest discomfort or dyspnea. A personal or family history of ACS or other cardiovascular disease, older age, diabetes, dyslipidemia, cigarette smoking, hypertension, or cocaine use all increase the likelihood.
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sure. (See "Evaluation of the adult with chest pain in the emergency department" and "Approach to the adult with dyspnea in the emergency department".) WHEN TO SUSPECT ACUTE CORONARY SYNDROME — <span>Clinicians should consider the possibility of ACS in any adult who presents to the emergency department complaining of chest discomfort or dyspnea. A personal or family history of ACS or other cardiovascular disease, older age, diabetes, dyslipidemia, cigarette smoking, hypertension, or cocaine use all increase the likelihood. (See "Overview of established risk factors for cardiovascular disease".) Characteristic presentations (as described below) heighten concern, but clinicians must keep in mind that many p




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Females are more likely to have associated dyspnea than males, and patients who are older or have diabetes are more likely to present with dyspnea without chest pain.
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(as described below) heighten concern, but clinicians must keep in mind that many patients with ACS present with symptoms such as dyspnea or malaise, either alone or in addition to chest pain. <span>Females are more likely to have associated dyspnea than males, and patients who are older or have diabetes are more likely to present with dyspnea without chest pain. (See 'Clinical presentation' below and 'Atypical presentations' below and "Clinical features and diagnosis of coronary heart disease in women" and "Silent myocardial ischemia: Epidemiol




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Pain from coronary-related ischemia is more often characterized as non-focal chest discomfort or pressure rather than pain, is generally gradual in onset, and is exacerbated by activity. Discomfort that radiates, particularly to either or both arms, should increase suspicion for ACS.
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and 'Atypical presentations' below and "Clinical features and diagnosis of coronary heart disease in women" and "Silent myocardial ischemia: Epidemiology, diagnosis, treatment, and prognosis".) <span>Pain from coronary-related ischemia is more often characterized as non-focal chest discomfort or pressure rather than pain, is generally gradual in onset, and is exacerbated by activity. Discomfort that radiates, particularly to either or both arms, should increase suspicion for ACS. IMMEDIATE EMERGENCY DEPARTMENT INTERVENTIONS — In the emergency department, patients presenting with chest pain or other symptoms possibly due to ACS (eg, dyspnea) should be rapidly eva




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If ACS is the leading diagnosis, initial assessment and interventions must be performed rapidly. The attached algorithm provides a simple approach to risk stratification while the table provides a concise outline of the immediate interventions needed to manage ST elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina (algorithm 1 and table 3).
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ning illness. (See 'Clinical presentation' below and "Evaluation of the adult with chest pain in the emergency department" and "Approach to the adult with dyspnea in the emergency department".) <span>If ACS is the leading diagnosis, initial assessment and interventions must be performed rapidly. The attached algorithm provides a simple approach to risk stratification while the table provides a concise outline of the immediate interventions needed to manage ST elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina (algorithm 1 and table 3). During the initial assessment phase, the following steps should be accomplished for any patient at significant risk for ACS: •Airway, breathing, and circulation assessed •Preliminary hi




#Diagnosis #Diagnostic #Emergency #Infarction #Infarctus #Myocarde #Myocardial #SAU #U2D

During the initial assessment phase, the following steps should be accomplished for any patient at significant risk for ACS:

• Airway, breathing, and circulation assessed

• Preliminary history and examination obtained

• 12-lead electrocardiogram (ECG) interpreted

• Resuscitation equipment brought to the bedside

• Cardiac monitor attached to patient

• Oxygen given as necessary

• Intravenous (IV) access and blood work (including high-sensitivity troponin, if available) obtained

Aspirin 162 to 325 mg given

• Nitrates given (contraindications to nitrates include severe aortic stenosis, hypertrophic cardiomyopathy, suspected right ventricular infarct, hypotension, marked bradycardia or tachycardia, and recent use of phosphodiesterase 5 inhibitor [eg, Viagra])

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tline of the immediate interventions needed to manage ST elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina (algorithm 1 and table 3). <span>During the initial assessment phase, the following steps should be accomplished for any patient at significant risk for ACS: •Airway, breathing, and circulation assessed •Preliminary history and examination obtained •12-lead electrocardiogram (ECG) interpreted •Resuscitation equipment brought to the bedside •Cardiac monitor attached to patient •Oxygen given as necessary •Intravenous (IV) access and blood work (including high-sensitivity troponin, if available) obtained •Aspirin 162 to 325 mg given •Nitrates given (contraindications to nitrates include severe aortic stenosis, hypertrophic cardiomyopathy, suspected right ventricular infarct, hypotension, marked bradycardia or tachycardia, and recent use of phosphodiesterase 5 inhibitor [eg, Viagra]) Caution should be employed in evaluating possible ACS in older adults and patients with diabetes, who are more likely to present with symptoms such as dyspnea or weakness without chest




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Large observational studies report that ECG acquisition is frequently delayed and that females are significantly less likely to be assessed within the recommended 10 minutes or to receive testing with a cardiac biomarker [2-4].
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of acute ischemia. The time for initial assessment, including ECG, and preliminary management of a patient with possible acute coronary-related ischemia is ideally 10 minutes from presentation. <span>Large observational studies report that ECG acquisition is frequently delayed and that females are significantly less likely to be assessed within the recommended 10 minutes or to receive testing with a cardiac biomarker [2-4]. ●Initial history and exam – Obtain a brief history and perform a focused physical examination. Important elements of the history include confirmation of the presenting symptoms, charact




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Initial history and exam – Obtain a brief history and perform a focused physical examination. Important elements of the history include confirmation of the presenting symptoms, characteristics of the pain, exacerbating and alleviating factors, and important associated symptoms, past history of or risk factors for cardiovascular disease, and potential contraindications to thrombolytic therapy (table 4).
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that ECG acquisition is frequently delayed and that females are significantly less likely to be assessed within the recommended 10 minutes or to receive testing with a cardiac biomarker [2-4]. ●<span>Initial history and exam – Obtain a brief history and perform a focused physical examination. Important elements of the history include confirmation of the presenting symptoms, characteristics of the pain, exacerbating and alleviating factors, and important associated symptoms, past history of or risk factors for cardiovascular disease, and potential contraindications to thrombolytic therapy (table 4). (See 'Clinical presentation' below.) The examination should include assessment of hemodynamic status and a screening neurologic examination, especially if thrombolysis is entertained as




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The history should address other potentially life-threatening, noncardiac causes of chest pain, such as acute aortic dissection, pulmonary embolism, tension pneumothorax, perforating peptic ulcer, and esophageal rupture (table 2A-B). Until the diagnosis of ACS is established, the clinician should keep these diagnoses in mind.
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ion should include assessment of hemodynamic status and a screening neurologic examination, especially if thrombolysis is entertained as a potential therapy. (See 'Physical examination' below.) <span>The history should address other potentially life-threatening, noncardiac causes of chest pain, such as acute aortic dissection, pulmonary embolism, tension pneumothorax, perforating peptic ulcer, and esophageal rupture (table 2A-B). Until the diagnosis of ACS is established, the clinician should keep these diagnoses in mind. (See "Evaluation of the adult with chest pain in the emergency department".) ●Twelve-lead electrocardiogram – A 12-lead ECG should be obtained within 10 minutes of arrival in all patien




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The initial ECG is often not diagnostic in patients with ACS. Thus, the ECG should be repeated at 15- to 30-minute intervals if the initial study is not diagnostic but the patient remains symptomatic and high clinical suspicion for ACS persists.
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dial infarction: Selecting a reperfusion strategy" and "Anticoagulant therapy in acute ST-elevation myocardial infarction" and "Acute ST-elevation myocardial infarction: Antiplatelet therapy".) <span>The initial ECG is often not diagnostic in patients with ACS. Thus, the ECG should be repeated at 15- to 30-minute intervals if the initial study is not diagnostic but the patient remains symptomatic and high clinical suspicion for ACS persists. ●Cardiac monitor – The patient should be placed on a cardiac monitor with emergency resuscitation equipment (including a defibrillator and airway equipment) nearby. ●Supplemental oxygen




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Supplemental oxygen – Supplemental oxygen should be given as necessary to maintain oxygen saturation above 90 percent.
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suspicion for ACS persists. ●Cardiac monitor – The patient should be placed on a cardiac monitor with emergency resuscitation equipment (including a defibrillator and airway equipment) nearby. ●<span>Supplemental oxygen – Supplemental oxygen should be given as necessary to maintain oxygen saturation above 90 percent. (See "Overview of the acute management of ST-elevation myocardial infarction", section on 'Therapy for specific symptoms and syndromes'.) ●Intravenous access – IV access should be estab




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Cardiac monitor – The patient should be placed on a cardiac monitor with emergency resuscitation equipment (including a defibrillator and airway equipment) nearby
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ith ACS. Thus, the ECG should be repeated at 15- to 30-minute intervals if the initial study is not diagnostic but the patient remains symptomatic and high clinical suspicion for ACS persists. ●<span>Cardiac monitor – The patient should be placed on a cardiac monitor with emergency resuscitation equipment (including a defibrillator and airway equipment) nearby. ●Supplemental oxygen – Supplemental oxygen should be given as necessary to maintain oxygen saturation above 90 percent. (See "Overview of the acute management of ST-elevation myocardia




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Aspirin – All patients with suspected ACS should be given aspirin in a dose of 162 to 325 mg to chew and swallow unless there is a compelling contraindication (eg, history of anaphylactic reaction) or it has been taken prior to presentation. Despite its well-demonstrated benefit, aspirin remains underutilized in the setting of ACS.
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f coagulopathy due to warfarin or heparin use, a history of liver disease, or a history of excessive or spontaneous bleeding [5]. (See 'Cardiac biomarkers and other laboratory testing' below.) ●<span>Aspirin – All patients with suspected ACS should be given aspirin in a dose of 162 to 325 mg to chew and swallow unless there is a compelling contraindication (eg, history of anaphylactic reaction) or it has been taken prior to presentation. Despite its well-demonstrated benefit, aspirin remains underutilized in the setting of ACS. (See "Aspirin for the secondary prevention of atherosclerotic cardiovascular disease".) ●Sublingual nitrates – In most cases of suspected ACS, sublingual nitroglycerin should be adminis




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Sublingual nitrates – In most cases of suspected ACS, sublingual nitroglycerin should be administered at a dose of 0.4 mg every five minutes for a total of three doses, after which an assessment of blood pressure and pain relief should guide the need for IV nitroglycerin.

Before this is done, all patients should be questioned about the use of phosphodiesterase-5 inhibitors, such as sildenafil (Viagra), vardenafil (Levitra), or tadalafil (Cialis); nitrates are contraindicated if these drugs have been used in the last 24 hours (or perhaps as long as 36 hours with tadalafil) because of the propensity to cause potentially severe hypotension.

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resentation. Despite its well-demonstrated benefit, aspirin remains underutilized in the setting of ACS. (See "Aspirin for the secondary prevention of atherosclerotic cardiovascular disease".) ●<span>Sublingual nitrates – In most cases of suspected ACS, sublingual nitroglycerin should be administered at a dose of 0.4 mg every five minutes for a total of three doses, after which an assessment of blood pressure and pain relief should guide the need for IV nitroglycerin. Before this is done, all patients should be questioned about the use of phosphodiesterase-5 inhibitors, such as sildenafil (Viagra), vardenafil (Levitra), or tadalafil (Cialis); nitrates are contraindicated if these drugs have been used in the last 24 hours (or perhaps as long as 36 hours with tadalafil) because of the propensity to cause potentially severe hypotension. (See "Nitrates in the management of acute coronary syndrome" and "Sexual activity in patients with cardiovascular disease", section on 'Treatment of sexual dysfunction'.) Extreme care s




#Diagnosis #Diagnostic #Emergency #Infarction #Infarctus #Myocarde #Myocardial #SAU #U2D
Pain that responds to sublingual nitroglycerin is frequently thought to have a cardiac etiology or to be due to esophageal spasm. However, pain relief with nitroglycerin in an acute care setting is not helpful in distinguishing cardiac from noncardiac chest pain [6]. In a study of 459 patients who presented to an emergency department with chest pain and were admitted to the hospital, the percentage of patients who had relief of chest pain with nitroglycerin was similar among the 141 patients with ACS and the 275 patients without active coronary disease (35 versus 41 percent experienced relief) [7]. As such, nitroglycerin administration should not be given as a diagnostic test in patients with chest pain or a presentation that is not consistent with ACS, as the response to treatment may cloud the clinical picture.
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tricle (waveform 1). In this setting, patients are dependent upon preload to maintain cardiac output, and nitrates can cause severe hypotension. (See "Right ventricular myocardial infarction".) <span>Pain that responds to sublingual nitroglycerin is frequently thought to have a cardiac etiology or to be due to esophageal spasm. However, pain relief with nitroglycerin in an acute care setting is not helpful in distinguishing cardiac from noncardiac chest pain [6]. In a study of 459 patients who presented to an emergency department with chest pain and were admitted to the hospital, the percentage of patients who had relief of chest pain with nitroglycerin was similar among the 141 patients with ACS and the 275 patients without active coronary disease (35 versus 41 percent experienced relief) [7]. As such, nitroglycerin administration should not be given as a diagnostic test in patients with chest pain or a presentation that is not consistent with ACS, as the response to treatment may cloud the clinical picture. (See "Evaluation of the adult with chest pain in the emergency department".) ●Intravenous morphine sulfate – IV morphine sulfate (initial dose of 2 to 4 mg, with increments of 2 to 8 mg




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Intravenous morphine sulfate – IV morphine sulfate (initial dose of 2 to 4 mg, with increments of 2 to 8 mg, repeated at 5- to 15-minute intervals) may be given for the relief of severe, persistent chest pain not relieved by other means but should not be given routinely. Morphine can reduce sympathetic stimulation caused by pain and anxiety, thereby decreasing cardiac workload and risks associated with excess catecholamines. However, morphine may worsen outcomes in patients with acute myocardial infarction
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ain or a presentation that is not consistent with ACS, as the response to treatment may cloud the clinical picture. (See "Evaluation of the adult with chest pain in the emergency department".) ●<span>Intravenous morphine sulfate – IV morphine sulfate (initial dose of 2 to 4 mg, with increments of 2 to 8 mg, repeated at 5- to 15-minute intervals) may be given for the relief of severe, persistent chest pain not relieved by other means but should not be given routinely. Morphine can reduce sympathetic stimulation caused by pain and anxiety, thereby decreasing cardiac workload and risks associated with excess catecholamines. However, morphine may worsen outcomes in patients with acute myocardial infarction. DETERMINING WHO NEEDS AN ELECTROCARDIOGRAM — In general, a resting electrocardiogram (ECG) should be obtained in all adults with chest discomfort that does not have an obvious noncardi




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One research group has proposed the following rule for identifying patients at high risk for ST elevation myocardial infarction (STEMI) who should be evaluated with an ECG [8]:

● Any patient over 30 with chest pain

● Any patient over 50 with any of the following: dyspnea, altered mental status, upper extremity pain, syncope, or weakness

● Any patient over 80 with abdominal pain, nausea, or vomiting

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st clear signs of ischemia in their initial ECG. Such presentations are discussed in detail separately. (See 'Atypical presentations' below and 'Importance of serial electrocardiograms' below.) <span>One research group has proposed the following rule for identifying patients at high risk for ST elevation myocardial infarction (STEMI) who should be evaluated with an ECG [8]: ●Any patient over 30 with chest pain ●Any patient over 50 with any of the following: dyspnea, altered mental status, upper extremity pain, syncope, or weakness ●Any patient over 80 with abdominal pain, nausea, or vomiting This rule was derived and validated using information from over three million emergency department visits included in a state-wide health surveillance database. Included in the database




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This proposed rule should not replace clinical judgement (in fact, the authors encourage clinicians to obtain an ECG based upon such judgement). As an example, a patient in whom a noncardiac diagnosis is likely (eg, younger patient with obvious zoster [shingles] lesions and no other symptoms) may not need an ECG.
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aset for the study. When applied to the validation sample (3294 STEMI cases), the rule had a sensitivity of 91.9 percent (95% CI 90.9-92.8) and a specificity of 76.2 percent (95% CI 76.1-76.2). <span>This proposed rule should not replace clinical judgement (in fact, the authors encourage clinicians to obtain an ECG based upon such judgement). As an example, a patient in whom a noncardiac diagnosis is likely (eg, younger patient with obvious zoster [shingles] lesions and no other symptoms) may not need an ECG. Nevertheless, this study provides some evidence for clinicians trying to devise appropriate triage protocols for the emergency department or to determine for which patients, including t




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Clinicians must be aware that the initial ECG is often not diagnostic in patients with ACS. Forty-one percent of patients with non-ST elevation myocardial infarction (NSTEMI) do not have the typical ST-depression or T-wave inversion [10]. In patients at intermediate to high risk for ACS without a clear diagnosis, ECGs should be repeated at frequent intervals until the patient's chest pain resolves or a definitive diagnosis is made.
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eparately; a focused review is provided below. (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction" and "Diagnosis of acute myocardial infarction", section on 'ECG'.) <span>Clinicians must be aware that the initial ECG is often not diagnostic in patients with ACS. Forty-one percent of patients with non-ST elevation myocardial infarction (NSTEMI) do not have the typical ST-depression or T-wave inversion [10]. In patients at intermediate to high risk for ACS without a clear diagnosis, ECGs should be repeated at frequent intervals until the patient's chest pain resolves or a definitive diagnosis is made. (See 'Importance of serial electrocardiograms' below.) When present, ECG abnormalities are an early sign of myocardial ischemia. Criteria for the two major categories of ECG manifestati




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Findings consistent with ST elevation myocardial infarction (STEMI):

• New or presumed new ST elevation at the J point in two anatomically contiguous leads using the following diagnostic thresholds:

≥0.1 mV (1 mm) in all leads other than V2 to V3, where the following diagnostic thresholds apply:

- ≥0.2 mV (2 mm) in males ≥ 40 years

- ≥0.25 mV (2.5 mm) in males <40 years

- ≥0.15 mV (1.5 mm) in females

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ams' below.) When present, ECG abnormalities are an early sign of myocardial ischemia. Criteria for the two major categories of ECG manifestations of acute myocardial ischemia are listed here: ●<span>Findings consistent with ST elevation myocardial infarction (STEMI): •New or presumed new ST elevation at the J point in two anatomically contiguous leads using the following diagnostic thresholds: ≥0.1 mV (1 mm) in all leads other than V2 to V3, where the following diagnostic thresholds apply: -≥0.2 mV (2 mm) in males ≥ 40 years -≥0.25 mV (2.5 mm) in males <40 years -≥0.15 mV (1.5 mm) in females ●Findings consistent with NSTEMI: •New or presumed new horizontal or down-sloping ST depression ≥0.05 mV (0.5 mm) in two anatomically contiguous leads and/or •T wave inversion ≥0.1 mV (




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Findings consistent with NSTEMI:

• New or presumed new horizontal or down-sloping ST depression ≥0.05 mV (0.5 mm) in two anatomically contiguous leads

and/or

• T wave inversion ≥0.1 mV (1 mm) in two anatomically contiguous leads with prominent R wave or R/S ratio >1

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m) in all leads other than V2 to V3, where the following diagnostic thresholds apply: -≥0.2 mV (2 mm) in males ≥ 40 years -≥0.25 mV (2.5 mm) in males <40 years -≥0.15 mV (1.5 mm) in females ●<span>Findings consistent with NSTEMI: •New or presumed new horizontal or down-sloping ST depression ≥0.05 mV (0.5 mm) in two anatomically contiguous leads and/or •T wave inversion ≥0.1 mV (1 mm) in two anatomically contiguous leads with prominent R wave or R/S ratio >1 Localization of ischemia — The ECG leads are more helpful in localizing regions of transmural than subendocardial ischemia. The anatomic location of a transmural infarct is determined b




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The anatomic location of a transmural infarct is determined by which ECG leads show ST elevation and/or increased T wave positivity:

Anterior wall ischemia – Two or more of the precordial leads (V1 to V6) (waveform 2A-B)

Anteroseptal ischemia – Leads V1 to V3 (waveform 3 and waveform 4)

Apical or lateral ischemia – Leads aVL and I, and leads V4 to V6 (waveform 5 and waveform 6)

Inferior wall ischemia – Leads II, III, and aVF (waveform 1)

Right ventricular ischemia – Right-sided precordial leads (waveform 1)

Posterior wall ischemia – Septal precordial leads (V1 to V2) (waveform 7) and posterior precordial leads (waveform 8)

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natomically contiguous leads with prominent R wave or R/S ratio >1 Localization of ischemia — The ECG leads are more helpful in localizing regions of transmural than subendocardial ischemia. <span>The anatomic location of a transmural infarct is determined by which ECG leads show ST elevation and/or increased T wave positivity: ●Anterior wall ischemia – Two or more of the precordial leads (V1 to V6) (waveform 2A-B) ●Anteroseptal ischemia – Leads V1 to V3 (waveform 3 and waveform 4) ●Apical or lateral ischemia – Leads aVL and I, and leads V4 to V6 (waveform 5 and waveform 6) ●Inferior wall ischemia – Leads II, III, and aVF (waveform 1) ●Right ventricular ischemia – Right-sided precordial leads (waveform 1) ●Posterior wall ischemia – Septal precordial leads (V1 to V2) (waveform 7) and posterior precordial leads (waveform 8) The right-sided leads V4R, V5R, and V6R (figure 1) should be obtained if there is evidence of inferior wall ischemia demonstrated by ST elevation in leads II, III, and aVF. The posterio




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The right-sided leads V4R, V5R, and V6R (figure 1) should be obtained if there is evidence of inferior wall ischemia demonstrated by ST elevation in leads II, III, and aVF.
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1) ●Right ventricular ischemia – Right-sided precordial leads (waveform 1) ●Posterior wall ischemia – Septal precordial leads (V1 to V2) (waveform 7) and posterior precordial leads (waveform 8) <span>The right-sided leads V4R, V5R, and V6R (figure 1) should be obtained if there is evidence of inferior wall ischemia demonstrated by ST elevation in leads II, III, and aVF. The posterior leads V7, V8, and V9 (figure 2) may also be helpful if there is evidence of posterior wall ischemia as suggested by prominent R waves and ST depressions in leads V1 and V2




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The posterior leads V7, V8, and V9 (figure 2) may also be helpful if there is evidence of posterior wall ischemia as suggested by prominent R waves and ST depressions in leads V1 and V2.
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l leads (waveform 8) The right-sided leads V4R, V5R, and V6R (figure 1) should be obtained if there is evidence of inferior wall ischemia demonstrated by ST elevation in leads II, III, and aVF. <span>The posterior leads V7, V8, and V9 (figure 2) may also be helpful if there is evidence of posterior wall ischemia as suggested by prominent R waves and ST depressions in leads V1 and V2. Importance of serial electrocardiograms — If the initial ECG is not diagnostic but the patient remains symptomatic and clinical suspicion for ACS remains high, the ECG should be repeate




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If the initial ECG is not diagnostic but the patient remains symptomatic and clinical suspicion for ACS remains high, the ECG should be repeated at least every 15 to 30 minutes.
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(figure 2) may also be helpful if there is evidence of posterior wall ischemia as suggested by prominent R waves and ST depressions in leads V1 and V2. Importance of serial electrocardiograms — <span>If the initial ECG is not diagnostic but the patient remains symptomatic and clinical suspicion for ACS remains high, the ECG should be repeated at least every 15 to 30 minutes. Patients whose repeat ECGs are diagnostic for or strongly suggestive of either STEMI or NSTEMI should be managed for those diagnoses. (See "Overview of the acute management of ST-elevat




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The initial ECG is often not diagnostic in patients with ACS. In two series, the initial ECG was nondiagnostic in 45 percent and normal in 20 percent of patients subsequently shown to have an acute myocardial infarction [1,11].
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managed for those diagnoses. (See "Overview of the acute management of ST-elevation myocardial infarction" and "Overview of the acute management of non-ST elevation acute coronary syndromes".) <span>The initial ECG is often not diagnostic in patients with ACS. In two series, the initial ECG was nondiagnostic in 45 percent and normal in 20 percent of patients subsequently shown to have an acute myocardial infarction [1,11]. In the early hours of infarction, peaked, hyperacute T waves may be the only abnormality. In addition to evolution of the ECG, an uncommon source of error is pseudonormalization of base




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In the early hours of infarction, peaked, hyperacute T waves may be the only abnormality. In addition to evolution of the ECG, an uncommon source of error is pseudonormalization of baseline T wave inversion [ 12].
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ostic in patients with ACS. In two series, the initial ECG was nondiagnostic in 45 percent and normal in 20 percent of patients subsequently shown to have an acute myocardial infarction [1,11]. <span>In the early hours of infarction, peaked, hyperacute T waves may be the only abnormality. In addition to evolution of the ECG, an uncommon source of error is pseudonormalization of baseline T wave inversion [12]. Some clinicians assume that an ECG obtained while the patient is experiencing chest pain that fails to show evidence of ischemia rules out the possibility of ACS. This assumption is fal




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Some clinicians assume that an ECG obtained while the patient is experiencing chest pain that fails to show evidence of ischemia rules out the possibility of ACS. This assumption is false, as demonstrated by two prospective observational studies [13,14].
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of infarction, peaked, hyperacute T waves may be the only abnormality. In addition to evolution of the ECG, an uncommon source of error is pseudonormalization of baseline T wave inversion [12]. <span>Some clinicians assume that an ECG obtained while the patient is experiencing chest pain that fails to show evidence of ischemia rules out the possibility of ACS. This assumption is false, as demonstrated by two prospective observational studies [13,14]. Left bundle branch block or pacemaker — Both left bundle branch block (LBBB) (waveform 9 and waveform 10), which is present in approximately 7 percent of patients with an acute myocardi




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Ischemic pain has a number of features that tend to distinguish it from noncardiac pain. These characteristics are described below using the OPQRST mnemonic
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esent with symptoms such as dyspnea, weakness, nausea and vomiting, palpitations, and syncope, and may not manifest chest discomfort. (See 'Atypical presentations' below.) Ischemic chest pain — <span>Ischemic pain has a number of features that tend to distinguish it from noncardiac pain. These characteristics are described below using the OPQRST mnemonic. Symptoms associated with the highest relative risk of myocardial infarction include radiation to an upper extremity, particularly when there is radiation to both arms, and pain associa




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Symptoms associated with the highest relative risk of myocardial infarction include radiation to an upper extremity, particularly when there is radiation to both arms, and pain associated with diaphoresis or with nausea and vomiting [ 19-21].
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ions' below.) Ischemic chest pain — Ischemic pain has a number of features that tend to distinguish it from noncardiac pain. These characteristics are described below using the OPQRST mnemonic. <span>Symptoms associated with the highest relative risk of myocardial infarction include radiation to an upper extremity, particularly when there is radiation to both arms, and pain associated with diaphoresis or with nausea and vomiting [19-21]. An important question is whether current pain is reminiscent of prior myocardial infarction. Of note, no one pain characteristic has sufficient positive or negative predictive value to




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An important question is whether current pain is reminiscent of prior myocardial infarction. Of note, no one pain characteristic has sufficient positive or negative predictive value to definitively diagnose or exclude ACS
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sk of myocardial infarction include radiation to an upper extremity, particularly when there is radiation to both arms, and pain associated with diaphoresis or with nausea and vomiting [19-21]. <span>An important question is whether current pain is reminiscent of prior myocardial infarction. Of note, no one pain characteristic has sufficient positive or negative predictive value to definitively diagnose or exclude ACS. ●Onset – Ischemic pain is typically gradual in onset, although the intensity of the discomfort may wax and wane. ●Provocation and palliation – Ischemic pain is generally provoked by an




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Onset – Ischemic pain is typically gradual in onset, although the intensity of the discomfort may wax and wane.
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er current pain is reminiscent of prior myocardial infarction. Of note, no one pain characteristic has sufficient positive or negative predictive value to definitively diagnose or exclude ACS. ●<span>Onset – Ischemic pain is typically gradual in onset, although the intensity of the discomfort may wax and wane. ●Provocation and palliation – Ischemic pain is generally provoked by an activity, such as exercise, that increases cardiac oxygen demand [20,22]. Ischemic pain does not change with resp




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Provocation and palliation – Ischemic pain is generally provoked by an activity, such as exercise, that increases cardiac oxygen demand [20,22]. Ischemic pain does not change with respiration or position. It may or may not respond to nitroglycerin and, if there is improvement, this may only be temporary. Relief of pain following the administration of therapeutic interventions (eg, nitroglycerin, "gastrointestinal cocktail" of viscous lidocaine and antacid) does not reliably distinguish nonischemic from ischemic chest pain [23-25].
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positive or negative predictive value to definitively diagnose or exclude ACS. ●Onset – Ischemic pain is typically gradual in onset, although the intensity of the discomfort may wax and wane. ●<span>Provocation and palliation – Ischemic pain is generally provoked by an activity, such as exercise, that increases cardiac oxygen demand [20,22]. Ischemic pain does not change with respiration or position. It may or may not respond to nitroglycerin and, if there is improvement, this may only be temporary. Relief of pain following the administration of therapeutic interventions (eg, nitroglycerin, "gastrointestinal cocktail" of viscous lidocaine and antacid) does not reliably distinguish nonischemic from ischemic chest pain [23-25]. ●Quality – Ischemic pain is often characterized more as a discomfort than pain, and it may be difficult for the patient to describe. Terms frequently used by patients include squeezing,




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Quality – Ischemic pain is often characterized more as a discomfort than pain, and it may be difficult for the patient to describe. Terms frequently used by patients include squeezing, tightness, pressure, constriction, crushing, strangling, burning, heartburn, fullness in the chest, band-like sensation, knot in the center of the chest, lump in throat, ache, heavy weight on chest (elephant sitting on chest), like a bra too tight, and toothache (when there is radiation to the lower jaw). It is generally not described as sharp, fleeting, knife-like, stabbing, or like "pins and needles" [20].
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ation of therapeutic interventions (eg, nitroglycerin, "gastrointestinal cocktail" of viscous lidocaine and antacid) does not reliably distinguish nonischemic from ischemic chest pain [23-25]. ●<span>Quality – Ischemic pain is often characterized more as a discomfort than pain, and it may be difficult for the patient to describe. Terms frequently used by patients include squeezing, tightness, pressure, constriction, crushing, strangling, burning, heartburn, fullness in the chest, band-like sensation, knot in the center of the chest, lump in throat, ache, heavy weight on chest (elephant sitting on chest), like a bra too tight, and toothache (when there is radiation to the lower jaw). It is generally not described as sharp, fleeting, knife-like, stabbing, or like "pins and needles" [20]. Increased pain severity does not appear to correlate with an increased likelihood of acute myocardial infarction [26]. In some cases, the patient cannot qualify the nature of the discom




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Increased pain severity does not appear to correlate with an increased likelihood of acute myocardial infarction [26].
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chest), like a bra too tight, and toothache (when there is radiation to the lower jaw). It is generally not described as sharp, fleeting, knife-like, stabbing, or like "pins and needles" [20]. <span>Increased pain severity does not appear to correlate with an increased likelihood of acute myocardial infarction [26]. In some cases, the patient cannot qualify the nature of the discomfort but places his or her clenched fist in the center of the chest, known as the "Levine sign." ●Radiation – Ischemic




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In some cases, the patient cannot qualify the nature of the discomfort but places his or her clenched fist in the center of the chest, known as the "Levine sign."
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as sharp, fleeting, knife-like, stabbing, or like "pins and needles" [20]. Increased pain severity does not appear to correlate with an increased likelihood of acute myocardial infarction [26]. <span>In some cases, the patient cannot qualify the nature of the discomfort but places his or her clenched fist in the center of the chest, known as the "Levine sign." ●Radiation – Ischemic pain often radiates to other parts of the body including the upper abdomen (epigastrium), shoulders, arms (upper and forearm), wrist, fingers, neck and throat, low




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Radiation – Ischemic pain often radiates to other parts of the body including the upper abdomen (epigastrium), shoulders, arms (upper and forearm), wrist, fingers, neck and throat, lower jaw and teeth (but not upper jaw), and not infrequently to the back (specifically the interscapular region). The old dictum that "pain above the nose or below the navel is rarely cardiac in origin" still holds. Pain radiating to the upper extremities is highly suggestive of ischemic pain [19,20,22,27].
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e myocardial infarction [26]. In some cases, the patient cannot qualify the nature of the discomfort but places his or her clenched fist in the center of the chest, known as the "Levine sign." ●<span>Radiation – Ischemic pain often radiates to other parts of the body including the upper abdomen (epigastrium), shoulders, arms (upper and forearm), wrist, fingers, neck and throat, lower jaw and teeth (but not upper jaw), and not infrequently to the back (specifically the interscapular region). The old dictum that "pain above the nose or below the navel is rarely cardiac in origin" still holds. Pain radiating to the upper extremities is highly suggestive of ischemic pain [19,20,22,27]. ●Site – Ischemic pain is not felt in one specific spot; rather, it is a diffuse discomfort that may be difficult to localize. The patient often indicates the entire chest, rather than l




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Site – Ischemic pain is not felt in one specific spot; rather, it is a diffuse discomfort that may be difficult to localize. The patient often indicates the entire chest, rather than localizing it to a specific area by pointing a single finger.
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e old dictum that "pain above the nose or below the navel is rarely cardiac in origin" still holds. Pain radiating to the upper extremities is highly suggestive of ischemic pain [19,20,22,27]. ●<span>Site – Ischemic pain is not felt in one specific spot; rather, it is a diffuse discomfort that may be difficult to localize. The patient often indicates the entire chest, rather than localizing it to a specific area by pointing a single finger. ●Time course – Angina is usually brief (two to five minutes) and is relieved by rest or with nitroglycerin. In comparison, patients with an ACS may have chest pain at rest, and the dura




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Time course – Angina is usually brief (two to five minutes) and is relieved by rest or with nitroglycerin. In comparison, patients with an ACS may have chest pain at rest, and the duration is variable but generally lasts longer than 30 minutes. Classic anginal pain lasting more than 20 minutes suggests ACS. Continuous pain that does not wax and wane and persists for over 24 hours is unlikely to be due to ACS [28].
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t; rather, it is a diffuse discomfort that may be difficult to localize. The patient often indicates the entire chest, rather than localizing it to a specific area by pointing a single finger. ●<span>Time course – Angina is usually brief (two to five minutes) and is relieved by rest or with nitroglycerin. In comparison, patients with an ACS may have chest pain at rest, and the duration is variable but generally lasts longer than 30 minutes. Classic anginal pain lasting more than 20 minutes suggests ACS. Continuous pain that does not wax and wane and persists for over 24 hours is unlikely to be due to ACS [28]. Historical features increasing likelihood of ACS — Historical features that increase the likelihood of ACS include the following: ●Patients with a prior history of ACS have a significan




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Historical features that increase the likelihood of ACS include the following:

● Patients with a prior history of ACS have a significantly increased risk of recurrent ischemic events.

● A prior history of other vascular disease is associated with a risk of cardiac ischemic events comparable to that seen with a prior history of ACS.

● Risk factors for ACS, particularly age, male sex, diabetes, hypertension, dyslipidemia, and cigarette smoking [29]. (See "Overview of established risk factors for cardiovascular disease".)

● Recent use of cocaine or other sympathomimetic drugs (eg, methamphetamine).

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ore than 20 minutes suggests ACS. Continuous pain that does not wax and wane and persists for over 24 hours is unlikely to be due to ACS [28]. Historical features increasing likelihood of ACS — <span>Historical features that increase the likelihood of ACS include the following: ●Patients with a prior history of ACS have a significantly increased risk of recurrent ischemic events. ●A prior history of other vascular disease is associated with a risk of cardiac ischemic events comparable to that seen with a prior history of ACS. ●Risk factors for ACS, particularly age, male sex, diabetes, hypertension, dyslipidemia, and cigarette smoking [29]. (See "Overview of established risk factors for cardiovascular disease".) ●Recent use of cocaine or other sympathomimetic drugs (eg, methamphetamine). (See "Clinical manifestations, diagnosis, and management of the cardiovascular complications of cocaine abuse".) Associated symptoms — Ischemic pain is often associated with other sympt




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Ischemic pain is often associated with other symptoms. The most common is shortness of breath, which may reflect mild pulmonary congestion resulting from ischemia-mediated diastolic dysfunction. Other symptoms may include belching, nausea, indigestion, vomiting, diaphoresis, dizziness, lightheadedness, clamminess, and fatigue
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aine or other sympathomimetic drugs (eg, methamphetamine). (See "Clinical manifestations, diagnosis, and management of the cardiovascular complications of cocaine abuse".) Associated symptoms — <span>Ischemic pain is often associated with other symptoms. The most common is shortness of breath, which may reflect mild pulmonary congestion resulting from ischemia-mediated diastolic dysfunction. Other symptoms may include belching, nausea, indigestion, vomiting, diaphoresis, dizziness, lightheadedness, clamminess, and fatigue. Noncardiac chest pain — Specific chest pain characteristics can be used to help differentiate cardiac from noncardiac causes. (See "Evaluation of the adult with chest pain in the emerg




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Systematic reviews have identified the following characteristics as more typical of nonischemic chest discomfort [19]:

● Pleuritic pain, sharp or knife-like pain related to respiratory movements or cough

● Primary or sole location in the mid or lower abdominal region

● Any discomfort localized with one finger

● Any discomfort reproduced by movement or palpation

● Constant pain lasting for days

● Fleeting pains lasting for a few seconds or less

● Pain radiating into the lower extremities or above the mandible

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c chest pain — Specific chest pain characteristics can be used to help differentiate cardiac from noncardiac causes. (See "Evaluation of the adult with chest pain in the emergency department".) <span>Systematic reviews have identified the following characteristics as more typical of nonischemic chest discomfort [19]: ●Pleuritic pain, sharp or knife-like pain related to respiratory movements or cough ●Primary or sole location in the mid or lower abdominal region ●Any discomfort localized with one finger ●Any discomfort reproduced by movement or palpation ●Constant pain lasting for days ●Fleeting pains lasting for a few seconds or less ●Pain radiating into the lower extremities or above the mandible However, some patients with ACS present with so-called "atypical" chest pain. This was illustrated in the Multicenter Chest Pain Study in which acute ischemia was diagnosed in 22 percen




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However, some patients with ACS present with so-called "atypical" chest pain. This was illustrated in the Multicenter Chest Pain Study in which acute ischemia was diagnosed in 22 percent of patients who presented with sharp or stabbing pain and 13 percent who presented with pleuritic-type pain [30].
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discomfort reproduced by movement or palpation ●Constant pain lasting for days ●Fleeting pains lasting for a few seconds or less ●Pain radiating into the lower extremities or above the mandible <span>However, some patients with ACS present with so-called "atypical" chest pain. This was illustrated in the Multicenter Chest Pain Study in which acute ischemia was diagnosed in 22 percent of patients who presented with sharp or stabbing pain and 13 percent who presented with pleuritic-type pain [30]. (See 'Atypical presentations' below.) In addition, some patients who appear to have a noncardiac cause of chest pain have other serious conditions including acute aortic dissection, pul




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In a review of over 430,000 patients with confirmed acute myocardial infarction from the National Registry of Myocardial Infarction II, one-third had no chest pain on presentation to the hospital [31]. These patients often present with symptoms such as dyspnea alone, weakness, nausea and/or vomiting, epigastric pain or discomfort, palpitations, syncope, or cardiac arrest. They are more likely to be older or have diabetes [20,31-33].
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tion of antiplatelet, anticoagulant, or thrombolytic therapy to a patient with an aortic dissection. ATYPICAL PRESENTATIONS — Some patients with ACS present with symptoms other than chest pain. <span>In a review of over 430,000 patients with confirmed acute myocardial infarction from the National Registry of Myocardial Infarction II, one-third had no chest pain on presentation to the hospital [31]. These patients often present with symptoms such as dyspnea alone, weakness, nausea and/or vomiting, epigastric pain or discomfort, palpitations, syncope, or cardiac arrest. They are more likely to be older or have diabetes [20,31-33]. (See "Clinical features and diagnosis of coronary heart disease in women", section on 'Clinical presentation' and "Prevalence of and risk factors for coronary heart disease in patients




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Focused neurologic examination – A screening neurologic examination should be performed to assess for focal lesions or cognitive deficits that might preclude safe use of thrombolytic therapy (table 4).
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ng upon the severity of the heart failure and the presence of other risk factors (table 7 and table 6) [34]. (See "Treatment of acute decompensated heart failure in acute coronary syndromes".) ●<span>Focused neurologic examination – A screening neurologic examination should be performed to assess for focal lesions or cognitive deficits that might preclude safe use of thrombolytic therapy (table 4). (See "Acute ST-elevation myocardial infarction: The use of fibrinolytic therapy".) The cardiac and general physical examinations of patients with possible ACS are reviewed in greater de




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Anemia can exacerbate myocardial ischemia, and patients with a low hemoglobin may require blood transfusion. Transfusion thresholds and implementation are reviewed separately. (See "Indications and hemoglobin thresholds for red blood cell transfusion in the adult", section on 'ACS (including MI)'.)
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absence of an acute coronary syndrome".) Basic electrolyte concentrations, kidney function studies, and a complete blood count with platelets should be obtained in patients with suspected ACS. <span>Anemia can exacerbate myocardial ischemia, and patients with a low hemoglobin may require blood transfusion. Transfusion thresholds and implementation are reviewed separately. (See "Indications and hemoglobin thresholds for red blood cell transfusion in the adult", section on 'ACS (including MI)'.) Indices of coagulation should be obtained in patients at increased risk of coagulopathy due to warfarin or heparin use, a history of liver disease, or a history of excessive or spontane




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Indices of coagulation should be obtained in patients at increased risk of coagulopathy due to warfarin or heparin use, a history of liver disease, or a history of excessive or spontaneous bleeding.
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n. Transfusion thresholds and implementation are reviewed separately. (See "Indications and hemoglobin thresholds for red blood cell transfusion in the adult", section on 'ACS (including MI)'.) <span>Indices of coagulation should be obtained in patients at increased risk of coagulopathy due to warfarin or heparin use, a history of liver disease, or a history of excessive or spontaneous bleeding. Additional laboratory testing is obtained depending on clinical circumstances, including patient comorbidities. MANAGEMENT ST elevation — The management of patients who meet the criteri




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The management of patients who meet the criteria for ST elevation myocardial infarction (STEMI) is discussed separately. The accompanying table provides a concise summary of the immediate treatment interventions needed in these patients (table 3).
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ase, or a history of excessive or spontaneous bleeding. Additional laboratory testing is obtained depending on clinical circumstances, including patient comorbidities. MANAGEMENT ST elevation — <span>The management of patients who meet the criteria for ST elevation myocardial infarction (STEMI) is discussed separately. The accompanying table provides a concise summary of the immediate treatment interventions needed in these patients (table 3). (See 'Electrocardiogram assessment' above and "Overview of the acute management of ST-elevation myocardial infarction".) Selection and implementation of the optimal reperfusion strategy




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Selection and implementation of the optimal reperfusion strategy is the most important step in the management of STEMI and is discussed separately. Reperfusion therapy, whether percutaneous coronary intervention (PCI) or thrombolytics, should not await the result of cardiac biomarker measurement.
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he immediate treatment interventions needed in these patients (table 3). (See 'Electrocardiogram assessment' above and "Overview of the acute management of ST-elevation myocardial infarction".) <span>Selection and implementation of the optimal reperfusion strategy is the most important step in the management of STEMI and is discussed separately. Reperfusion therapy, whether percutaneous coronary intervention (PCI) or thrombolytics, should not await the result of cardiac biomarker measurement. (See "Acute ST-elevation myocardial infarction: Selecting a reperfusion strategy" and "Primary percutaneous coronary intervention in acute ST elevation myocardial infarction: Determinan




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Unstable angina and NSTEMI comprise part of the spectrum of ACS. Angina is considered unstable if it presents in any of the following three ways:

● Rest angina, generally lasting longer than 20 minutes

● New-onset angina that markedly limits physical activity

● Increasing angina that is more frequent, lasts longer, or occurs with less exertion than previous angina

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diate treatment interventions needed in these patients (table 3). (See 'Electrocardiogram assessment' above and "Overview of the acute management of non-ST elevation acute coronary syndromes".) <span>Unstable angina and NSTEMI comprise part of the spectrum of ACS. Angina is considered unstable if it presents in any of the following three ways: ●Rest angina, generally lasting longer than 20 minutes ●New-onset angina that markedly limits physical activity ●Increasing angina that is more frequent, lasts longer, or occurs with less exertion than previous angina NSTEMI is distinguished from unstable angina by the presence of elevated serum biomarkers. ST segment elevations and Q waves are absent in both unstable angina and NSTEMI. As a result,




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NSTEMI is distinguished from unstable angina by the presence of elevated serum biomarkers. ST segment elevations and Q waves are absent in both unstable angina and NSTEMI. As a result, unstable angina and NSTEMI can be indistinguishable at initial evaluation since an elevation in serum biomarkers may not be detectable for two to four hours after a myocardial infarction with contemporary troponin assays and one to three hours with high-sensitivity assays, and at least 12 hours are required to detect elevations in all patients.
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lasting longer than 20 minutes ●New-onset angina that markedly limits physical activity ●Increasing angina that is more frequent, lasts longer, or occurs with less exertion than previous angina <span>NSTEMI is distinguished from unstable angina by the presence of elevated serum biomarkers. ST segment elevations and Q waves are absent in both unstable angina and NSTEMI. As a result, unstable angina and NSTEMI can be indistinguishable at initial evaluation since an elevation in serum biomarkers may not be detectable for two to four hours after a myocardial infarction with contemporary troponin assays and one to three hours with high-sensitivity assays, and at least 12 hours are required to detect elevations in all patients. (See 'Cardiac biomarkers and other laboratory testing' above and "Acute coronary syndrome: Terminology and classification".) Thrombolytic therapy should not be administered to patients




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Thrombolytic therapy should not be administered to patients with unstable angina or NSTEMI unless subsequent ECG monitoring documents ST segment elevations that persist. Repeat ECGs are an essential part of management in these patients.
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at least 12 hours are required to detect elevations in all patients. (See 'Cardiac biomarkers and other laboratory testing' above and "Acute coronary syndrome: Terminology and classification".) <span>Thrombolytic therapy should not be administered to patients with unstable angina or NSTEMI unless subsequent ECG monitoring documents ST segment elevations that persist. Repeat ECGs are an essential part of management in these patients. (See "Overview of the acute management of non-ST elevation acute coronary syndromes" and 'Importance of serial electrocardiograms' above.) An aggressive approach to reperfusion using PC




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● Sustained ventricular tachyarrhythmias in the peri-infarction period must be treated immediately because of their deleterious effect on cardiac output, possible exacerbation of myocardial ischemia, and the risk of deterioration into ventricular fibrillation (algorithm 2). (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features".)

● While supraventricular tachyarrhythmias in the peri-infarction period may pose less immediate risk of cardiac arrest, the management of such arrhythmias is important because any tachycardia can increase myocardial oxygen demand, thereby exacerbating ischemia and possibly decreasing cardiac output (algorithm 4). (See "Supraventricular arrhythmias after myocardial infarction".)

● Bradyarrhythmias occurring early in the setting of an inferior wall myocardial infarction (within the first 24 hours) may respond to treatment with atropine (algorithm 3). Later bradyarrhythmias, wide QRS-complex bradyarrhythmias, and those occurring in the setting of an anterior wall myocardial infarction may require temporary pacemaker placement. (See "Conduction abnormalities after myocardial infarction".)

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ols'.) Cardiac arrhythmias during ACS — Disturbances of cardiac rhythm during a myocardial infarction are usually detected by cardiac monitor rather than by physical examination or 12-lead ECG: <span>●Sustained ventricular tachyarrhythmias in the peri-infarction period must be treated immediately because of their deleterious effect on cardiac output, possible exacerbation of myocardial ischemia, and the risk of deterioration into ventricular fibrillation (algorithm 2). (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features".) ●While supraventricular tachyarrhythmias in the peri-infarction period may pose less immediate risk of cardiac arrest, the management of such arrhythmias is important because any tachycardia can increase myocardial oxygen demand, thereby exacerbating ischemia and possibly decreasing cardiac output (algorithm 4). (See "Supraventricular arrhythmias after myocardial infarction".) ●Bradyarrhythmias occurring early in the setting of an inferior wall myocardial infarction (within the first 24 hours) may respond to treatment with atropine (algorithm 3). Later bradyarrhythmias, wide QRS-complex bradyarrhythmias, and those occurring in the setting of an anterior wall myocardial infarction may require temporary pacemaker placement. (See "Conduction abnormalities after myocardial infarction".) Disposition of patient without STEMI — For patients without STEMI, the ECG remains a critical component in determining risk for adverse outcomes in ACS. The patient's hemodynamic status




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The patient is at high risk for ACS if ST segment depression (≥0.05 mV [0.5 mm]) is present in two or more contiguous leads or serum biomarkers are elevated. A high score on a validated ACS risk stratification tool suggests the patient is at high risk. Such scores include the HEART Score (table 8) and EDACS Score [37].
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for any case in which the diagnosis or treatment plan are unclear. The utility of epidemiologic risk factors in determining acute, individual risk has been questioned [36]. High-risk patient — <span>The patient is at high risk for ACS if ST segment depression (≥0.05 mV [0.5 mm]) is present in two or more contiguous leads or serum biomarkers are elevated. A high score on a validated ACS risk stratification tool suggests the patient is at high risk. Such scores include the HEART Score (table 8) and EDACS Score [37]. (See "Risk stratification after non-ST elevation acute coronary syndrome", section on 'Very high-risk patients' and "Risk stratification after non-ST elevation acute coronary syndrome",




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Low- and moderate-risk patient — The management, including methods for risk assessment, of patients who have no ECG changes and normal serum biomarkers but are still considered to be at low or moderate risk for ACS is discussed separately.
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y department course should be admitted and considered for early PCI. (See "Overview of the acute management of non-ST elevation acute coronary syndromes", section on 'Early revascularization'.) <span>Low- and moderate-risk patient — The management, including methods for risk assessment, of patients who have no ECG changes and normal serum biomarkers but are still considered to be at low or moderate risk for ACS is discussed separately. (See "Evaluation of emergency department patients with chest pain at low or intermediate risk for acute coronary syndrome".) IMPACT OF MISSED DIAGNOSIS — With careful evaluation using e




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With careful evaluation using effective risk scores, serial electrocardiograms (ECGs), and appropriate diagnostic testing, only a very small percentage of patients with an ACS are mistakenly discharged from the emergency department [38,39]. However, patients whose diagnosis is missed initially have an increase in short-term mortality [32,38,40,41]
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e risk for ACS is discussed separately. (See "Evaluation of emergency department patients with chest pain at low or intermediate risk for acute coronary syndrome".) IMPACT OF MISSED DIAGNOSIS — <span>With careful evaluation using effective risk scores, serial electrocardiograms (ECGs), and appropriate diagnostic testing, only a very small percentage of patients with an ACS are mistakenly discharged from the emergency department [38,39]. However, patients whose diagnosis is missed initially have an increase in short-term mortality [32,38,40,41]. This issue was evaluated in a review of 10,689 Black, White, and Hispanic American patients who presented to the emergency department with symptoms suggesting acute coronary-related is




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The patients with missed myocardial infarction had the following characteristics:

● Females less than 55 years of age

● Not White Americans

● Shortness of breath as the major presenting symptom

● Normal or nondiagnostic ECG

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nt had unstable angina [32]. Among the patients with an ACS, 2.2 percent were mistakenly discharged from the emergency department. Atypical presentation most frequently led to missed diagnosis. <span>The patients with missed myocardial infarction had the following characteristics: ●Females less than 55 years of age ●Not White Americans ●Shortness of breath as the major presenting symptom ●Normal or nondiagnostic ECG Misreading of the ECG was an infrequent problem. There was a nonsignificant trend toward an increased risk-adjusted 30-day mortality ratio for patients who were not hospitalized (1.9 an




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Angina pectoris, or angina for short, is the term used when chest discomfort is thought to be attributable to myocardial ischemia.
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current through: Jun 2022. | This topic last updated: Feb 09, 2021. INTRODUCTION — Myocardial ischemia is one of the more common causes of chest pain (also termed "chest discomfort") in adults. <span>Angina pectoris, or angina for short, is the term used when chest discomfort is thought to be attributable to myocardial ischemia. In patients with myocardial ischemia, chest discomfort is often but not always present, although other associated symptoms with ischemia may be present (such as exertional shortness of




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Myocardial ischemia in the absence of chest discomfort or another anginal equivalent symptoms is termed "silent ischemia."
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lways present, although other associated symptoms with ischemia may be present (such as exertional shortness of breath, nausea, diaphoresis, fatigue). This has been termed "anginal equivalent." <span>Myocardial ischemia in the absence of chest discomfort or another anginal equivalent symptoms is termed "silent ischemia." (See "Silent myocardial ischemia: Epidemiology, diagnosis, treatment, and prognosis".) For patients with suspected myocardial ischemia, timely diagnosis and treatment is necessary to tr




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Myocardial ischemia can occur due to fixed epicardial coronary artery ("macrovascular") obstruction, coronary microvascular obstruction (ischemia with no obstructive coronary artery disease [INOCA]), or coronary artery spasm.
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ion, or ST-elevation myocardial infarction). (See "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department".) <span>Myocardial ischemia can occur due to fixed epicardial coronary artery ("macrovascular") obstruction, coronary microvascular obstruction (ischemia with no obstructive coronary artery disease [INOCA]), or coronary artery spasm. (See "Microvascular angina: Angina pectoris with normal coronary arteries" and "Vasospastic angina" and "Chronic coronary syndrome: Overview of care", section on 'Introduction'.) This t




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Myocardial oxygen demand — There are four major factors that determine myocardial work and therefore myocardial oxygen demand:

● Heart rate

● Systolic blood pressure (the clinical marker of afterload)

● Myocardial wall tension or stress (the product of ventricular end-diastolic volume or preload and myocardial muscle mass)

● Myocardial contractility

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ntly angina, occurs when myocardial oxygen demand exceeds oxygen supply (table 1). Detailed reviews of the pathophysiology of myocardial ischemia are available in the scientific literature [1]. <span>Myocardial oxygen demand — There are four major factors that determine myocardial work and therefore myocardial oxygen demand: ●Heart rate ●Systolic blood pressure (the clinical marker of afterload) ●Myocardial wall tension or stress (the product of ventricular end-diastolic volume or preload and myocardial muscle mass) ●Myocardial contractility Myocardial contractility and wall stress cannot be measured clinically. As a result, myocardial oxygen demands are estimated clinically by the multiplication product (also called the do




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Myocardial oxygen supply — The major determinants of oxygen supply are the oxygen carrying capacity of the blood, which is affected by a variety of factors including oxygen tension and the hemoglobin concentration; the degree of oxygen unloading from hemoglobin to the tissues, which is related to 2,3 diphosphoglycerate levels; and the coronary artery blood flow delivered to the myocardium. The latter is influenced by:

● Coronary artery diameter and tone (resistance) [2,3].

● Collateral blood flow.

● Perfusion pressure. This is determined by the pressure gradients from the aorta to the coronary arteries. Coronary blood flow from the epicardium to endocardial capillaries is determined by the left ventricular end-diastolic pressure.

● Heart rate, which affects the duration of diastole; importantly, coronary artery flow primarily occurs during diastole. The percent of diastolic time decreases as the heart rate increases. Thus, heart rate is a determining factor for both oxygen demand and supply.

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he systolic blood pressure. Individuals reproducibly experience angina during exercise testing when functional capacity exceeds a well-defined angina threshold or absolute double product value. <span>Myocardial oxygen supply — The major determinants of oxygen supply are the oxygen carrying capacity of the blood, which is affected by a variety of factors including oxygen tension and the hemoglobin concentration; the degree of oxygen unloading from hemoglobin to the tissues, which is related to 2,3 diphosphoglycerate levels; and the coronary artery blood flow delivered to the myocardium. The latter is influenced by: ●Coronary artery diameter and tone (resistance) [2,3]. ●Collateral blood flow. ●Perfusion pressure. This is determined by the pressure gradients from the aorta to the coronary arteries. Coronary blood flow from the epicardium to endocardial capillaries is determined by the left ventricular end-diastolic pressure. ●Heart rate, which affects the duration of diastole; importantly, coronary artery flow primarily occurs during diastole. The percent of diastolic time decreases as the heart rate increases. Thus, heart rate is a determining factor for both oxygen demand and supply. MECHANISMS OF ANGINA — The mechanisms responsible for the sensation of angina are complex and not entirely understood. An important feature is that myocardial ischemia results in the de




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The nerve fibers travel along the sympathetic afferent pathways from the heart and enter the sympathetic ganglia in lower cervical and upper thoracic spinal cord (C5-6 and T1-T6). Impulses are then transmitted via the ascending spinothalamic pathways to the medial and lateral thalamus and ultimately activate several areas of the cerebral cortex [4].
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the primary mediator of angina is adenosine, via stimulation of the A1 adenosine receptor [10-13]. It is also possible that venodilation as a response to ischemia can activate these receptors. <span>The nerve fibers travel along the sympathetic afferent pathways from the heart and enter the sympathetic ganglia in lower cervical and upper thoracic spinal cord (C5-6 and T1-T6). Impulses are then transmitted via the ascending spinothalamic pathways to the medial and lateral thalamus and ultimately activate several areas of the cerebral cortex [4]. Angina is a discomfort that is referred to the corresponding dermatomes that supply sympathetic afferent nerves to the same segments of the spinal cord as the heart [4]. Furthermore, st




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Angina is a discomfort that is referred to the corresponding dermatomes that supply sympathetic afferent nerves to the same segments of the spinal cord as the heart [4]. Furthermore, stimulation of sensory receptors in different myocardial regions results in the transmission via the same neural pathway [13]. These characteristics account for two typical features of angina: It is often a diffuse discomfort felt in the chest, neck, lower jaw, and down the arm (typically the left arm, although some patients experience right arm discomfort). Most patients experience angina in the same distribution, regardless of which area of the myocardium is ischemic [13]. An exception is often post-cardiac surgery, as this may interrupt and alter the neural supply to the heart, which may affect the distribution of angina
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ord (C5-6 and T1-T6). Impulses are then transmitted via the ascending spinothalamic pathways to the medial and lateral thalamus and ultimately activate several areas of the cerebral cortex [4]. <span>Angina is a discomfort that is referred to the corresponding dermatomes that supply sympathetic afferent nerves to the same segments of the spinal cord as the heart [4]. Furthermore, stimulation of sensory receptors in different myocardial regions results in the transmission via the same neural pathway [13]. These characteristics account for two typical features of angina: It is often a diffuse discomfort felt in the chest, neck, lower jaw, and down the arm (typically the left arm, although some patients experience right arm discomfort). Most patients experience angina in the same distribution, regardless of which area of the myocardium is ischemic [13]. An exception is often post-cardiac surgery, as this may interrupt and alter the neural supply to the heart, which may affect the distribution of angina. CLINICAL ENTITIES ASSOCIATED WITH MYOCARDIAL ISCHEMIA — As mentioned above, any significant imbalance between myocardial oxygen supply and demand can lead to myocardial ischemia and an




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Left ventricular hypertrophy may result in a reduction in subendocardial blood flow and oxygen supply; this may result in angina. This may be particularly important with the development of arterial hypertension, which may increase left ventricular end-diastolic pressure, resulting in impairment of capillary flow in the subendocardium.
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in supply due to disease in one or more coronary arteries include coronary artery vasospasm, coronary microvascular disease, myocardial bridging, fibrosis, embolism, dissection, and arteritis. <span>Left ventricular hypertrophy may result in a reduction in subendocardial blood flow and oxygen supply; this may result in angina. This may be particularly important with the development of arterial hypertension, which may increase left ventricular end-diastolic pressure, resulting in impairment of capillary flow in the subendocardium. Other examples of inadequate supply include shock (any cause), hypoxemia, anemia, and postprandial angina resulting from a redistribution of blood flow away from territories supplied by




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Other examples of inadequate supply include shock (any cause), hypoxemia, anemia, and postprandial angina resulting from a redistribution of blood flow away from territories supplied by severely stenosed coronary arteries to those supplied by less diseased or normal arteries (ie, a steal phenomenon) [14,15]
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articularly important with the development of arterial hypertension, which may increase left ventricular end-diastolic pressure, resulting in impairment of capillary flow in the subendocardium. <span>Other examples of inadequate supply include shock (any cause), hypoxemia, anemia, and postprandial angina resulting from a redistribution of blood flow away from territories supplied by severely stenosed coronary arteries to those supplied by less diseased or normal arteries (ie, a steal phenomenon) [14,15]. Increased demand — Clinical conditions associated with an increase in myocardial oxygen demand include any situation in which there are increased catecholamines or sympathetic tone, as




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The initial presentation of myocardial ischemia with angina may be one of a stable pattern or an acute coronary syndrome. Patients with recent onset of chest discomfort, episodes of rest chest discomfort, or one or more prolonged episodes (more than 20 minutes), should be evaluated in an acute care facility for the possibility of an acute coronary syndrome. However, every patient has their first episode of chest discomfort so that recent onset is not necessarily an acute coronary syndrome, particularly if the pattern of occurrence is stable and predictable (ie, with exertion)
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t. Patients may also experience ischemic episodes without chest discomfort or anginal equivalent symptoms. (See "Silent myocardial ischemia: Epidemiology, diagnosis, treatment, and prognosis".) <span>The initial presentation of myocardial ischemia with angina may be one of a stable pattern or an acute coronary syndrome. Patients with recent onset of chest discomfort, episodes of rest chest discomfort, or one or more prolonged episodes (more than 20 minutes), should be evaluated in an acute care facility for the possibility of an acute coronary syndrome. However, every patient has their first episode of chest discomfort so that recent onset is not necessarily an acute coronary syndrome, particularly if the pattern of occurrence is stable and predictable (ie, with exertion). (See "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department".) History — Elements of the history t




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Quality − Angina is usually characterized more as a discomfort rather than pain. Terms frequently used by patients include squeezing, tightness, pressure, constriction, strangling, burning, heart burn, fullness in the chest, band-like sensation, knot in the center of the chest, lump in throat, ache, heavy weight on chest (elephant sitting on chest), like a bra too tight, and toothache (when there is radiation to the lower jaw) [17]. In some cases, the patient cannot qualify the nature of the discomfort, but places his or her fist in the center of the chest, known as the "Levine sign."

It is generally not described as sharp, dull-aching, knife-like, stabbing, or pins and needles-like. In a report of patients presenting to the emergency department, "sharp" or "stabbing" pain was a low risk description, particularly when the pain was pleuritic or positional, was fully reproducible by palpation, and the patient had no history of angina or myocardial infarction [18].

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ors, and information about social and family history. Typical qualities of anginal pain — Clinicians should attempt to elicit information about the following characteristics of the discomfort: ●<span>Quality − Angina is usually characterized more as a discomfort rather than pain. Terms frequently used by patients include squeezing, tightness, pressure, constriction, strangling, burning, heart burn, fullness in the chest, band-like sensation, knot in the center of the chest, lump in throat, ache, heavy weight on chest (elephant sitting on chest), like a bra too tight, and toothache (when there is radiation to the lower jaw) [17]. In some cases, the patient cannot qualify the nature of the discomfort, but places his or her fist in the center of the chest, known as the "Levine sign." It is generally not described as sharp, dull-aching, knife-like, stabbing, or pins and needles-like. In a report of patients presenting to the emergency department, "sharp" or "stabbing" pain was a low risk description, particularly when the pain was pleuritic or positional, was fully reproducible by palpation, and the patient had no history of angina or myocardial infarction [18]. The following additional characteristics are typically seen: •Angina is typically gradual in onset and offset, with the intensity of the discomfort increasing and decreasing over severa




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Angina is typically gradual in onset and offset, with the intensity of the discomfort increasing and decreasing over several minutes. In contrast, noncardiac pain is often of greatest intensity at its onset and often has an abrupt onset and offset.
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euritic or positional, was fully reproducible by palpation, and the patient had no history of angina or myocardial infarction [18]. The following additional characteristics are typically seen: •<span>Angina is typically gradual in onset and offset, with the intensity of the discomfort increasing and decreasing over several minutes. In contrast, noncardiac pain is often of greatest intensity at its onset and often has an abrupt onset and offset. •Since angina is a referred discomfort, patients tend to have the same quality of chest discomfort with recurrent ischemic episodes [13]. Generally, it is felt in the same location. The




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Since angina is a referred discomfort, patients tend to have the same quality of chest discomfort with recurrent ischemic episodes [13]. Generally, it is felt in the same location. The discomfort is generally the same prior to or with a myocardial infarction and is the same quality as prior to revascularization by either surgery (although the location may be different due to disruption of neural innervation of the heart) or percutaneous coronary intervention.
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e intensity of the discomfort increasing and decreasing over several minutes. In contrast, noncardiac pain is often of greatest intensity at its onset and often has an abrupt onset and offset. •<span>Since angina is a referred discomfort, patients tend to have the same quality of chest discomfort with recurrent ischemic episodes [13]. Generally, it is felt in the same location. The discomfort is generally the same prior to or with a myocardial infarction and is the same quality as prior to revascularization by either surgery (although the location may be different due to disruption of neural innervation of the heart) or percutaneous coronary intervention. •Angina is a constant discomfort that does not change with respiration or most changes in position (one exception is lying down, which increases venous return). It is also not provoked




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Angina is a constant discomfort that does not change with respiration or most changes in position (one exception is lying down, which increases venous return). It is also not provoked or worsened with palpation of the chest wall. However, the presence of a change in pain with respiration (or position) or pain elicited by palpation does not exclude angina as the cause.
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ame quality as prior to revascularization by either surgery (although the location may be different due to disruption of neural innervation of the heart) or percutaneous coronary intervention. •<span>Angina is a constant discomfort that does not change with respiration or most changes in position (one exception is lying down, which increases venous return). It is also not provoked or worsened with palpation of the chest wall. However, the presence of a change in pain with respiration (or position) or pain elicited by palpation does not exclude angina as the cause. ●Location and radiation − As noted above, angina is a referred pain due to involvement of a neural reflex pathway via the thoracic and cervical nerves. As a result, it is not felt in a




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The patient often indicates the entire chest when asked where the discomfort is felt. Pain that localizes to one small area of the chest is more likely of chest wall or pleural origin rather than visceral.
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volvement of a neural reflex pathway via the thoracic and cervical nerves. As a result, it is not felt in a specific spot, but is usually a diffuse discomfort that may be difficult to localize. <span>The patient often indicates the entire chest when asked where the discomfort is felt. Pain that localizes to one small area of the chest is more likely of chest wall or pleural origin rather than visceral. Angina is referred to the corresponding dermatomes (C5-6 and T1-T6) that supply afferent nerves to the same segments of the spinal cord as the heart. Thus, angina often radiates to othe




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Angina is referred to the corresponding dermatomes (C5-6 and T1-T6) that supply afferent nerves to the same segments of the spinal cord as the heart. Thus, angina often radiates to other parts of the body, including the upper abdomen (epigastric), shoulders, arms (upper and forearm), wrist, fingers, neck and throat, lower jaw and teeth (but not upper jaw), and rarely to the back (specifically the interscapular region) [19,20]
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often indicates the entire chest when asked where the discomfort is felt. Pain that localizes to one small area of the chest is more likely of chest wall or pleural origin rather than visceral. <span>Angina is referred to the corresponding dermatomes (C5-6 and T1-T6) that supply afferent nerves to the same segments of the spinal cord as the heart. Thus, angina often radiates to other parts of the body, including the upper abdomen (epigastric), shoulders, arms (upper and forearm), wrist, fingers, neck and throat, lower jaw and teeth (but not upper jaw), and rarely to the back (specifically the interscapular region) [19,20]. Radiation to both arms is a stronger predictor of acute myocardial infarction. The location and radiation of angina is usually the same each time. Occasionally, the location and radiat




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Radiation to both arms is a stronger predictor of acute myocardial infarction. The location and radiation of angina is usually the same each time. Occasionally, the location and radiation, but not quality, may be different after bypass surgery due to the disruption of the neural innervation of the heart.
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igastric), shoulders, arms (upper and forearm), wrist, fingers, neck and throat, lower jaw and teeth (but not upper jaw), and rarely to the back (specifically the interscapular region) [19,20]. <span>Radiation to both arms is a stronger predictor of acute myocardial infarction. The location and radiation of angina is usually the same each time. Occasionally, the location and radiation, but not quality, may be different after bypass surgery due to the disruption of the neural innervation of the heart. Isolated back pain is unusual in patients with angina. However, it may be seen with an aortic dissection that also involves the coronary arteries. (See "Clinical features and diagnosis




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Isolated back pain is unusual in patients with angina. However, it may be seen with an aortic dissection that also involves the coronary arteries.
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ina is usually the same each time. Occasionally, the location and radiation, but not quality, may be different after bypass surgery due to the disruption of the neural innervation of the heart. <span>Isolated back pain is unusual in patients with angina. However, it may be seen with an aortic dissection that also involves the coronary arteries. (See "Clinical features and diagnosis of acute aortic dissection".) ●Provoking factors − Angina is often elicited by activities and situations that increase myocardial oxygen demand, in




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Provoking factors Angina is often elicited by activities and situations that increase myocardial oxygen demand, including physical activity, cold, emotional stress, sexual intercourse, meals, or lying down (which results in an increase in venous return and increase in wall stress) [21-23]. Patients should be questioned about the use of cocaine or other recreational drugs, as they may trigger myocardial ischemia.
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unusual in patients with angina. However, it may be seen with an aortic dissection that also involves the coronary arteries. (See "Clinical features and diagnosis of acute aortic dissection".) ●<span>Provoking factors − Angina is often elicited by activities and situations that increase myocardial oxygen demand, including physical activity, cold, emotional stress, sexual intercourse, meals, or lying down (which results in an increase in venous return and increase in wall stress) [21-23]. Patients should be questioned about the use of cocaine or other recreational drugs, as they may trigger myocardial ischemia. (See "Clinical manifestations, diagnosis, and management of the cardiovascular complications of cocaine abuse", section on 'Myocardial ischemia/infarction'.) Postprandial pain is genera




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Postprandial pain is generally considered to be gastrointestinal in origin. However, it may also be anginal, especially in patients with severe ischemia (eg, left main or three vessel coronary disease) [15].
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ey may trigger myocardial ischemia. (See "Clinical manifestations, diagnosis, and management of the cardiovascular complications of cocaine abuse", section on 'Myocardial ischemia/infarction'.) <span>Postprandial pain is generally considered to be gastrointestinal in origin. However, it may also be anginal, especially in patients with severe ischemia (eg, left main or three vessel coronary disease) [15]. ●Timing − Angina occurs more commonly in the morning due to a diurnal increase in sympathetic tone. Enhanced sympathetic activity raises heart rate, blood pressure, vessel tone and resi




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Timing Angina occurs more commonly in the morning due to a diurnal increase in sympathetic tone. Enhanced sympathetic activity raises heart rate, blood pressure, vessel tone and resistance (resulting in a reduced vessel diameter that causes any fixed lesion to be more occlusive), and promotes platelet aggregation (resulting in the release of vasoactive substances, such as serotonin and thromboxane A2) [8,9].
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in is generally considered to be gastrointestinal in origin. However, it may also be anginal, especially in patients with severe ischemia (eg, left main or three vessel coronary disease) [15]. ●<span>Timing − Angina occurs more commonly in the morning due to a diurnal increase in sympathetic tone. Enhanced sympathetic activity raises heart rate, blood pressure, vessel tone and resistance (resulting in a reduced vessel diameter that causes any fixed lesion to be more occlusive), and promotes platelet aggregation (resulting in the release of vasoactive substances, such as serotonin and thromboxane A2) [8,9]. ●Duration and relief − Classic angina is often relieved with termination of the provoking factor. Angina generally lasts for two to five minutes. It is not a fleeting discomfort, which




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Duration and relief Classic angina is often relieved with termination of the provoking factor. Angina generally lasts for two to five minutes. It is not a fleeting discomfort, which lasts only for a few seconds or less than a minute, and it generally does not last for 20 to 30 minutes, unless the patient is experiencing an acute coronary syndrome, especially myocardial infarction.
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diameter that causes any fixed lesion to be more occlusive), and promotes platelet aggregation (resulting in the release of vasoactive substances, such as serotonin and thromboxane A2) [8,9]. ●<span>Duration and relief − Classic angina is often relieved with termination of the provoking factor. Angina generally lasts for two to five minutes. It is not a fleeting discomfort, which lasts only for a few seconds or less than a minute, and it generally does not last for 20 to 30 minutes, unless the patient is experiencing an acute coronary syndrome, especially myocardial infarction. Factors that reduce oxygen demand or increase oxygen supply will result in relief of angina. These include cessation of activity or termination of the provoking factor, use of nitroglyc




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Factors that reduce oxygen demand or increase oxygen supply will result in relief of angina. These include cessation of activity or termination of the provoking factor, use of nitroglycerin (which is a venodilator, reducing venous return, and a coronary artery vasodilator that increases coronary blood flow), and sitting up (which reduces venous return and preload).
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ly for a few seconds or less than a minute, and it generally does not last for 20 to 30 minutes, unless the patient is experiencing an acute coronary syndrome, especially myocardial infarction. <span>Factors that reduce oxygen demand or increase oxygen supply will result in relief of angina. These include cessation of activity or termination of the provoking factor, use of nitroglycerin (which is a venodilator, reducing venous return, and a coronary artery vasodilator that increases coronary blood flow), and sitting up (which reduces venous return and preload). Relief of chest discomfort with nitroglycerin is not specific for angina, since a similar response may be seen with esophageal spasm or other gastrointestinal problems as nitroglycerin




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However, some patients with an acute coronary syndrome present with atypical types of chest pain. In one study, acute ischemia was diagnosed in 22 percent of patients who presented with sharp or stabbing pain and 13 percent who presented with pleuritic-type pain [18].
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omfort reproduced by movement or palpation. ●Constant pain lasting for days. ●Fleeting pains lasting for a few seconds or less. ●Pain radiating into the lower extremities or above the mandible. <span>However, some patients with an acute coronary syndrome present with atypical types of chest pain. In one study, acute ischemia was diagnosed in 22 percent of patients who presented with sharp or stabbing pain and 13 percent who presented with pleuritic-type pain [18]. In addition, some patients who appear to have a noncardiac cause of chest pain have other serious conditions including acute aortic dissection, pulmonary embolism, tension pneumothorax,




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Angina is often associated with other symptoms. Dyspnea is a common anginal equivalent, and its presence is associated with a higher cardiovascular death rate compared with patients with typical angina. Dyspnea in the setting of angina may reflect pulmonary congestion due to an elevation in left ventricular end diastolic pressure related to failure of the myocardium to relax normally in diastole (as relaxation or lusitropy is energy dependent). The resulting diastolic "stiffness" or diastolic dysfunction results in an increase in left ventricular end diastolic pressure, left atrial pressure, and pulmonary venous pressure, which is transmitted to the pulmonary vessels.
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r these alternate diagnoses to avoid potentially dangerous errors in management, such as the administration of thrombolytic therapy to a patient with an aortic dissection. Associated symptoms — <span>Angina is often associated with other symptoms. Dyspnea is a common anginal equivalent, and its presence is associated with a higher cardiovascular death rate compared with patients with typical angina. Dyspnea in the setting of angina may reflect pulmonary congestion due to an elevation in left ventricular end diastolic pressure related to failure of the myocardium to relax normally in diastole (as relaxation or lusitropy is energy dependent). The resulting diastolic "stiffness" or diastolic dysfunction results in an increase in left ventricular end diastolic pressure, left atrial pressure, and pulmonary venous pressure, which is transmitted to the pulmonary vessels. (See "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis".) Other symptoms may include belching, nausea, indigestion, diaphoresis, dizziness, lighthea




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Other symptoms may include belching, nausea, indigestion, diaphoresis, dizziness, lightheadedness, clamminess, and fatigue. These have been referred to as "angina equivalent" symptoms and appear to be more common in women compared with men. However, these symptoms may be seen with other etiologies for chest pain, especially gastrointestinal causes.
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eft atrial pressure, and pulmonary venous pressure, which is transmitted to the pulmonary vessels. (See "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis".) <span>Other symptoms may include belching, nausea, indigestion, diaphoresis, dizziness, lightheadedness, clamminess, and fatigue. These have been referred to as "angina equivalent" symptoms and appear to be more common in women compared with men. However, these symptoms may be seen with other etiologies for chest pain, especially gastrointestinal causes. It is common for patients with diabetes mellitus, who often have autonomic (sympathetic) dysfunction, to experience "silent ischemia" or best termed "discomfortless ischemia." (see "Sil




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It is common for patients with diabetes mellitus, who often have autonomic (sympathetic) dysfunction, to experience "silent ischemia" or best termed "discomfortless ischemia." (see "Silent myocardial ischemia: Epidemiology, diagnosis, treatment, and prognosis"). They may also present with anginal equivalent symptoms.
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ngina equivalent" symptoms and appear to be more common in women compared with men. However, these symptoms may be seen with other etiologies for chest pain, especially gastrointestinal causes. <span>It is common for patients with diabetes mellitus, who often have autonomic (sympathetic) dysfunction, to experience "silent ischemia" or best termed "discomfortless ischemia." (see "Silent myocardial ischemia: Epidemiology, diagnosis, treatment, and prognosis"). They may also present with anginal equivalent symptoms. Social and family history — Many patients who are ultimately diagnosed with myocardial ischemia have key pieces of information in the social and family histories. For example, risk fact




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Physical examination — Ischemia can produce impairment in myocardial function, which may result in the following findings on physical examination. All disappear with resolution of the ischemia. Some patients have none of these features.
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family history may reveal members with premature cardiovascular disease or hypertrophic cardiomyopathy. (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation".) <span>Physical examination — Ischemia can produce impairment in myocardial function, which may result in the following findings on physical examination. All disappear with resolution of the ischemia. Some patients have none of these features. Increase in heart rate — Ischemia can raise the heart rate even if the patient is receiving a beta blocker or calcium channel blocker. The increase in heart rate is induced by reflex sy




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Increase in heart rate — Ischemia can raise the heart rate even if the patient is receiving a beta blocker or calcium channel blocker. The increase in heart rate is induced by reflex sympathetic nervous system activation as a response to ischemia.
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impairment in myocardial function, which may result in the following findings on physical examination. All disappear with resolution of the ischemia. Some patients have none of these features. <span>Increase in heart rate — Ischemia can raise the heart rate even if the patient is receiving a beta blocker or calcium channel blocker. The increase in heart rate is induced by reflex sympathetic nervous system activation as a response to ischemia. Elevation in blood pressure — Ischemia often causes a hypertensive blood pressure response. The elevation in blood pressure is induced by both sympathetic activation in response to isch




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Elevation in blood pressure — Ischemia often causes a hypertensive blood pressure response. The elevation in blood pressure is induced by both sympathetic activation in response to ischemia and stimulation of the left anterior descending coronary artery chemoreceptor. This chemoreceptor is stimulated by serotonin secreted as a result of platelet aggregation, which often occurs in association with angina.
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rate even if the patient is receiving a beta blocker or calcium channel blocker. The increase in heart rate is induced by reflex sympathetic nervous system activation as a response to ischemia. <span>Elevation in blood pressure — Ischemia often causes a hypertensive blood pressure response. The elevation in blood pressure is induced by both sympathetic activation in response to ischemia and stimulation of the left anterior descending coronary artery chemoreceptor. This chemoreceptor is stimulated by serotonin secreted as a result of platelet aggregation, which often occurs in association with angina. New heart sounds — Ischemia-induced myocardial dysfunction can lead to changes in the normal heart sounds. The second heart sound may become paradoxically split due to delayed relaxatio




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New heart sounds — Ischemia-induced myocardial dysfunction can lead to changes in the normal heart sounds. The second heart sound may become paradoxically split due to delayed relaxation of the left ventricular myocardium and delayed closure of the aortic valve. There may also be a third or fourth heart sound.
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eft anterior descending coronary artery chemoreceptor. This chemoreceptor is stimulated by serotonin secreted as a result of platelet aggregation, which often occurs in association with angina. <span>New heart sounds — Ischemia-induced myocardial dysfunction can lead to changes in the normal heart sounds. The second heart sound may become paradoxically split due to delayed relaxation of the left ventricular myocardium and delayed closure of the aortic valve. There may also be a third or fourth heart sound. (See "Auscultation of heart sounds".) New/changed murmurs — Impaired myocardial function may result in a new mitral regurgitation murmur, which appears to be due to papillary muscle dys




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New/changed murmurs — Impaired myocardial function may result in a new mitral regurgitation murmur, which appears to be due to papillary muscle dysfunction causing apical tethering or tenting of the leaflets, or changes in the intensity or timing of pre-existing murmurs.
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plit due to delayed relaxation of the left ventricular myocardium and delayed closure of the aortic valve. There may also be a third or fourth heart sound. (See "Auscultation of heart sounds".) <span>New/changed murmurs — Impaired myocardial function may result in a new mitral regurgitation murmur, which appears to be due to papillary muscle dysfunction causing apical tethering or tenting of the leaflets, or changes in the intensity or timing of pre-existing murmurs. (See "Auscultation of cardiac murmurs in adults" and "Management and prognosis of chronic secondary mitral regurgitation".) Precordial pulsation — Palpation of the chest wall may reveal




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Precordial pulsation — Palpation of the chest wall may reveal abnormal pulsations that correlate with transient left ventricular dysfunction. An area of dyskinesis may develop, especially at the apex of the left ventricle or at the anterior axillary line (location of the left ventricular wall), reflecting disease of the left anterior descending coronary artery. (See "Examination of the precordial pulsation".)
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flets, or changes in the intensity or timing of pre-existing murmurs. (See "Auscultation of cardiac murmurs in adults" and "Management and prognosis of chronic secondary mitral regurgitation".) <span>Precordial pulsation — Palpation of the chest wall may reveal abnormal pulsations that correlate with transient left ventricular dysfunction. An area of dyskinesis may develop, especially at the apex of the left ventricle or at the anterior axillary line (location of the left ventricular wall), reflecting disease of the left anterior descending coronary artery. (See "Examination of the precordial pulsation".) Palpation of the left anterior chest wall at the anterior axillary line may reveal an abnormal tapping in systole, which reflects the presence of an area of dyskinetic contraction or an




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Palpation of the left anterior chest wall at the anterior axillary line may reveal an abnormal tapping in systole, which reflects the presence of an area of dyskinetic contraction or aneurysm. Transient right ventricular dysfunction may lead to a transient right ventricular heave or sternal pulsation.
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le or at the anterior axillary line (location of the left ventricular wall), reflecting disease of the left anterior descending coronary artery. (See "Examination of the precordial pulsation".) <span>Palpation of the left anterior chest wall at the anterior axillary line may reveal an abnormal tapping in systole, which reflects the presence of an area of dyskinetic contraction or aneurysm. Transient right ventricular dysfunction may lead to a transient right ventricular heave or sternal pulsation. Laboratory tests — For patients in whom the history and physical examination raise the possibility of myocardial ischemia as the cause of chest discomfort, an electrocardiogram should b




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Cardiac biomarkers (eg, troponin) are often obtained in patients with angina. They are unlikely to be elevated in patients with intermittent and relatively brief angina episodes. However, they may be useful when the anginal episode is more prolonged and for prognostication.
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s performed to screen for other causes of chest pain (eg, enlarged aorta, broken rib). (See "Outpatient evaluation of the adult with chest pain", section on 'Indications for chest radiograph'.) <span>Cardiac biomarkers (eg, troponin) are often obtained in patients with angina. They are unlikely to be elevated in patients with intermittent and relatively brief angina episodes. However, they may be useful when the anginal episode is more prolonged and for prognostication. If high-sensitivity troponin assays are used, low levels of troponin are often detected in patients experiencing stable angina. Increased high-sensitivity troponin levels are associated




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The term "ACS" is applied to patients in whom there is evidence of myocardial ischemia or infarction. There are three types of ACS: ST-elevation myocardial infarction (STEMI), non-ST-elevation MI (NSTEMI), and unstable angina (UA). The first two are characterized by a typical rise and/or fall in serum troponin [2]. UA is characterized by new or worsening myocardial ischemia without elevated biomarkers and is often a clinical diagnosis based on history, dynamic ECG changes, or inducible ischemia on stress testing. UA accounts for a smaller proportion of ACS now that there is widespread use of highly sensitive troponin, which can detect very small amounts of myocardial injury
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nt, and care pathways is presented. A major goal of the topic is to help clinicians identify patients who are candidates for early discharge from the ED. DEFINITION OF ACUTE CORONARY SYNDROME — <span>The term "ACS" is applied to patients in whom there is evidence of myocardial ischemia or infarction. There are three types of ACS: ST-elevation myocardial infarction (STEMI), non-ST-elevation MI (NSTEMI), and unstable angina (UA). The first two are characterized by a typical rise and/or fall in serum troponin [2]. UA is characterized by new or worsening myocardial ischemia without elevated biomarkers and is often a clinical diagnosis based on history, dynamic ECG changes, or inducible ischemia on stress testing. UA accounts for a smaller proportion of ACS now that there is widespread use of highly sensitive troponin, which can detect very small amounts of myocardial injury. Establishing whether a patient has ACS requires integration of information obtained from a careful patient interview and examination, as well as from serial evaluation of the ECG, trop




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The primary focus in the very early evaluation (generally within the first 15 minutes after presentation) of patients with possible ACS is to reasonably confirm or exclude in an expeditious manner ACS as the cause for the patient's symptoms (algorithm 1). In this early time period, reasonable confirmation of ACS is generally secured by the finding of diagnostic ECG changes. ACS is reasonably excluded when the probability of ACS is very low (generally considered below a 1 to 2 percent threshold [3,4]).
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rom serial evaluation of the ECG, troponin levels, and occasionally provocative testing results. (See "Diagnosis of acute myocardial infarction", section on 'Definitions'.) INITIAL EVALUATION — <span>The primary focus in the very early evaluation (generally within the first 15 minutes after presentation) of patients with possible ACS is to reasonably confirm or exclude in an expeditious manner ACS as the cause for the patient's symptoms (algorithm 1). In this early time period, reasonable confirmation of ACS is generally secured by the finding of diagnostic ECG changes. ACS is reasonably excluded when the probability of ACS is very low (generally considered below a 1 to 2 percent threshold [3,4]). (See 'Risk assessment' below.) For patients who have or are likely to have an ACS, appropriate management strategies should be initiated (algorithm 2). (See "Initial evaluation and mana




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An initial 12-lead ECG within 10 minutes of arrival (even if one has been performed in an ambulance, unless that ECG showed ST-segment elevation) in patients ≥25 years of age with chest pain, or age ≥50 years with chest pain or other symptoms that could represent myocardial ischemia like shortness of breath, altered mental status, upper extremity pain, syncope, or generalized weakness. Very elderly (≥80 years of age) patients with abdominal pain or nausea/vomiting should have an immediate 12-lead ECG as well [2,5].
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owing performed (see "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department"): ●Continuous ECG monitoring. ●<span>An initial 12-lead ECG within 10 minutes of arrival (even if one has been performed in an ambulance, unless that ECG showed ST-segment elevation) in patients ≥25 years of age with chest pain, or age ≥50 years with chest pain or other symptoms that could represent myocardial ischemia like shortness of breath, altered mental status, upper extremity pain, syncope, or generalized weakness. Very elderly (≥80 years of age) patients with abdominal pain or nausea/vomiting should have an immediate 12-lead ECG as well [2,5]. It is recommended that the ECG be repeated at 20- to 30-minute intervals for any patient with ongoing pain in whom a suspicion of ACS continues. Patients whose ECGs are diagnostic for o




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While patients who are assessed to be at very low risk of an ACS do not need a troponin test, many institutions have protocols that direct nursing staff to order them based on their assessment, which may be prior to physician evaluation. We believe this is a reasonable strategy.

The results of the first high sensitivity troponin should be available within 60 minutes.

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where available), serum electrolytes, serum creatinine, and a complete blood count. (See "Evaluation of the adult with chest pain in the emergency department", section on 'Laboratory studies'.) <span>While patients who are assessed to be at very low risk of an ACS do not need a troponin test, many institutions have protocols that direct nursing staff to order them based on their assessment, which may be prior to physician evaluation. We believe this is a reasonable strategy. The results of the first high sensitivity troponin should be available within 60 minutes. (See "Troponin testing: Clinical use", section on 'Diagnosis of acute MI'.) ●A chest radiograph is usually performed in patients suspected of having an ACS, since alternative diagnoses




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We attempt to assign patients to low, intermediate, or high risk for ACS category, or definite ACS (table 1), based on information obtained from the history, physical examination, ECG, and continuous ECG monitoring (algorithm 1) but before the first troponin level is available.
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ected of having an ACS, since alternative diagnoses such as heart failure, pneumonia, aortic dissection, pulmonary embolism, or large pericardial effusion may be detected [6]. Risk assessment — <span>We attempt to assign patients to low, intermediate, or high risk for ACS category, or definite ACS (table 1), based on information obtained from the history, physical examination, ECG, and continuous ECG monitoring (algorithm 1) but before the first troponin level is available. Multiple scoring systems have been evaluated. We prefer the History, ECG, Age, Risk factors, and a single sensitive Troponin (HEART) score, which is used in the HEART Pathway (see 'Care




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Multiple scoring systems have been evaluated. We prefer the History, ECG, Age, Risk factors, and a single sensitive Troponin (HEART) score, which is used in the HEART Pathway (see 'Care pathways' below). Using this score, individuals with a score of 0 to 3 are considered low risk. There is an element of subjectivity in the HEART score, so internal discussions to improve consistency of use are suggested [7].
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definite ACS (table 1), based on information obtained from the history, physical examination, ECG, and continuous ECG monitoring (algorithm 1) but before the first troponin level is available. <span>Multiple scoring systems have been evaluated. We prefer the History, ECG, Age, Risk factors, and a single sensitive Troponin (HEART) score, which is used in the HEART Pathway (see 'Care pathways' below). Using this score, individuals with a score of 0 to 3 are considered low risk. There is an element of subjectivity in the HEART score, so internal discussions to improve consistency of use are suggested [7]. Low-risk patients generally have none of the risk factors found in the table (table 1). Specifically, low-risk patients cannot have a history of coronary artery disease or have ST-segme




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Low-risk patients generally have none of the risk factors found in the table (table 1). Specifically, low-risk patients cannot have a history of coronary artery disease or have ST-segment elevation, significant ST-segment depression, or new T wave inversion.
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ore, individuals with a score of 0 to 3 are considered low risk. There is an element of subjectivity in the HEART score, so internal discussions to improve consistency of use are suggested [7]. <span>Low-risk patients generally have none of the risk factors found in the table (table 1). Specifically, low-risk patients cannot have a history of coronary artery disease or have ST-segment elevation, significant ST-segment depression, or new T wave inversion. We manage patients as follows: ●If the patient's likelihood of ACS is very low (<1 to 2 percent) based on the history, physical examination, and initial ECG, additional testing for A




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At some lower threshold of pretest probability, the clinician is more likely to cause harm by further testing. It has been suggested that an acceptable lower limit of pretest probability for ACS, above which further testing should be done, is 1 to 2 percent [3,4]. We believe patients below this threshold are very low risk and are unlikely to benefit from additional testing for an ACS. All other patients should receive further testing and risk stratification.
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gement of ST-elevation myocardial infarction" and "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department".) <span>At some lower threshold of pretest probability, the clinician is more likely to cause harm by further testing. It has been suggested that an acceptable lower limit of pretest probability for ACS, above which further testing should be done, is 1 to 2 percent [3,4]. We believe patients below this threshold are very low risk and are unlikely to benefit from additional testing for an ACS. All other patients should receive further testing and risk stratification. Providers commonly identify very low-risk patients using an experienced clinician's unstructured clinical estimate. In an evaluation of this method, approximately 25 percent of chest pa




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Providers commonly identify very low-risk patients using an experienced clinician's unstructured clinical estimate. In an evaluation of this method, approximately 25 percent of chest pain patients were classified as very low risk (<2 percent risk), and these patients experienced an event rate of 0.7 percent (95% CI 0-2.4) [8].
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elieve patients below this threshold are very low risk and are unlikely to benefit from additional testing for an ACS. All other patients should receive further testing and risk stratification. <span>Providers commonly identify very low-risk patients using an experienced clinician's unstructured clinical estimate. In an evaluation of this method, approximately 25 percent of chest pain patients were classified as very low risk (<2 percent risk), and these patients experienced an event rate of 0.7 percent (95% CI 0-2.4) [8]. With the introduction of clinical decision aids, many clinicians and health systems have moved toward more objective classification systems, typically incorporating serum troponin measu




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When formulating the clinician's pretest (before the troponin) probability, it is important to avoid eliminating the possibility of an ACS even when an alternative diagnosis is possible. In patients being evaluated for chest pain, it has been shown that those with a "clear-cut" alternative noncardiac diagnosis still have a 4 percent rate of ACS at 30 days [9].
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l decision aids, many clinicians and health systems have moved toward more objective classification systems, typically incorporating serum troponin measurements. (See 'Troponin testing' below.) <span>When formulating the clinician's pretest (before the troponin) probability, it is important to avoid eliminating the possibility of an ACS even when an alternative diagnosis is possible. In patients being evaluated for chest pain, it has been shown that those with a "clear-cut" alternative noncardiac diagnosis still have a 4 percent rate of ACS at 30 days [9]. Similarly, patients with a "clear-cut" alternative noncardiac diagnosis and a Thrombolysis in Myocardial Infarction (TIMI) risk score of 0 had a 2.9 percent rate of ACS at 30 days [10].




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As an example, among patients with ACS, a common misdiagnosis is gastroesophageal reflux disease. In two different datasets, it has been shown that patients with ACS commonly describe their pain as burning [11,12]. A gastrointestinal etiology should be assigned only after the diagnosis of a cardiac emergency has been excluded.
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ys [9]. Similarly, patients with a "clear-cut" alternative noncardiac diagnosis and a Thrombolysis in Myocardial Infarction (TIMI) risk score of 0 had a 2.9 percent rate of ACS at 30 days [10]. <span>As an example, among patients with ACS, a common misdiagnosis is gastroesophageal reflux disease. In two different datasets, it has been shown that patients with ACS commonly describe their pain as burning [11,12]. A gastrointestinal etiology should be assigned only after the diagnosis of a cardiac emergency has been excluded. Further, a trial of antacids or nitroglycerin should not be used as a reliable method to determine whether pain is of gastrointestinal or cardiac origin. The diagnosis of ACS is more li




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While we have identified specific times in this process when evaluation must take place rapidly, evaluation is a continuous process, and new information at any time point can alter a patient's risk category. For example, worsening of symptoms, arrhythmias, or new ECG changes on continuous monitoring can make the possibility of an ACS more likely.
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nts when forming an unstructured estimate of ACS probability, avoid overreliance on the presence of an alternative diagnosis, and use caution when defining the very low-risk patient population. <span>While we have identified specific times in this process when evaluation must take place rapidly, evaluation is a continuous process, and new information at any time point can alter a patient's risk category. For example, worsening of symptoms, arrhythmias, or new ECG changes on continuous monitoring can make the possibility of an ACS more likely. TROPONIN TESTING — In those patients for whom the diagnosis of ACS remains a possibility after rapid evaluation of the history, physical examination, and 12-lead ECG (see 'Risk assessme




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Compared with a standard troponin assay, hs-cTn leads to the diagnosis of acute MI in a modest additional number of chest pain patients and may do so earlier in the patients' emergency department (ED) stay [14]. This occurs because hs-cTn detects biochemical evidence of myocardial injury at lower concentrations, and hs-cTn assays allow for discrimination of small changes in concentration even within the normal reference range. However, MI is not ruled in unless there is both a rising and/or falling pattern of values and one value above the upper reference limit (URL) [15]
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assessment' above), a high-sensitivity cardiac troponin (hs-cTn) should be obtained as soon as possible. (See "Troponin testing: Clinical use", section on 'Diagnosis of acute MI'.) Background — <span>Compared with a standard troponin assay, hs-cTn leads to the diagnosis of acute MI in a modest additional number of chest pain patients and may do so earlier in the patients' emergency department (ED) stay [14]. This occurs because hs-cTn detects biochemical evidence of myocardial injury at lower concentrations, and hs-cTn assays allow for discrimination of small changes in concentration even within the normal reference range. However, MI is not ruled in unless there is both a rising and/or falling pattern of values and one value above the upper reference limit (URL) [15] (see "Diagnosis of acute myocardial infarction", section on 'Definitions'). However, the issue of whether this improves long-term cardiovascular outcomes is debated [16]. In addition, v




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With hs-cTn, serial values <99th percentile of the URL make the diagnosis of acute MI quite unlikely, but the value does not exclude the possibility of unstable angina [17,18]
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'Definitions'). However, the issue of whether this improves long-term cardiovascular outcomes is debated [16]. In addition, very low hs-cTn values identify patients at low risk of MI in the ED. <span>With hs-cTn, serial values <99th percentile of the URL make the diagnosis of acute MI quite unlikely, but the value does not exclude the possibility of unstable angina [17,18]. The use of sex-dependent 99th percentile URL is advocated by the Universal Definition of Myocardial Infarction and will be different depending on the assay used. A value of <5 ng/L




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If the first troponin returns clearly elevated in a patient with clinical findings consistent with ACS, the management for NSTEMI likely begins. (See "Overview of the acute management of non-ST elevation acute coronary syndromes".)

However, this paradigm may be changing with the routine use of increasingly sensitive troponin assays. Data from outside the United States suggest that 11 to 15 percent of patients will be classified as having NSTEMI based on that initial hs-cTn result, of whom 68 to 79 percent will ultimately be adjudicated as having NSTEMI [22]. As these hs-cTn assays are applied to broader patient populations with concomitant medical conditions such as sepsis and renal failure, this positive predictive value is likely to be reduced. This fact needs to be considered by clinicians.

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cluded individuals who presented in two hours or less from the onset of symptoms. Caution is necessary with these early rapid approaches for early presenting patients. Elevated first troponin — <span>If the first troponin returns clearly elevated in a patient with clinical findings consistent with ACS, the management for NSTEMI likely begins. (See "Overview of the acute management of non-ST elevation acute coronary syndromes".) However, this paradigm may be changing with the routine use of increasingly sensitive troponin assays. Data from outside the United States suggest that 11 to 15 percent of patients will be classified as having NSTEMI based on that initial hs-cTn result, of whom 68 to 79 percent will ultimately be adjudicated as having NSTEMI [22]. As these hs-cTn assays are applied to broader patient populations with concomitant medical conditions such as sepsis and renal failure, this positive predictive value is likely to be reduced. This fact needs to be considered by clinicians. Normal first troponin — If the troponin value is less than the upper reference limit, further evaluation is directed by the clinical presentation and risk factors. (See 'Risk scores' be




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If the troponin value is less than the upper reference limit, further evaluation is directed by the clinical presentation and risk factors. (See 'Risk scores' below.)

● For patients whose symptoms remain suspicious for an ACS or who have a low or intermediate risk of ACS (Heart Score ≥1), obtain a second troponin (algorithm 1). For most patients, we obtain a second troponin three hours after the first troponin and use the HEART Pathway approach (see 'Care pathways' below). Monitoring continues until a second troponin returns.

● For selected patients whose symptoms are best explained by a noncardiac diagnosis (eg, costochondritis, pneumonia), and who have a risk for ACS less than 2 percent by clinical evaluation or a Heart Score of zero, the evaluation for ACS can stop [23].

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concomitant medical conditions such as sepsis and renal failure, this positive predictive value is likely to be reduced. This fact needs to be considered by clinicians. Normal first troponin — <span>If the troponin value is less than the upper reference limit, further evaluation is directed by the clinical presentation and risk factors. (See 'Risk scores' below.) ●For patients whose symptoms remain suspicious for an ACS or who have a low or intermediate risk of ACS (Heart Score ≥1), obtain a second troponin (algorithm 1). For most patients, we obtain a second troponin three hours after the first troponin and use the HEART Pathway approach (see 'Care pathways' below). Monitoring continues until a second troponin returns. ●For selected patients whose symptoms are best explained by a noncardiac diagnosis (eg, costochondritis, pneumonia), and who have a risk for ACS less than 2 percent by clinical evaluation or a Heart Score of zero, the evaluation for ACS can stop [23]. On occasion, some patients will require a third troponin. Examples include those with stuttering pain, new return of pain while in the ED, patients presenting very soon after the onset




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On occasion, some patients will require a third troponin. Examples include those with stuttering pain, new return of pain while in the ED, patients presenting very soon after the onset of symptoms, and those in whom the clinician has a high degree of concern.
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y a noncardiac diagnosis (eg, costochondritis, pneumonia), and who have a risk for ACS less than 2 percent by clinical evaluation or a Heart Score of zero, the evaluation for ACS can stop [23]. <span>On occasion, some patients will require a third troponin. Examples include those with stuttering pain, new return of pain while in the ED, patients presenting very soon after the onset of symptoms, and those in whom the clinician has a high degree of concern. For low-risk patients or those with normal ECGs who present more than three hours after the onset of chest pain [21,24], a value of hs-cTn below the limit of detection of the assay is a




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For low-risk patients or those with normal ECGs who present more than three hours after the onset of chest pain [21,24], a value of hs-cTn below the limit of detection of the assay is a sensitive way to rule out acute MI.
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include those with stuttering pain, new return of pain while in the ED, patients presenting very soon after the onset of symptoms, and those in whom the clinician has a high degree of concern. <span>For low-risk patients or those with normal ECGs who present more than three hours after the onset of chest pain [21,24], a value of hs-cTn below the limit of detection of the assay is a sensitive way to rule out acute MI. However, even those who endorse the European Society of Cardiology (ESC) guidelines concur with the need for caution in those who present early after the onset of symptoms [25,26]. The




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With hs-cTn assays, one- to three-hour rule-outs using assay specific change criteria are usually adequate. There are only rare patients who rule in thereafter [34].
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>3 to 6 hours after the onset of symptoms (assuming no recurrences) and who has a normal cTn value (either hs-cTn or contemporary cTn) can be considered to have ruled out for acute MI [36]. <span>With hs-cTn assays, one- to three-hour rule-outs using assay specific change criteria are usually adequate. There are only rare patients who rule in thereafter [34]. Borderline or indeterminate first troponin — Uncertainty exists around the optimal management strategy for patients with borderline or indeterminate troponin elevations or changes over




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Thus, any patient who is >3 to 6 hours after the onset of symptoms (assuming no recurrences) and who has a normal cTn value (either hs-cTn or contemporary cTn) can be considered to have ruled out for acute MI [36].
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ost patients, a rule-out diagnosis can be accomplished in two to three hours. This is facilitated by the fact that most patients do not arrive early (within two hours of the onset of symptoms). <span>Thus, any patient who is >3 to 6 hours after the onset of symptoms (assuming no recurrences) and who has a normal cTn value (either hs-cTn or contemporary cTn) can be considered to have ruled out for acute MI [36]. With hs-cTn assays, one- to three-hour rule-outs using assay specific change criteria are usually adequate. There are only rare patients who rule in thereafter [34]. Borderline or indet




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Late presenters — Patients who present 12 hours or more after the onset of symptoms can be diagnostically challenging. If the first hs-cTn is elevated in these patients, clinicians should be careful in their interpretation of changes or deltas between first and second values. Patients with adjudicated NSTEMI with less acute presentations, and those with longer ischemic times, are more likely to present near their peak hs-cTn value. Subsequent values may downtrend or stay about the same, providing false reassurance or misleading the clinician away from the diagnosis of NSTEMI, but still leaving the patient with substantial risk for mortality from ACS [37]. These patients potentially require additional testing.
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atient unit for serial troponin measurement and consideration of specialty consultation and/or imaging are prudent. Additional data are needed to define the optimal approach for these patients. <span>Late presenters — Patients who present 12 hours or more after the onset of symptoms can be diagnostically challenging. If the first hs-cTn is elevated in these patients, clinicians should be careful in their interpretation of changes or deltas between first and second values. Patients with adjudicated NSTEMI with less acute presentations, and those with longer ischemic times, are more likely to present near their peak hs-cTn value. Subsequent values may downtrend or stay about the same, providing false reassurance or misleading the clinician away from the diagnosis of NSTEMI, but still leaving the patient with substantial risk for mortality from ACS [37]. These patients potentially require additional testing. (See 'Noninvasive evaluation' below.) Risk scores — Risk scores or prediction models have been developed and integrated into care pathways. These tools predict the risk of adverse short




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The TIMI score (calculator 1) was derived and validated in patients enrolled in clinical trials with ACS, but has since been validated in patients suspected to have ACS [40]. Advantages include simplicity, lack of a need for a nomogram or computer algorithm, and its ability to predict a risk of short-term (30 days) outcome [40].
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●The TIMI risk prediction score (for unstable angina/NSTEMI) has proven predictive ability in patients with suspected or known ACS and has undergone multiple validation investigations [38,39]. <span>The TIMI score (calculator 1) was derived and validated in patients enrolled in clinical trials with ACS, but has since been validated in patients suspected to have ACS [40]. Advantages include simplicity, lack of a need for a nomogram or computer algorithm, and its ability to predict a risk of short-term (30 days) outcome [40]. Among the elements of the TIMI risk score, troponin elevation was the most powerful factor. However, even TIMI 0 patients had a significant 2.1 percent incidence of the composite outcom




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Among the elements of the TIMI risk score, troponin elevation was the most powerful factor. However, even TIMI 0 patients had a significant 2.1 percent incidence of the composite outcome. As such, the TIMI score has limited utility as a tool to determine who can be discharged as very low risk with no further testing. Once ACS has been documented, then the GRACE risk score performs better than the TIMI score [ 33]
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patients suspected to have ACS [40]. Advantages include simplicity, lack of a need for a nomogram or computer algorithm, and its ability to predict a risk of short-term (30 days) outcome [40]. <span>Among the elements of the TIMI risk score, troponin elevation was the most powerful factor. However, even TIMI 0 patients had a significant 2.1 percent incidence of the composite outcome. As such, the TIMI score has limited utility as a tool to determine who can be discharged as very low risk with no further testing. Once ACS has been documented, then the GRACE risk score performs better than the TIMI score [33]. ●The HEART score (table 1) uses similar components to the TIMI risk score. The HEART score has been widely validated [23,41,42]. However, validation studies have shown the need to add




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The HEART score (table 1) uses similar components to the TIMI risk score. The HEART score has been widely validated [23,41,42]. However, validation studies have shown the need to add a three-hour troponin to achieve acceptable sensitivity [7]. A score of 0 to 3 identifies a patient at low risk of major adverse cardiovascular events; patients with a score of 4 to 6 have intermediate risk, and those with a score of 7 or greater are high risk. A meta-analysis of 30 studies of the HEART risk score found that a score of 4 or greater had a sensitivity of about 96 percent for the prediction of short-term (39 days or 6 weeks) incidence of major adverse cardiovascular events [43].
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utility as a tool to determine who can be discharged as very low risk with no further testing. Once ACS has been documented, then the GRACE risk score performs better than the TIMI score [33]. ●<span>The HEART score (table 1) uses similar components to the TIMI risk score. The HEART score has been widely validated [23,41,42]. However, validation studies have shown the need to add a three-hour troponin to achieve acceptable sensitivity [7]. A score of 0 to 3 identifies a patient at low risk of major adverse cardiovascular events; patients with a score of 4 to 6 have intermediate risk, and those with a score of 7 or greater are high risk. A meta-analysis of 30 studies of the HEART risk score found that a score of 4 or greater had a sensitivity of about 96 percent for the prediction of short-term (39 days or 6 weeks) incidence of major adverse cardiovascular events [43]. The HEART pathway is discussed below. (See 'Care pathways' below.) ●The Calculation Of MI risk probabilities to Manage Patients with SuSpicion of Myocardial Infarction (COMPASS-MI) Proj




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If the second troponin value is also normal, we use the HEART score to reestimate risk (table 1) and the HEART Pathway (algorithm 1) to determine the next step in management.
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e being evaluated for possible MI. Prior to recommending wide-spread use of this tool, additional validation is needed, particularly in populations with differing baseline risk. Care pathways — <span>If the second troponin value is also normal, we use the HEART score to reestimate risk (table 1) and the HEART Pathway (algorithm 1) to determine the next step in management. Most EDs use a care pathway, also called an "accelerated diagnostic pathway," for patients at low to moderate risk of an ACS. These pathways are used to facilitate the discharge of pati




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It is generally agreed upon by the medical community that protocols designed to facilitate early discharge of patients who are initially suspected to be at low or moderate risk of ACS should have a negative predictive value of greater than 99 percent; that is, 99 percent of individuals chosen for early discharge will not have an adverse cardiovascular event within 30 days.
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ng further ED evaluation or treatment), using the results from an initial (and sometimes a follow-up) troponin and from an ECG. Some pathways integrate information from a risk prediction score. <span>It is generally agreed upon by the medical community that protocols designed to facilitate early discharge of patients who are initially suspected to be at low or moderate risk of ACS should have a negative predictive value of greater than 99 percent; that is, 99 percent of individuals chosen for early discharge will not have an adverse cardiovascular event within 30 days. Patients with objective signs of ischemia (ie, elevated troponin, ST-elevation, ST-depression) or a history of ischemic heart disease (ie, prior MI, history of coronary artery diseases




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The HEART Pathway consists of a modified HEART score (table 1), which is estimated from clinical data, and two troponin values at zero and three hours (algorithm 1) [7]. (See 'Risk assessment' above.)

• If the HEART score is ≤3 points and two troponin measurements are negative (ie, below the 99th percentile), and no new ischemic ECG changes are present, the risk of incident ischemic events is considered sufficiently low for discharge without further observation or diagnostic testing [23,45-48].

• For HEART scores >3 points, the patient is at intermediate or high risk and should be appropriately managed for ACS [46].

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prior coronary revascularization) should not be managed using this type of care pathway. The following pathways have been evaluated and are in clinical use to varying degrees: ●HEART Pathway – <span>The HEART Pathway consists of a modified HEART score (table 1), which is estimated from clinical data, and two troponin values at zero and three hours (algorithm 1) [7]. (See 'Risk assessment' above.) •If the HEART score is ≤3 points and two troponin measurements are negative (ie, below the 99th percentile), and no new ischemic ECG changes are present, the risk of incident ischemic events is considered sufficiently low for discharge without further observation or diagnostic testing [23,45-48]. •For HEART scores >3 points, the patient is at intermediate or high risk and should be appropriately managed for ACS [46]. The use of the HEART Pathway approach with sensitive and hs-cTn assays is supported by randomized trials and prospective registry data [7,41,45,47,49]. Examples include: •Using sensitiv




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Similar to the 0/2- and 0/3-hour pathways, the very low troponin value at presentation in a 0/1-hour pathway is not helpful for patients with recent onset (<3 hours) chest pain [33].
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values less than the lower limit of the reference range demonstrated a higher rate of all-cause mortality and MI in the 0/1-hour pathway arm (3.7 versus 2.3 percent; HR 1.60, 95% CI 1.05–2.46). <span>Similar to the 0/2- and 0/3-hour pathways, the very low troponin value at presentation in a 0/1-hour pathway is not helpful for patients with recent onset (<3 hours) chest pain [33]. The ESC 0/1-hour pathway has limitations due to reliance on cutoffs below what the FDA allows to be reported, uncertainty about the ideal cutoff and ability to measure those values for




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Patients identified as low risk with these approaches can be discharged home with primary care follow-up. However, with all decision aids, it is important to incorporate the provider's clinical gestalt into this decision
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scharges compared with previously reported rates. ●Two 2017 studies compared two or more of these approaches and found that all but the single-hs-cTn approach have an acceptable NPV [26,57-59]. <span>Patients identified as low risk with these approaches can be discharged home with primary care follow-up. However, with all decision aids, it is important to incorporate the provider's clinical gestalt into this decision. The decision to pursue outpatient evaluation, especially if additional testing is likely to be required, should be discussed with the patient. There are many reasonable evaluation stra




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Some patients will have been assessed to be at high risk, despite a normal biomarker, because of the presence of ongoing chest pain, new ECG changes, or heart failure. These patients should be admitted and managed as having unstable angina and/or heart failure.
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ed as low risk. When pursuing this strategy, we encourage clinicians to discuss this with their patients and consider patient preferences in this decision. (See 'Noninvasive evaluation' below.) <span>Some patients will have been assessed to be at high risk, despite a normal biomarker, because of the presence of ongoing chest pain, new ECG changes, or heart failure. These patients should be admitted and managed as having unstable angina and/or heart failure. (See "Overview of the acute management of non-ST elevation acute coronary syndromes".) In patients classified as not low risk, subsequent noninvasive provocative testing remains an impo




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In patients classified as not low risk, subsequent noninvasive provocative testing remains an important part of the evaluation. Among patients with normal or nondiagnostic ECG and normal troponin results, up to 10 percent may still have ACS [3], and 2 to 4 percent may have early adverse events [4,60]. Such patients may be cared for in the ED, in an observation unit, or are admitted.
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art failure. These patients should be admitted and managed as having unstable angina and/or heart failure. (See "Overview of the acute management of non-ST elevation acute coronary syndromes".) <span>In patients classified as not low risk, subsequent noninvasive provocative testing remains an important part of the evaluation. Among patients with normal or nondiagnostic ECG and normal troponin results, up to 10 percent may still have ACS [3], and 2 to 4 percent may have early adverse events [4,60]. Such patients may be cared for in the ED, in an observation unit, or are admitted. Observation unit approach — Observation units can be used to complete subsequent assessment with additional troponin values and/or stress chemical cardiac imaging in patients requiring




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If the results of stress testing or imaging are negative for a cardiac cause, and other life-threatening components of the differential diagnosis have been ruled out, discharge is appropriate for stable patients. These patients are labeled as having noncardiac chest pain. Many of these patients will carry the diagnosis of nonspecific chest pain while some will ultimately be diagnosed with cardiac causes such as myocarditis/pericarditis, stress cardiomyopathy, or heart failure [67].
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obtained. Many such patients will be admitted. ●Patients with positive stress testing or imaging results should be evaluated by a cardiologist and should generally be admitted to the hospital. ●<span>If the results of stress testing or imaging are negative for a cardiac cause, and other life-threatening components of the differential diagnosis have been ruled out, discharge is appropriate for stable patients. These patients are labeled as having noncardiac chest pain. Many of these patients will carry the diagnosis of nonspecific chest pain while some will ultimately be diagnosed with cardiac causes such as myocarditis/pericarditis, stress cardiomyopathy, or heart failure [67]. We suggest the following at the time of discharge: •Provide care for the most likely cause of pain. •Inform the patient about the basis for the presumptive diagnosis and discuss areas o




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One of the primary goals that researchers look to achieve through customer base analysis is to leverage historical records of individual customer transactions and related context factors to forecast future behavior, and to link these forecasts with actionable characteristics of individuals, managerially significant customer sub-groups, and entire cohorts.
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One of the primary goals that researchers look to achieve through customer base analysis is to leverage historical records of individual customer transactions and related context factors to forecast future behavior, and to link these forecasts with actionable characteristics of individuals, managerially significant customer sub-groups, and entire cohorts. This paper presents a new approach that helps firms leverage the automatic feature extraction capabilities of a specific type of deep learning models when applied to customer transactio

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We suggest the following at the time of discharge:

• Provide care for the most likely cause of pain.

• Inform the patient about the basis for the presumptive diagnosis and discuss areas of uncertainty in the diagnosis.

• Establish a plan for follow-up with a care provider, ideally within 72 hours.

• Provide clear and concise written discharge instructions that describe specific reasons for reevaluation and where and when to return.

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ts will carry the diagnosis of nonspecific chest pain while some will ultimately be diagnosed with cardiac causes such as myocarditis/pericarditis, stress cardiomyopathy, or heart failure [67]. <span>We suggest the following at the time of discharge: •Provide care for the most likely cause of pain. •Inform the patient about the basis for the presumptive diagnosis and discuss areas of uncertainty in the diagnosis. •Establish a plan for follow-up with a care provider, ideally within 72 hours. •Provide clear and concise written discharge instructions that describe specific reasons for reevaluation and where and when to return. INDICATIONS FOR CONSULTATION — Indications for cardiology consultation will vary among institutions. The following are reasonable indications for obtaining consultation from a cardiolog




#Data #GAN #reading #synthetic

We end up with the following attributes for the parent and child components:

| | | | | --- | --- | --- |Parent attributes | Name | Type | Description | | Employee_id | Categorical | 78 levels | | order_date | Datetime | 1996-1998 | | required_date | Datetime | 1996-1998 | | shipped_date | Datetime | 1996-1998 | | ship_via | Categorical | 3 levels | | freight | Numerical | [0.02 - 1007] | | ship_region | Categorical | 19 levels | | ship_country | Categorical | 21 levels | | customer_city | Categorical | 70 levels | | customer_region | Categorical | 19 levels | | customer_country | Categorical | 21 levels | | order_lenght | Numerical | [1 - 22] | | | | | | --- | --- | --- |Table 3: Child attributes Name Type Description product_id Categorical 77 levels supplier_id Categorical 29 levels category_id Categorical 8 levels unit_price Numerical [2 - 263.5] quantity_per_unit Numerical [0 - 70]

All data is converted into a one-hot encoding, including datetime and numerical types (previously binned into 20 levels). One-hot encoding converts categorical variables (occupation, city names, etc) into a numeric format to be ingested by machine learning algorithms.

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hierarchical GAN Data processing¶ The first step in data processing is to remove all personally identifiable information — like names and addresses — and any free-text fields. We end up with the following attributes for the parent and child components: | | | | | --- | --- | --- |Parent attributes | Name | Type | Description | | Employee_id | Categorical | 78 levels | | order_date | Datetime | 1996-1998 | | required_date | Datetime | 1996-1998 | | shipped_date | Datetime | 1996-1998 | | ship_via | Categorical | 3 levels | | freight | Numerical | [0.02 - 1007] | | ship_region | Categorical | 19 levels | | ship_country | Categorical | 21 levels | | customer_city | Categorical | 70 levels | | customer_region | Categorical | 19 levels | | customer_country | Categorical | 21 levels | | order_lenght | Numerical | [1 - 22] | | | | | | --- | --- | --- |Table 3: Child attributes Name Type Description product_id Categorical 77 levels supplier_id Categorical 29 levels category_id Categorical 8 levels unit_price Numerical [2 - 263.5] quantity_per_unit Numerical [0 - 70] All data is converted into a one-hot encoding, including datetime and numerical types (previously binned into 20 levels). One-hot encoding converts categorical variables (occupation, city names, etc) into a numeric format to be ingested by machine learning algorithms. The final generated tabular data is converted back into tables to recreate the original database

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[unknown IMAGE 7100438023436] #has-images #recurrent-neural-networks #rnn
Based on our initial discussion, an ideal model for customer base analysis in data-rich environments would combine a robust forecasting capability both in the short and in the long-term with limited engineering requirements at low computational cost and providing a direct link toward managerial decision-making.
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Based on our initial discussion, an ideal model for customer base analysis in data-rich environments would combine a robust forecasting capability both in the short and in the long-term with limited engineering requirements at low computational cost and providing a direct link toward managerial decision-making. Recognizing that traditional statistical forecasting models often suffer from poor efficiency when increasing model complexity and heavily rely on manual feature engineering and data la

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Normal first troponin If the troponin value is less than the upper reference limit, further evaluation is directed by the clinical presentation and risk factors. (See 'Normal first troponin' above and 'Late presenters' above and 'Risk scores' above.)

• For most patients whose symptoms are best explained by a noncardiac diagnosis (eg, costochondritis, pneumonia), and who have a risk for ACS less than 2 by clinical evaluation or a Heart Score of zero, the evaluation for ACS can stop (algorithm 1).

• For patients whose symptoms remain suspicious for an ACS or who have a low or intermediate risk of ACS (HEART Score ≥1), obtain a second troponin (algorithm 1). For most patients, we obtain a second troponin three hours after the first troponin and use the HEART Pathway approach. (See 'Troponin testing' above and 'Care pathways' above.)

Normal second troponin – If the second troponin value is also normal, we use the HEART score to reestimate risk (table 1) and the HEART Pathway (algorithm 1) to determine the next step in management (see 'Care pathways' above):

• For HEART Pathway score values ≤3 and two negative troponin measurements three hours apart, the patient can be discharged with follow-up in the next week.

• For HEART Pathway score values >3 and two negative troponin measurements three hours apart, the patient should remain under observation and undergo non-invasive ischemia evaluation prior to discharge.

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al evaluation' above and "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department", section on 'Management'.) <span>●Normal first troponin – If the troponin value is less than the upper reference limit, further evaluation is directed by the clinical presentation and risk factors. (See 'Normal first troponin' above and 'Late presenters' above and 'Risk scores' above.) •For most patients whose symptoms are best explained by a noncardiac diagnosis (eg, costochondritis, pneumonia), and who have a risk for ACS less than 2 by clinical evaluation or a Heart Score of zero, the evaluation for ACS can stop (algorithm 1). •For patients whose symptoms remain suspicious for an ACS or who have a low or intermediate risk of ACS (HEART Score ≥1), obtain a second troponin (algorithm 1). For most patients, we obtain a second troponin three hours after the first troponin and use the HEART Pathway approach. (See 'Troponin testing' above and 'Care pathways' above.) ●Normal second troponin – If the second troponin value is also normal, we use the HEART score to reestimate risk (table 1) and the HEART Pathway (algorithm 1) to determine the next step in management (see 'Care pathways' above): •For HEART Pathway score values ≤3 and two negative troponin measurements three hours apart, the patient can be discharged with follow-up in the next week. •For HEART Pathway score values >3 and two negative troponin measurements three hours apart, the patient should remain under observation and undergo non-invasive ischemia evaluation prior to discharge. ●Noninvasive evaluation – For those patients in whom a decision is made to perform further testing, the timing and location should be guided by patient and institutional characteristics




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Cardiac disease is the leading cause of death in the United States, yet only 2 to 4 percent of patients presenting to a primary care office with chest pain will have unstable angina or an acute myocardial infarction [2-4].
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allenge given the wide array of possible etiologies, including a potentially life-threatening condition. Approximately 1 percent of all ambulatory visits in primary care are for chest pain [1]. <span>Cardiac disease is the leading cause of death in the United States, yet only 2 to 4 percent of patients presenting to a primary care office with chest pain will have unstable angina or an acute myocardial infarction [2-4]. The most common causes of chest pain in the primary care population are chest wall pain (20 to 50 percent), reflux esophagitis (10 to 20 percent), and costochondritis (13 percent). This




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The most common causes of chest pain in the primary care population are chest wall pain (20 to 50 percent), reflux esophagitis (10 to 20 percent), and costochondritis (13 percent).
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g cause of death in the United States, yet only 2 to 4 percent of patients presenting to a primary care office with chest pain will have unstable angina or an acute myocardial infarction [2-4]. <span>The most common causes of chest pain in the primary care population are chest wall pain (20 to 50 percent), reflux esophagitis (10 to 20 percent), and costochondritis (13 percent). This topic reviews those causes of chest pain that are most common in primary care practice and the office-based diagnostic approach to chest pain. The evaluation of chest pain in the e




#recurrent-neural-networks #rnn
n this specific domain of customer base analysis, probabilistic approaches from the ‘‘Buy ’Till You Die” (BTYD) model family represent the gold standard, leveraging easily observable Recency and Frequency (RF, or RFM when including also the monetary value) metrics together with a latent attrition process to deliver accurate predictions (Schmittlein, Morrison, & Colombo, 1987; Fader, Hardie, & Lee, 2005; Fader & Hardie, 2009)
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n this specific domain of customer base analysis, probabilistic approaches from the ‘‘Buy ’Till You Die” (BTYD) model family represent the gold standard, leveraging easily observable Recency and Frequency (RF, or RFM when including also the monetary value) metrics together with a latent attrition process to deliver accurate predictions (Schmittlein, Morrison, & Colombo, 1987; Fader, Hardie, & Lee, 2005; Fader & Hardie, 2009). The simple behavioral story which sits at the core of BTYD models – while ”alive”, customers make purchases until they drop out – gives these models robust predictive power, especially

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Flashcard 7106700905740

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#causality #statistics
Question
The potential outcome that is observed is sometimes referred to as a factual. Note that there are no [...] or factuals until the outcome is observed. Before that, there are only potential outcomes
Answer
counterfactuals

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The potential outcome that is observed is sometimes referred to as a factual. Note that there are no counterfactuals or factuals until the outcome is observed. Before that, there are only potential outcomes

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Flashcard 7106702478604

Tags
#causality #statistics
Question
The potential outcome that is [...] is sometimes referred to as a factual. Note that there are no counterfactuals or factuals until the outcome is observed. Before that, there are only potential outcomes
Answer
observed

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The potential outcome that is observed is sometimes referred to as a factual. Note that there are no counterfactuals or factuals until the outcome is observed. Before that, there are only potential outcomes

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#Chest #Diagnosis #Diagnostic #Douleur #U2D #pain #thoracique
Aortic dissection – Aortic dissection is rare but may be a surgical emergency. Patients with acute aortic dissection typically present with acute chest and back pain that is severe and sharp and may have a ripping or tearing quality [5]. Pain can radiate anywhere in the chest or into the abdomen.
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g, sublingual nitroglycerin), if available. (See "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department".) ●<span>Aortic dissection – Aortic dissection is rare but may be a surgical emergency. Patients with acute aortic dissection typically present with acute chest and back pain that is severe and sharp and may have a ripping or tearing quality [5]. Pain can radiate anywhere in the chest or into the abdomen. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Symptoms and signs'.) ●Pulmonary embolism – The most common symptoms of pulmonary embolism include dyspnea




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Pulmonary embolism – The most common symptoms of pulmonary embolism include dyspnea followed by pleuritic chest pain, cough, and symptoms of deep venous thrombosis. Risk factors that may predispose to thromboembolic disease are listed in the table (table 1). In addition, the Wells score is useful for calculating the probability of pulmonary embolism (calculator 1).
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ripping or tearing quality [5]. Pain can radiate anywhere in the chest or into the abdomen. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Symptoms and signs'.) ●<span>Pulmonary embolism – The most common symptoms of pulmonary embolism include dyspnea followed by pleuritic chest pain, cough, and symptoms of deep venous thrombosis. Risk factors that may predispose to thromboembolic disease are listed in the table (table 1). In addition, the Wells score is useful for calculating the probability of pulmonary embolism (calculator 1). (See "Overview of acute pulmonary embolism in adults", section on 'Clinical presentation, evaluation, and diagnosis'.) ●Tension pneumothorax – Patients with spontaneous pneumothorax pre




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Tension pneumothorax – Patients with spontaneous pneumothorax present with sudden onset of pleuritic chest pain and dyspnea. Evidence of labored breathing, or accessory muscle use suggest a sizeable pneumothorax. Hemodynamic compromise (eg, tachycardia, hypotension) is an ominous sign and suggests a tension pneumothorax and/or impending cardiopulmonary collapse.
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ful for calculating the probability of pulmonary embolism (calculator 1). (See "Overview of acute pulmonary embolism in adults", section on 'Clinical presentation, evaluation, and diagnosis'.) ●<span>Tension pneumothorax – Patients with spontaneous pneumothorax present with sudden onset of pleuritic chest pain and dyspnea. Evidence of labored breathing, or accessory muscle use suggest a sizeable pneumothorax. Hemodynamic compromise (eg, tachycardia, hypotension) is an ominous sign and suggests a tension pneumothorax and/or impending cardiopulmonary collapse. (See "Evaluation of the adult with chest pain in the emergency department", section on 'Life-threatening conditions' and "Pneumothorax in adults: Epidemiology and etiology".) ●Esophagea




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Esophageal rupture, perforation – Spontaneous perforation of the esophagus (Boerhaave syndrome) caused by straining or vomiting presents as excruciating retrosternal chest pain [6].
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lmonary collapse. (See "Evaluation of the adult with chest pain in the emergency department", section on 'Life-threatening conditions' and "Pneumothorax in adults: Epidemiology and etiology".) ●<span>Esophageal rupture, perforation – Spontaneous perforation of the esophagus (Boerhaave syndrome) caused by straining or vomiting presents as excruciating retrosternal chest pain [6]. (See "Boerhaave syndrome: Effort rupture of the esophagus", section on 'Clinical features'.) ●Cardiac tamponade – In a patient with pericarditis, development of cardiac tamponade can be




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Cardiac tamponade – In a patient with pericarditis, development of cardiac tamponade can be life-threatening. Symptoms are sudden in onset and include chest pain, tachypnea, and dyspnea. The jugular venous pressure is markedly elevated and may be associated with venous distension in the forehead and scalp. The heart sounds are often muted.
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ave syndrome) caused by straining or vomiting presents as excruciating retrosternal chest pain [6]. (See "Boerhaave syndrome: Effort rupture of the esophagus", section on 'Clinical features'.) ●<span>Cardiac tamponade – In a patient with pericarditis, development of cardiac tamponade can be life-threatening. Symptoms are sudden in onset and include chest pain, tachypnea, and dyspnea. The jugular venous pressure is markedly elevated and may be associated with venous distension in the forehead and scalp. The heart sounds are often muted. (See "Cardiac tamponade", section on 'Clinical presentation'.) ●Sarcoidosis-related arrhythmias – Cardiac sarcoidosis can cause arrhythmias (including heart block and ventricular tachyc




#Chest #Diagnosis #Diagnostic #Douleur #U2D #pain #thoracique
Sarcoidosis-related arrhythmias – Cardiac sarcoidosis can cause arrhythmias (including heart block and ventricular tachycardia) and sudden death, which may be heralded by chest pain, palpitations, syncope, or dizziness.
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re is markedly elevated and may be associated with venous distension in the forehead and scalp. The heart sounds are often muted. (See "Cardiac tamponade", section on 'Clinical presentation'.) ●<span>Sarcoidosis-related arrhythmias – Cardiac sarcoidosis can cause arrhythmias (including heart block and ventricular tachycardia) and sudden death, which may be heralded by chest pain, palpitations, syncope, or dizziness. (See "Clinical manifestations and diagnosis of cardiac sarcoidosis".) Other etiologies — Other etiologies of chest pain are listed in the table (table 2), with a synopsis of selected co




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Heart failure – Patients with acute decompensated heart failure may present with chest discomfort, usually along with progressive dyspnea, cough, fatigue, and peripheral edema.
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oronary heart disease and myocardial infarction in young men and women", section on 'Clinical presentation'.) Nonischemic cardiac causes — Nonischemic cardiac etiologies of chest pain include: ●<span>Heart failure – Patients with acute decompensated heart failure may present with chest discomfort, usually along with progressive dyspnea, cough, fatigue, and peripheral edema. (See "Approach to diagnosis and evaluation of acute decompensated heart failure in adults", section on 'Clinical manifestations'.) ●Pericarditis/myopericarditis – Acute pericarditis ref




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Pericarditis/myopericarditis – Acute pericarditis refers to inflammation of the pericardial sac. Etiologies include infection, medications, autoimmune disorders, uremia, and malignancy. The term myopericarditis indicates a primarily pericarditic syndrome with minor myocardial involvement. Key symptoms include sharp, pleuritic chest pain which is decreased by leaning forward from a seated position, and radiates to the trapezius ridge. There is often associated fever.
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th progressive dyspnea, cough, fatigue, and peripheral edema. (See "Approach to diagnosis and evaluation of acute decompensated heart failure in adults", section on 'Clinical manifestations'.) ●<span>Pericarditis/myopericarditis – Acute pericarditis refers to inflammation of the pericardial sac. Etiologies include infection, medications, autoimmune disorders, uremia, and malignancy. The term myopericarditis indicates a primarily pericarditic syndrome with minor myocardial involvement. Key symptoms include sharp, pleuritic chest pain which is decreased by leaning forward from a seated position, and radiates to the trapezius ridge. There is often associated fever. (See "Acute pericarditis: Clinical presentation and diagnosis", section on 'Clinical features' and "Myopericarditis".) ●Myocarditis – Acute myocarditis refers to inflammation of the car




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Myocarditis – Acute myocarditis refers to inflammation of the cardiac muscle, due to infectious and noninfectious causes. Symptoms are similar to those of pericarditis described above.
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on, and radiates to the trapezius ridge. There is often associated fever. (See "Acute pericarditis: Clinical presentation and diagnosis", section on 'Clinical features' and "Myopericarditis".) ●<span>Myocarditis – Acute myocarditis refers to inflammation of the cardiac muscle, due to infectious and noninfectious causes. Symptoms are similar to those of pericarditis described above. (See "Clinical manifestations and diagnosis of myocarditis in adults".) ●Stress cardiomyopathy – Stress (takotsubo) cardiomyopathy is a syndrome characterized by transient regional syst




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Stress cardiomyopathy – Stress (takotsubo) cardiomyopathy is a syndrome characterized by transient regional systolic dysfunction of the left ventricle that often occurs in the setting of physical or emotional stress or critical illness. Symptoms, including substernal chest pain, are similar to that of acute myocardial infarction
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rdiac muscle, due to infectious and noninfectious causes. Symptoms are similar to those of pericarditis described above. (See "Clinical manifestations and diagnosis of myocarditis in adults".) ●<span>Stress cardiomyopathy – Stress (takotsubo) cardiomyopathy is a syndrome characterized by transient regional systolic dysfunction of the left ventricle that often occurs in the setting of physical or emotional stress or critical illness. Symptoms, including substernal chest pain, are similar to that of acute myocardial infarction. (See "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy", section on 'Pathogenesis' and "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyop




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Aortic valve disease – Symptoms of aortic stenosis include exertional angina, exertional dyspnea and decreased exercise tolerance, as well as exertional presyncope or syncope.
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gnosis of stress (takotsubo) cardiomyopathy", section on 'Pathogenesis' and "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy", section on 'Clinical manifestations'.) ●<span>Aortic valve disease – Symptoms of aortic stenosis include exertional angina, exertional dyspnea and decreased exercise tolerance, as well as exertional presyncope or syncope. (See "Clinical manifestations and diagnosis of aortic stenosis in adults", section on 'Symptoms'.) ●Mitral valve disease – Patients with mitral stenosis infrequently experience chest pa




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Mitral valve disease – Patients with mitral stenosis infrequently experience chest pain which resembles angina, due to pulmonary hypertension and right ventricular hypertrophy. Symptoms of mitral stenosis typically include slowly progressive exertional dyspnea.
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tional dyspnea and decreased exercise tolerance, as well as exertional presyncope or syncope. (See "Clinical manifestations and diagnosis of aortic stenosis in adults", section on 'Symptoms'.) ●<span>Mitral valve disease – Patients with mitral stenosis infrequently experience chest pain which resembles angina, due to pulmonary hypertension and right ventricular hypertrophy. Symptoms of mitral stenosis typically include slowly progressive exertional dyspnea. (See "Rheumatic mitral stenosis: Clinical manifestations and diagnosis", section on 'Chest pain'.) Patients with mitral valve prolapse may have chest pain, but it is generally mild and




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Patients with mitral valve prolapse may have chest pain, but it is generally mild and not typical for angina. (See "Mitral valve prolapse syndrome", section on 'Chest pain'.)


Chest pain — The chest pain attributed to MVP is usually atypical and easily distinguishable from angina. The pain is generally mild but can be disabling and recurrent.

Patients with chest pain and MVP should be evaluated in the same manner as any patient with chest discomfort. (See "Outpatient evaluation of the adult with chest pain".) If no cause is found, we do not recommend the use of beta blockers, because there is no evidence that they are effective. However, a modest change in lifestyle including the initiation of an exercise program may be beneficial [7].

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ertrophy. Symptoms of mitral stenosis typically include slowly progressive exertional dyspnea. (See "Rheumatic mitral stenosis: Clinical manifestations and diagnosis", section on 'Chest pain'.) <span>Patients with mitral valve prolapse may have chest pain, but it is generally mild and not typical for angina. (See "Mitral valve prolapse syndrome", section on 'Chest pain'.) Pulmonary — Patients with pulmonary etiologies for chest pain generally also have respiratory symptoms and may be hypoxemic. ●Pneumothorax – A primary spontaneous pneumothorax usually o




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Pulmonary — Patients with pulmonary etiologies for chest pain generally also have respiratory symptoms and may be hypoxemic.
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on 'Chest pain'.) Patients with mitral valve prolapse may have chest pain, but it is generally mild and not typical for angina. (See "Mitral valve prolapse syndrome", section on 'Chest pain'.) <span>Pulmonary — Patients with pulmonary etiologies for chest pain generally also have respiratory symptoms and may be hypoxemic. ●Pneumothorax – A primary spontaneous pneumothorax usually occurs without a precipitating event in young patients (typically in their twenties) with no clinical lung disease. A secondar




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Pneumothorax – A primary spontaneous pneumothorax usually occurs without a precipitating event in young patients (typically in their twenties) with no clinical lung disease. A secondary spontaneous pneumothorax occurs as a complication of underlying lung disease (eg, chronic obstructive pulmonary disease [COPD]). Typically symptoms include sudden onset of dyspnea and pleuritic chest pain, usually unilateral.
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a. (See "Mitral valve prolapse syndrome", section on 'Chest pain'.) Pulmonary — Patients with pulmonary etiologies for chest pain generally also have respiratory symptoms and may be hypoxemic. ●<span>Pneumothorax – A primary spontaneous pneumothorax usually occurs without a precipitating event in young patients (typically in their twenties) with no clinical lung disease. A secondary spontaneous pneumothorax occurs as a complication of underlying lung disease (eg, chronic obstructive pulmonary disease [COPD]). Typically symptoms include sudden onset of dyspnea and pleuritic chest pain, usually unilateral. (See "Clinical presentation and diagnosis of pneumothorax", section on 'Clinical presentation'.) Hemodynamic instability suggests a tension pneumothorax, which can be life-threatening a




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Pneumonia – Patients with pneumonia may have chest pain, which is often pleuritic. They also have fever and productive cough.
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ife-threatening and requires prompt transfer to the emergency department. (See "Evaluation of the adult with chest pain in the emergency department", section on 'Life-threatening conditions'.) ●<span>Pneumonia – Patients with pneumonia may have chest pain, which is often pleuritic. They also have fever and productive cough. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults", section on 'Clinical evaluation'.) ●Malignancy – Patients with lung cancer may complain of




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Malignancy – Patients with lung cancer may complain of chest pain, typically on the same side as the primary tumor. Other symptoms can include cough, hemoptysis, and dyspnea.
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is often pleuritic. They also have fever and productive cough. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults", section on 'Clinical evaluation'.) ●<span>Malignancy – Patients with lung cancer may complain of chest pain, typically on the same side as the primary tumor. Other symptoms can include cough, hemoptysis, and dyspnea. (See "Clinical manifestations of lung cancer", section on 'Chest pain'.) ●Asthma and COPD – Asthma and COPD exacerbations are often associated with chest tightness along with dyspnea. T




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Asthma and COPD – Asthma and COPD exacerbations are often associated with chest tightness along with dyspnea. Triggers for exacerbation (eg, pneumonia) may also cause chest pain
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chest pain, typically on the same side as the primary tumor. Other symptoms can include cough, hemoptysis, and dyspnea. (See "Clinical manifestations of lung cancer", section on 'Chest pain'.) ●<span>Asthma and COPD – Asthma and COPD exacerbations are often associated with chest tightness along with dyspnea. Triggers for exacerbation (eg, pneumonia) may also cause chest pain. (See "Asthma in adolescents and adults: Evaluation and diagnosis", section on 'Clinical features' and "Chronic obstructive pulmonary disease: Definition, clinical manifestations, diagn




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Pleuritis – Pleuritis is an inflammation of the lung pleura and causes pleuritic chest pain. Causes include autoimmune diseases (eg, systemic lupus erythematosus) and drugs (eg, procainamide, hydralazine, isoniazid). Associated systemic signs and symptoms of autoimmune disease include fever, rash, arthralgias, and constitutional symptoms.
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iagnosis", section on 'Clinical features' and "Chronic obstructive pulmonary disease: Definition, clinical manifestations, diagnosis, and staging", section on 'Symptoms and pattern of onset'.) ●<span>Pleuritis – Pleuritis is an inflammation of the lung pleura and causes pleuritic chest pain. Causes include autoimmune diseases (eg, systemic lupus erythematosus) and drugs (eg, procainamide, hydralazine, isoniazid). Associated systemic signs and symptoms of autoimmune disease include fever, rash, arthralgias, and constitutional symptoms. (See "Pulmonary manifestations of systemic lupus erythematosus in adults", section on 'Pleural disease' and "Overview of pleuropulmonary diseases associated with rheumatoid arthritis",




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Sarcoidosis – Chest pain is a common manifestation of pulmonary sarcoidosis, most commonly in association with cough and dyspnea (see "Clinical manifestations and diagnosis of pulmonary sarcoidosis"). Sarcoidosis can also cause arrhythmias [7].
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' and "Overview of pleuropulmonary diseases associated with rheumatoid arthritis", section on 'Pleural disease' and "Drug-induced lupus", section on 'Clinical spectrum of drug-induced lupus'.) ●<span>Sarcoidosis – Chest pain is a common manifestation of pulmonary sarcoidosis, most commonly in association with cough and dyspnea (see "Clinical manifestations and diagnosis of pulmonary sarcoidosis"). Sarcoidosis can also cause arrhythmias [7]. (See 'Life-threatening conditions' above.). ●Acute chest syndrome – Patients with sickle cell anemia may present with chest pain in the setting of acute chest syndrome. These patients w




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Acute chest syndrome – Patients with sickle cell anemia may present with chest pain in the setting of acute chest syndrome. These patients will also have an infiltrate on chest radiograph; other symptoms include fever, tachypnea, cough, and decreased oxygen saturation.
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sociation with cough and dyspnea (see "Clinical manifestations and diagnosis of pulmonary sarcoidosis"). Sarcoidosis can also cause arrhythmias [7]. (See 'Life-threatening conditions' above.). ●<span>Acute chest syndrome – Patients with sickle cell anemia may present with chest pain in the setting of acute chest syndrome. These patients will also have an infiltrate on chest radiograph; other symptoms include fever, tachypnea, cough, and decreased oxygen saturation. (See "Acute chest syndrome (ACS) in sickle cell disease (adults and children)", section on 'Clinical features'.) ●Pulmonary hypertension – Patients with pulmonary hypertension may have




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Pulmonary hypertension – Patients with pulmonary hypertension may have exertional chest pain in addition to exertional dyspnea and syncope.
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ther symptoms include fever, tachypnea, cough, and decreased oxygen saturation. (See "Acute chest syndrome (ACS) in sickle cell disease (adults and children)", section on 'Clinical features'.) ●<span>Pulmonary hypertension – Patients with pulmonary hypertension may have exertional chest pain in addition to exertional dyspnea and syncope. (See "Clinical features and diagnosis of pulmonary hypertension of unclear etiology in adults", section on 'Clinical manifestations'.) Gastrointestinal — Gastroesophageal reflux disease




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Gastrointestinal — Gastroesophageal reflux disease (GERD) is a common cause of noncardiac chest pain.
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chest pain in addition to exertional dyspnea and syncope. (See "Clinical features and diagnosis of pulmonary hypertension of unclear etiology in adults", section on 'Clinical manifestations'.) <span>Gastrointestinal — Gastroesophageal reflux disease (GERD) is a common cause of noncardiac chest pain. ●GERD – Chest pain due to GERD can mimic angina pectoris and may be described as squeezing or burning, located substernally and radiating to the back, neck, jaw, or arms. It can last mi




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GERD – Chest pain due to GERD can mimic angina pectoris and may be described as squeezing or burning, located substernally and radiating to the back, neck, jaw, or arms. It can last minutes to hours and resolves spontaneously or with antacids. It may occur after meals, awaken patients from sleep, and be exacerbated by emotional stress.
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monary hypertension of unclear etiology in adults", section on 'Clinical manifestations'.) Gastrointestinal — Gastroesophageal reflux disease (GERD) is a common cause of noncardiac chest pain. ●<span>GERD – Chest pain due to GERD can mimic angina pectoris and may be described as squeezing or burning, located substernally and radiating to the back, neck, jaw, or arms. It can last minutes to hours and resolves spontaneously or with antacids. It may occur after meals, awaken patients from sleep, and be exacerbated by emotional stress. (See "Clinical manifestations and diagnosis of gastroesophageal reflux in adults".) ●Peptic ulcer disease – Symptomatic peptic ulcers commonly present with epigastric pain or food-provo




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Peptic ulcer disease – Symptomatic peptic ulcers commonly present with epigastric pain or food-provoked epigastric discomfort and fullness, early satiety, and nausea.
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with antacids. It may occur after meals, awaken patients from sleep, and be exacerbated by emotional stress. (See "Clinical manifestations and diagnosis of gastroesophageal reflux in adults".) ●<span>Peptic ulcer disease – Symptomatic peptic ulcers commonly present with epigastric pain or food-provoked epigastric discomfort and fullness, early satiety, and nausea. (See "Peptic ulcer disease: Clinical manifestations and diagnosis", section on 'Clinical manifestations'.) ●Esophageal pain – Chest pain may have an esophageal origin (other than GERD),




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Esophageal pain – Chest pain may have an esophageal origin (other than GERD), such as motility disorders, which may include spasm. Clues that suggest an esophageal etiology include persistent pain >1 hour, postprandial pain, lack of radiation, associated symptoms of heartburn or regurgitation, and pain relieved by antacids.
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pain or food-provoked epigastric discomfort and fullness, early satiety, and nausea. (See "Peptic ulcer disease: Clinical manifestations and diagnosis", section on 'Clinical manifestations'.) ●<span>Esophageal pain – Chest pain may have an esophageal origin (other than GERD), such as motility disorders, which may include spasm. Clues that suggest an esophageal etiology include persistent pain >1 hour, postprandial pain, lack of radiation, associated symptoms of heartburn or regurgitation, and pain relieved by antacids. (See "Evaluation of the adult with chest pain of esophageal origin".) ●Esophagitis – Patients with medication-induced esophagitis may present with sudden-onset retrosternal chest pain i




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Esophagitis – Patients with medication-induced esophagitis may present with sudden-onset retrosternal chest pain in addition to odynophagia. Esophagitis may also be related to candidiasis, cytomegalovirus (as a complication of acquired immunodeficiency syndrome [AIDS]), or radiation injury.
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r, postprandial pain, lack of radiation, associated symptoms of heartburn or regurgitation, and pain relieved by antacids. (See "Evaluation of the adult with chest pain of esophageal origin".) ●<span>Esophagitis – Patients with medication-induced esophagitis may present with sudden-onset retrosternal chest pain in addition to odynophagia. Esophagitis may also be related to candidiasis, cytomegalovirus (as a complication of acquired immunodeficiency syndrome [AIDS]), or radiation injury. (See "Pill esophagitis", section on 'Clinical manifestations' and "Esophageal candidiasis in adults" and "AIDS-related cytomegalovirus gastrointestinal disease" and "Overview of gastroi




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Eosinophilic esophagitis – Eosinophilic esophagitis may mimic GERD in its presentation, with complaints of heartburn, dysphagia, or chest pain; however, symptoms associated with eosinophilic esophagitis may be resistant to antacid therapy.
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'Clinical manifestations' and "Esophageal candidiasis in adults" and "AIDS-related cytomegalovirus gastrointestinal disease" and "Overview of gastrointestinal toxicity of radiation therapy".) ●<span>Eosinophilic esophagitis – Eosinophilic esophagitis may mimic GERD in its presentation, with complaints of heartburn, dysphagia, or chest pain; however, symptoms associated with eosinophilic esophagitis may be resistant to antacid therapy. (See "Clinical manifestations and diagnosis of eosinophilic esophagitis (EoE)", section on 'Clinical manifestations in adults'.) ●Other – Hiatus hernias may cause chest pain in addition




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Other – Hiatus hernias may cause chest pain in addition to reflux symptoms. Acute cholecystitis, biliary colic, and pancreatitis may have pain that involves the chest.
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h eosinophilic esophagitis may be resistant to antacid therapy. (See "Clinical manifestations and diagnosis of eosinophilic esophagitis (EoE)", section on 'Clinical manifestations in adults'.) ●<span>Other – Hiatus hernias may cause chest pain in addition to reflux symptoms. Acute cholecystitis, biliary colic, and pancreatitis may have pain that involves the chest. (See "Hiatus hernia", section on 'Clinical features' and "Acute calculous cholecystitis: Clinical features and diagnosis" and "Clinical manifestations and diagnosis of acute pancreatiti




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Isolated musculoskeletal chest pain syndrome – Patients with isolated musculoskeletal chest pain syndromes have local or regional chest tenderness (table 4) without other symptoms. The most common are costosternal (costochondritis) and lower rib pain syndromes.
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loskeletal — Musculoskeletal etiologies are common in patients who present to the primary care clinician's office with chest pain. (See "Major causes of musculoskeletal chest pain in adults".) ●<span>Isolated musculoskeletal chest pain syndrome – Patients with isolated musculoskeletal chest pain syndromes have local or regional chest tenderness (table 4) without other symptoms. The most common are costosternal (costochondritis) and lower rib pain syndromes. (See "Major causes of musculoskeletal chest pain in adults", section on 'Isolated musculoskeletal chest pain syndromes'.) ●Rheumatic diseases – Rheumatic diseases can be associated with




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Rheumatic diseases – Rheumatic diseases can be associated with musculoskeletal chest wall pain, but patients generally do not have isolated chest wall pain and have other symptoms of rheumatic disease. Pain may be from increased sensitivity to ordinarily nonpainful stimuli (eg, in fibromyalgia) or involvement of thoracic joints (eg, in rheumatoid arthritis). Common rheumatologic causes of chest pain are presented in the table (table 5).
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ommon are costosternal (costochondritis) and lower rib pain syndromes. (See "Major causes of musculoskeletal chest pain in adults", section on 'Isolated musculoskeletal chest pain syndromes'.) ●<span>Rheumatic diseases – Rheumatic diseases can be associated with musculoskeletal chest wall pain, but patients generally do not have isolated chest wall pain and have other symptoms of rheumatic disease. Pain may be from increased sensitivity to ordinarily nonpainful stimuli (eg, in fibromyalgia) or involvement of thoracic joints (eg, in rheumatoid arthritis). Common rheumatologic causes of chest pain are presented in the table (table 5). (See "Major causes of musculoskeletal chest pain in adults", section on 'Rheumatic diseases causing musculoskeletal chest wall pain'.) ●Rib pain – Rib fractures are associated with pleu




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Rib pain – Rib fractures are associated with pleuritic chest pain that is localized and reproducible with palpation. Patients often describe an associated injury, though some may occur without trauma (eg, osteoporosis).
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auses of chest pain are presented in the table (table 5). (See "Major causes of musculoskeletal chest pain in adults", section on 'Rheumatic diseases causing musculoskeletal chest wall pain'.) ●<span>Rib pain – Rib fractures are associated with pleuritic chest pain that is localized and reproducible with palpation. Patients often describe an associated injury, though some may occur without trauma (eg, osteoporosis). (See "Initial evaluation and management of rib fractures", section on 'Clinical presentation and examination'.) A variety of systemic disorders can also lead to chest wall pain from rib




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A variety of systemic disorders can also lead to chest wall pain from rib pathology. These are uncommon but include neoplasm involvement of the ribs, including sarcomas, invasive primary lung cancer; and rib infarct from sickle cell anemia.
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be an associated injury, though some may occur without trauma (eg, osteoporosis). (See "Initial evaluation and management of rib fractures", section on 'Clinical presentation and examination'.) <span>A variety of systemic disorders can also lead to chest wall pain from rib pathology. These are uncommon but include neoplasm involvement of the ribs, including sarcomas, invasive primary lung cancer; and rib infarct from sickle cell anemia. (See "Major causes of musculoskeletal chest pain in adults", section on 'Nonrheumatic systemic causes of chest wall pain'.) ●Trauma – Patients can have a variety of injuries from trauma




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One in four people with a panic attack will have chest pain and shortness of breath [8].
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ypically present with spontaneous, discrete episodes of intense fear that begin abruptly and last for several minutes to an hour. In panic disorder, patients experience recurrent panic attacks. <span>One in four people with a panic attack will have chest pain and shortness of breath [8]. Panic disorder may be present in 30 percent or more of patients with chest pain who have no or minimal coronary heart disease (CHD) [9]. Hyperventilation during a panic attack can resul




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Panic disorder may be present in 30 percent or more of patients with chest pain who have no or minimal coronary heart disease (CHD) [ 9]. Hyperventilation during a panic attack can result in nonanginal chest pain and occasionally ECG changes, particularly nonspecific ST and T wave abnormalities [10,11].
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and last for several minutes to an hour. In panic disorder, patients experience recurrent panic attacks. One in four people with a panic attack will have chest pain and shortness of breath [8]. <span>Panic disorder may be present in 30 percent or more of patients with chest pain who have no or minimal coronary heart disease (CHD) [9]. Hyperventilation during a panic attack can result in nonanginal chest pain and occasionally ECG changes, particularly nonspecific ST and T wave abnormalities [10,11]. (See "Panic disorder in adults: Epidemiology, clinical manifestations, and diagnosis".) Patients with psychiatric disorders may develop or have coexisting CHD, and in such patients, isc




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Patients with psychiatric disorders may develop or have coexisting CHD, and in such patients, ischemia may occur during a panic attack [9,12,13].
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al chest pain and occasionally ECG changes, particularly nonspecific ST and T wave abnormalities [10,11]. (See "Panic disorder in adults: Epidemiology, clinical manifestations, and diagnosis".) <span>Patients with psychiatric disorders may develop or have coexisting CHD, and in such patients, ischemia may occur during a panic attack [9,12,13]. In a subgroup analysis of the Women's Health Initiative Observational Study, panic disorder was an independent risk factor for CHD in postmenopausal women [14]. ●Other – Other psychiatr




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Other – Other psychiatric etiologies of chest pain include depression, somatization, or factitious disorder.
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uring a panic attack [9,12,13]. In a subgroup analysis of the Women's Health Initiative Observational Study, panic disorder was an independent risk factor for CHD in postmenopausal women [14]. ●<span>Other – Other psychiatric etiologies of chest pain include depression, somatization, or factitious disorder. (See "Unipolar minor depression in adults: Epidemiology, clinical presentation, and diagnosis", section on 'Symptoms' and "Somatic symptom disorder: Epidemiology and clinical presentati




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Cocaine – Myocardial ischemia is the most common cardiac condition associated with cocaine use and is usually due to coronary artery spasm [15]. Other cardiac complications include aortic dissection, coronary artery aneurysm, myocarditis and cardiomyopathy, and arrhythmias.
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n, and diagnosis", section on 'Symptoms' and "Somatic symptom disorder: Epidemiology and clinical presentation" and "Factitious disorder imposed on self (Munchausen syndrome)".) Drugs of abuse ●<span>Cocaine – Myocardial ischemia is the most common cardiac condition associated with cocaine use and is usually due to coronary artery spasm [15]. Other cardiac complications include aortic dissection, coronary artery aneurysm, myocarditis and cardiomyopathy, and arrhythmias. (See "Clinical manifestations, diagnosis, and management of the cardiovascular complications of cocaine abuse".) The pulmonary complications of cocaine use can also cause chest pain but




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The pulmonary complications of cocaine use can also cause chest pain but with associated respiratory symptoms. These include acute pulmonary toxicity ("crack lung"), acute eosinophilic pneumonia, pneumothorax and pneumomediastinum, and pulmonary vascular disease.
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tion, coronary artery aneurysm, myocarditis and cardiomyopathy, and arrhythmias. (See "Clinical manifestations, diagnosis, and management of the cardiovascular complications of cocaine abuse".) <span>The pulmonary complications of cocaine use can also cause chest pain but with associated respiratory symptoms. These include acute pulmonary toxicity ("crack lung"), acute eosinophilic pneumonia, pneumothorax and pneumomediastinum, and pulmonary vascular disease. (See "Pulmonary complications of cocaine use".) ●Methamphetamine – Methamphetamine intoxication may mimic cocaine intoxication and cause similar cardiac complications. (See "Methampheta




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Methamphetamine – Methamphetamine intoxication may mimic cocaine intoxication and cause similar cardiac complications.
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clude acute pulmonary toxicity ("crack lung"), acute eosinophilic pneumonia, pneumothorax and pneumomediastinum, and pulmonary vascular disease. (See "Pulmonary complications of cocaine use".) ●<span>Methamphetamine – Methamphetamine intoxication may mimic cocaine intoxication and cause similar cardiac complications. (See "Methamphetamine: Acute intoxication", section on 'Examination findings associated with intoxication and complications'.) Referred pain — Chest wall pain may be referred from painf




#Chest #Diagnosis #Diagnostic #Douleur #U2D #pain #thoracique
Herpes zoster — Chest pain, especially in older adults, may be the presenting symptom of herpes zoster, preceding the characteristic rash usually by two to three days. Dysesthesia is usually present in the affected dermatome. Postherpetic neuralgia may also cause chest pain.
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cal features and diagnosis" and "Clinical manifestations and diagnosis of acute pancreatitis" and "Clinical manifestations and diagnosis of acute pancreatitis", section on 'Clinical features'.) <span>Herpes zoster — Chest pain, especially in older adults, may be the presenting symptom of herpes zoster, preceding the characteristic rash usually by two to three days. Dysesthesia is usually present in the affected dermatome. Postherpetic neuralgia may also cause chest pain. (See "Epidemiology, clinical manifestations, and diagnosis of herpes zoster", section on 'Clinical manifestations' and "Postherpetic neuralgia", section on 'Clinical manifestations'.) D




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Referred pain — Chest wall pain may be referred from painful disorders in visceral or somatic structures sharing the same spinal cord segments. The pain is perceived in the corresponding dermatomes and myotomes.
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imic cocaine intoxication and cause similar cardiac complications. (See "Methamphetamine: Acute intoxication", section on 'Examination findings associated with intoxication and complications'.) <span>Referred pain — Chest wall pain may be referred from painful disorders in visceral or somatic structures sharing the same spinal cord segments. The pain is perceived in the corresponding dermatomes and myotomes. For example, referred pain can come from abdominal organs, cervical disc disease, or from the ligaments, muscles, and periosteum of the cervical and thoracic spines. Acute cholecystitis




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Domestic violence — Patients suffering from domestic violence may complain of chest pain or have chest pain in the setting of associated psychiatric conditions (eg, panic disorder).
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est pain. (See "Epidemiology, clinical manifestations, and diagnosis of herpes zoster", section on 'Clinical manifestations' and "Postherpetic neuralgia", section on 'Clinical manifestations'.) <span>Domestic violence — Patients suffering from domestic violence may complain of chest pain or have chest pain in the setting of associated psychiatric conditions (eg, panic disorder). In a community-based population of 1900 primary care patients, chest pain was one of many specific physical symptoms associated with current domestic violence [16]. (See "Intimate partn




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Initial triage

● All patients should have vital sign and oxygen saturation measurement.

● Patients with unstable vital signs should be evaluated urgently by a clinician.

● If symptoms are concerning for aortic dissection (acute chest and back pain that is severe, sharp, with a ripping or tearing quality), blood pressure should be obtained in both arms.

● If pericarditis is suspected, based on pleuritic chest pain and relief when sitting forward, pulsus paradoxus should be evaluated. (See 'Nonischemic cardiac disease' below.)

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valuation should then proceed to a thorough history and physical examination which are used to assess the probability of various causes of chest pain and determine the need for further testing. <span>Initial triage ●All patients should have vital sign and oxygen saturation measurement. ●Patients with unstable vital signs should be evaluated urgently by a clinician. ●If symptoms are concerning for aortic dissection (acute chest and back pain that is severe, sharp, with a ripping or tearing quality), blood pressure should be obtained in both arms. ●If pericarditis is suspected, based on pleuritic chest pain and relief when sitting forward, pulsus paradoxus should be evaluated. (See 'Nonischemic cardiac disease' below.) Patients who have unstable vital signs or symptoms of life-threatening conditions should be sent to the emergency department by ambulance. Symptoms of life-threatening conditions includ




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The most common ECG findings in patients with pulmonary embolism are tachycardia, T-wave inversion in lead V1, and ST elevation in lead aVR [17]
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on on 'Electrocardiogram'.) Pericarditis is discussed below (see 'Nonischemic cardiac disease' below), and treatment is presented elsewhere. (See "Acute pericarditis: Treatment and prognosis".) <span>The most common ECG findings in patients with pulmonary embolism are tachycardia, T-wave inversion in lead V1, and ST elevation in lead aVR [17] (see "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism", section on 'Electrocardiography') The treatment of pulmonary em




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After excluding life-threatening causes of chest pain, identifying patients with stable myocardial ischemia is the next priority.
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Indications for chest radiograph — Indications for chest radiograph include suspected pulmonary causes of chest pain, heart failure or rib fracture. Evaluation for stable myocardial ischemia — <span>After excluding life-threatening causes of chest pain, identifying patients with stable myocardial ischemia is the next priority. Evaluation is indicated in patients with classic symptoms but also in those without classic angina who have no other obvious etiology for their chest pain, or in those with multiple ris




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Features of chest pain that increase and decrease the likelihood of myocardial ischemia are presented in the table ( table 6).
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ngina who have no other obvious etiology for their chest pain, or in those with multiple risk factors for cardiovascular disease (eg, diabetes, hyperlipidemia, hypertension and/or tobacco use). <span>Features of chest pain that increase and decrease the likelihood of myocardial ischemia are presented in the table (table 6). Certain medical conditions may worsen ischemic symptoms (table 3). ●Symptoms – Classic symptoms of stable angina include a pressure, heaviness, tightness, or constriction in the center




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Risk factors – Elements of patient history which increase the likelihood of myocardial ischemia include older age, family history of cardiovascular disease (table 7), tobacco or cocaine use, diabetes mellitus, hypertension, hyperlipidemia, and certain lifestyle factors.
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2-25]. (See "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department", section on 'Atypical presentations'.) ●<span>Risk factors – Elements of patient history which increase the likelihood of myocardial ischemia include older age, family history of cardiovascular disease (table 7), tobacco or cocaine use, diabetes mellitus, hypertension, hyperlipidemia, and certain lifestyle factors. The Multi-Ethnic Study of Atherosclerosis (MESA) risk calculator can be used for risk stratification. This calculator utilizes a coronary artery calcium score, although an estimate of r




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Nonischemic cardiac disease — Key diagnoses include pericarditis, heart failure, and aortic stenosis.
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f other etiologies — If the evaluation for myocardial ischemia is negative or there is low suspicion, further evaluation is directed by the most likely etiology based on the initial evaluation. <span>Nonischemic cardiac disease — Key diagnoses include pericarditis, heart failure, and aortic stenosis. (See 'Nonischemic cardiac causes' above.) Elements of the history include elicitation of symptoms of pericarditis (sharp pleuritic chest pain), heart failure (dyspnea, peripheral edema,




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Patients in whom pericarditis is suspected should have the following examinations performed:

● A cardiac examination while lying supine and while sitting up and leaning forward (picture 1). Classically, patients will have symptom relief with sitting up, and this is also the best position in which to evaluate the patient for a pericardial rub (movie 1) (see "Acute pericarditis: Clinical presentation and diagnosis", section on 'Pericardial friction rub' and "Acute pericarditis: Clinical presentation and diagnosis", section on 'Clinical features'). Diagnostic criteria of ECG indicative of acute pericarditis and myopericarditis are presented in the table (table 8).

● Evaluation for pulsus paradoxus (an abnormally large decrease in systolic blood pressure [>10 mmHg] on inspiration), which is indicative of cardiac tamponade (see "Cardiac tamponade", section on 'Pulsus paradoxus'). If pulsus paradoxus if found, the patient should be sent to the emergency department.

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nea, peripheral edema, cough), aortic stenosis (exertional dyspnea, exertional angina, exertional presyncope or syncope), and mitral stenosis (exertional dyspnea, decreased exercise tolerance). <span>Patients in whom pericarditis is suspected should have the following examinations performed: ●A cardiac examination while lying supine and while sitting up and leaning forward (picture 1). Classically, patients will have symptom relief with sitting up, and this is also the best position in which to evaluate the patient for a pericardial rub (movie 1) (see "Acute pericarditis: Clinical presentation and diagnosis", section on 'Pericardial friction rub' and "Acute pericarditis: Clinical presentation and diagnosis", section on 'Clinical features'). Diagnostic criteria of ECG indicative of acute pericarditis and myopericarditis are presented in the table (table 8). ●Evaluation for pulsus paradoxus (an abnormally large decrease in systolic blood pressure [>10 mmHg] on inspiration), which is indicative of cardiac tamponade (see "Cardiac tamponade", section on 'Pulsus paradoxus'). If pulsus paradoxus if found, the patient should be sent to the emergency department. The approach to management of patients with pericarditis is discussed separately. (See "Acute pericarditis: Treatment and prognosis".) Patients with symptoms and physical examination co




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Gastrointestinal disease — Evaluation for gastrointestinal disease involves elicitation of symptoms of heartburn, indigestion, regurgitation, and pain associated with food intake, all of which make a gastrointestinal etiology more likely.
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and diagnosis".) The approach to management of patients with heart failure is reviewed separately. (See "Overview of the management of heart failure with reduced ejection fraction in adults".) <span>Gastrointestinal disease — Evaluation for gastrointestinal disease involves elicitation of symptoms of heartburn, indigestion, regurgitation, and pain associated with food intake, all of which make a gastrointestinal etiology more likely. Common etiologies are discussed above. (See 'Gastrointestinal' above.) There is considerable overlap between symptoms of gastrointestinal disease and myocardial ischemia. Discomfort tha




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There is considerable overlap between symptoms of gastrointestinal disease and myocardial ischemia. Discomfort that reliably occurs with eating, or that is reliably and repeatedly palliated by antacids or food is likely of gastroesophageal origin. However, relief of pain following the administration of a "gastrointestinal cocktail" (eg, viscous lidocaine and antacid) does not reliably distinguish gastrointestinal from ischemic chest pain [27].
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digestion, regurgitation, and pain associated with food intake, all of which make a gastrointestinal etiology more likely. Common etiologies are discussed above. (See 'Gastrointestinal' above.) <span>There is considerable overlap between symptoms of gastrointestinal disease and myocardial ischemia. Discomfort that reliably occurs with eating, or that is reliably and repeatedly palliated by antacids or food is likely of gastroesophageal origin. However, relief of pain following the administration of a "gastrointestinal cocktail" (eg, viscous lidocaine and antacid) does not reliably distinguish gastrointestinal from ischemic chest pain [27]. Similarly, pain that responds to sublingual nitroglycerin is frequently thought to have a cardiac etiology but may also be due to esophageal origin [28]. Patients whose symptoms are con




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Patients with a negative cardiac evaluation and anginal-like chest pain often have gastroesophageal reflux disease (GERD) [29-31]. GERD is associated with heartburn, regurgitation, cough, and dysphagia (table 9). GERD can be diagnosed based on symptoms and response to therapy, with initial therapy depending on the severity of symptoms.
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eatment for gastrointestinal etiologies, particularly if they have risk factors for cardiovascular disease. (See 'Gastrointestinal' above and 'Evaluation for stable myocardial ischemia' above.) <span>Patients with a negative cardiac evaluation and anginal-like chest pain often have gastroesophageal reflux disease (GERD) [29-31]. GERD is associated with heartburn, regurgitation, cough, and dysphagia (table 9). GERD can be diagnosed based on symptoms and response to therapy, with initial therapy depending on the severity of symptoms. (See "Medical management of gastroesophageal reflux disease in adults", section on 'Initial management' and "Evaluation of the adult with chest pain of esophageal origin" and "Clinical




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Belching, a bad taste in the mouth, and difficult or painful swallowing are suggestive of esophageal disease (see "Pill esophagitis", section on 'Clinical manifestations' and "Evaluation of the adult with chest pain of esophageal origin"). Patients with dysphagia should be evaluated based on potential etiologies (table 10).
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in adults", section on 'Initial management' and "Evaluation of the adult with chest pain of esophageal origin" and "Clinical manifestations and diagnosis of gastroesophageal reflux in adults".) <span>Belching, a bad taste in the mouth, and difficult or painful swallowing are suggestive of esophageal disease (see "Pill esophagitis", section on 'Clinical manifestations' and "Evaluation of the adult with chest pain of esophageal origin"). Patients with dysphagia should be evaluated based on potential etiologies (table 10). (See "Approach to the evaluation of dysphagia in adults".) Further evaluation of esophageal or peptic ulcer disease will likely involve consultation with a gastroenterologist for determ




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Pulmonary disease — Key symptoms in patients with pulmonary disease include pleuritic chest pain, dyspnea, and cough. Obtaining a history of chronic lung disease (eg, asthma, chronic obstructive pulmonary disease [COPD], sarcoidosis), malignancy, prior pulmonary embolism, or systemic autoimmune disease can be helpful in the diagnosis.
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hagia in adults".) Further evaluation of esophageal or peptic ulcer disease will likely involve consultation with a gastroenterologist for determination of the appropriate diagnostic procedure. <span>Pulmonary disease — Key symptoms in patients with pulmonary disease include pleuritic chest pain, dyspnea, and cough. Obtaining a history of chronic lung disease (eg, asthma, chronic obstructive pulmonary disease [COPD], sarcoidosis), malignancy, prior pulmonary embolism, or systemic autoimmune disease can be helpful in the diagnosis. A chest radiograph is usually necessary. Potential etiologies include pulmonary embolism, pneumothorax, pleuritis, asthma or COPD exacerbation, or pneumonia. (See 'Pulmonary' above.) Ph




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Physical examination findings in patients with a small pneumothorax may be limited to signs of the underlying lung disease, if present. However, characteristic physical findings when a large pneumothorax is present include decreased chest excursion on the affected side, enlarged hemithorax on the affected side, diminished breath sounds, absent tactile or vocal fremitus, and hyperresonant percussion, as well as, rarely, subcutaneous emphysema.
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diagnosis. A chest radiograph is usually necessary. Potential etiologies include pulmonary embolism, pneumothorax, pleuritis, asthma or COPD exacerbation, or pneumonia. (See 'Pulmonary' above.) <span>Physical examination findings in patients with a small pneumothorax may be limited to signs of the underlying lung disease, if present. However, characteristic physical findings when a large pneumothorax is present include decreased chest excursion on the affected side, enlarged hemithorax on the affected side, diminished breath sounds, absent tactile or vocal fremitus, and hyperresonant percussion, as well as, rarely, subcutaneous emphysema. (See "Clinical presentation and diagnosis of pneumothorax", section on 'Clinical manifestations'.) Musculoskeletal disease — Musculoskeletal etiologies are the most common causes of che




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Musculoskeletal disease — Musculoskeletal etiologies are the most common causes of chest pain. Well-localized pain associated with point tenderness is more likely to be musculoskeletal in origin [32]. Body position or movement may exacerbate chest pain of musculoskeletal origin. Musculoskeletal complaints outside the chest are suggestive of a musculoskeletal etiology for chest pain. For example, pain in the neck, thoracic spine, or shoulder may cause referred pain to the chest. Chronic widespread musculoskeletal pain is associated with fibromyalgia.
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e or vocal fremitus, and hyperresonant percussion, as well as, rarely, subcutaneous emphysema. (See "Clinical presentation and diagnosis of pneumothorax", section on 'Clinical manifestations'.) <span>Musculoskeletal disease — Musculoskeletal etiologies are the most common causes of chest pain. Well-localized pain associated with point tenderness is more likely to be musculoskeletal in origin [32]. Body position or movement may exacerbate chest pain of musculoskeletal origin. Musculoskeletal complaints outside the chest are suggestive of a musculoskeletal etiology for chest pain. For example, pain in the neck, thoracic spine, or shoulder may cause referred pain to the chest. Chronic widespread musculoskeletal pain is associated with fibromyalgia. (See "Clinical evaluation of musculoskeletal chest pain".) If the evaluation is consistent with musculoskeletal pain (eg, point tenderness that is reproducible with palpation) with no e




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If the evaluation is consistent with musculoskeletal pain (eg, point tenderness that is reproducible with palpation) with no evidence of underlying systemic etiology, it is reasonable to defer diagnostic studies and prescribe a therapeutic trial of physical therapy or nonsteroidal antiinflammatory medication which may help confirm the diagnosis if there is improvement [33].
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acic spine, or shoulder may cause referred pain to the chest. Chronic widespread musculoskeletal pain is associated with fibromyalgia. (See "Clinical evaluation of musculoskeletal chest pain".) <span>If the evaluation is consistent with musculoskeletal pain (eg, point tenderness that is reproducible with palpation) with no evidence of underlying systemic etiology, it is reasonable to defer diagnostic studies and prescribe a therapeutic trial of physical therapy or nonsteroidal antiinflammatory medication which may help confirm the diagnosis if there is improvement [33]. If there is concern for underlying systemic disease, then the appropriate evaluation should be initiated. (See 'Musculoskeletal' above and "Management of isolated musculoskeletal chest




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Psychiatric disease — The most common psychiatric diseases associated with chest pain are panic disorder and depression. Patients with depressed mood, decreased appetite, or sleep disturbances may have depression. Classic associated symptoms in patients with panic attack include fear and tachycardia.
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ld be initiated. (See 'Musculoskeletal' above and "Management of isolated musculoskeletal chest pain" and "Clinical evaluation of musculoskeletal chest pain", section on 'Diagnostic approach'.) <span>Psychiatric disease — The most common psychiatric diseases associated with chest pain are panic disorder and depression. Patients with depressed mood, decreased appetite, or sleep disturbances may have depression. Classic associated symptoms in patients with panic attack include fear and tachycardia. A validated screening question that is good at supporting a diagnosis of panic disorder when patients answer yes, and good at ruling it out when the answer is no, is the following: “In




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A validated screening question that is good at supporting a diagnosis of panic disorder when patients answer yes, and good at ruling it out when the answer is no, is the following: “In the past four weeks, have you had an anxiety attack (suddenly feeling fear or panic)?” [ 34].
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depression. Patients with depressed mood, decreased appetite, or sleep disturbances may have depression. Classic associated symptoms in patients with panic attack include fear and tachycardia. <span>A validated screening question that is good at supporting a diagnosis of panic disorder when patients answer yes, and good at ruling it out when the answer is no, is the following: “In the past four weeks, have you had an anxiety attack (suddenly feeling fear or panic)?” [34]. A therapeutic trial of cognitive behavioral therapy and/or antidepressant medication may be indicated. (See "Psychotherapy for panic disorder with or without agoraphobia in adults", sec




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Other conditions — If other etiologies have been evaluated and ruled out or the history and physical examination are not consistent with those etiologies, we use a knowledge of dermatomes and spinal and visceral pain referral patterns to guide to the evaluation of other less common causes of chest pain (eg, zoster) and pain referred to the chest (eg, from the gallbladder, diaphragm, or from a disc herniation).
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ychotherapy for panic disorder with or without agoraphobia in adults", section on 'Cognitive-behavioral therapy' and "Pharmacotherapy for panic disorder with or without agoraphobia in adults".) <span>Other conditions — If other etiologies have been evaluated and ruled out or the history and physical examination are not consistent with those etiologies, we use a knowledge of dermatomes and spinal and visceral pain referral patterns to guide to the evaluation of other less common causes of chest pain (eg, zoster) and pain referred to the chest (eg, from the gallbladder, diaphragm, or from a disc herniation). Hyperesthesia, particularly when associated with a rash, is often due to herpes zoster. Patients with referred pain will often have associated symptoms or physical examination findings




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Hyperesthesia, particularly when associated with a rash, is often due to herpes zoster.
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erral patterns to guide to the evaluation of other less common causes of chest pain (eg, zoster) and pain referred to the chest (eg, from the gallbladder, diaphragm, or from a disc herniation). <span>Hyperesthesia, particularly when associated with a rash, is often due to herpes zoster. Patients with referred pain will often have associated symptoms or physical examination findings that support a particular diagnosis. INFORMATION FOR PATIENTS — UpToDate offers two type




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Patients with referred pain will often have associated symptoms or physical examination findings that support a particular diagnosis.
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zoster) and pain referred to the chest (eg, from the gallbladder, diaphragm, or from a disc herniation). Hyperesthesia, particularly when associated with a rash, is often due to herpes zoster. <span>Patients with referred pain will often have associated symptoms or physical examination findings that support a particular diagnosis. INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain langu




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ST elevation — RBBB does not usually interfere with the diagnosis of an acute ST-elevation MI (STEMI). The reason is that MI most often involves the left ventricle and therefore affects the initial phase of ventricular depolarization, sometimes producing abnormal Q waves. In contrast, RBBB primarily affects the terminal phase of ventricular depolarization, producing a wide R' wave in the right chest leads and a wide S wave in the left chest leads (waveform 1A-B). These changes are due to delayed depolarization of the right ventricle, while depolarization of the left ventricle is not substantially affected. (See "Right bundle branch block".)
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pital mortality. RIGHT BUNDLE BRANCH BLOCK WITH MI — Clinicians should be familiar with the effects of right bundle branch block (RBBB) in the settings of acute and prior myocardial infarction. <span>ST elevation — RBBB does not usually interfere with the diagnosis of an acute ST-elevation MI (STEMI). The reason is that MI most often involves the left ventricle and therefore affects the initial phase of ventricular depolarization, sometimes producing abnormal Q waves. In contrast, RBBB primarily affects the terminal phase of ventricular depolarization, producing a wide R' wave in the right chest leads and a wide S wave in the left chest leads (waveform 1A-B). These changes are due to delayed depolarization of the right ventricle, while depolarization of the left ventricle is not substantially affected. (See "Right bundle branch block".) The net effect is that the ECG patterns are combined when complete RBBB and a Q wave infarct occur together, and the criteria for the diagnosis of a Q wave MI are the same as in patient




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The net effect is that the ECG patterns are combined when complete RBBB and a Q wave infarct occur together, and the criteria for the diagnosis of a Q wave MI are the same as in patients with normal conduction:

● Due to the bundle branch block, the QRS complex will be abnormally wide (duration of 120 ms or more), lead V1 will show a terminal, positive deflection, and lead V6 will show a terminal negative deflection (wide S wave).

● If the infarction is anterior, there will be a loss of R wave progression with abnormal Q waves in the anterior leads and characteristic ST-T changes; if the infarction is inferior, Q waves will appear in leads II, III, and aVF.

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eform 1A-B). These changes are due to delayed depolarization of the right ventricle, while depolarization of the left ventricle is not substantially affected. (See "Right bundle branch block".) <span>The net effect is that the ECG patterns are combined when complete RBBB and a Q wave infarct occur together, and the criteria for the diagnosis of a Q wave MI are the same as in patients with normal conduction: ●Due to the bundle branch block, the QRS complex will be abnormally wide (duration of 120 ms or more), lead V1 will show a terminal, positive deflection, and lead V6 will show a terminal negative deflection (wide S wave). ●If the infarction is anterior, there will be a loss of R wave progression with abnormal Q waves in the anterior leads and characteristic ST-T changes; if the infarction is inferior, Q waves will appear in leads II, III, and aVF. However, problems can occur with interpretation of the ECG in patients with RBBB and acute MI: ●Large clinical trials in which serial ECGs are performed have shown both false-positive a




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Large clinical trials in which serial ECGs are performed have shown both false-positive and false-negative diagnoses of MI in the presence of RBBB [8]. After revascularization, for example, Q wave durations in patients who develop RBBB can shorten significantly, primarily in the inferior leads, suggesting that the initial orientation of wavefronts can change and that false-negative results may be obtained in patients with inferior infarctions [9].
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istic ST-T changes; if the infarction is inferior, Q waves will appear in leads II, III, and aVF. However, problems can occur with interpretation of the ECG in patients with RBBB and acute MI: ●<span>Large clinical trials in which serial ECGs are performed have shown both false-positive and false-negative diagnoses of MI in the presence of RBBB [8]. After revascularization, for example, Q wave durations in patients who develop RBBB can shorten significantly, primarily in the inferior leads, suggesting that the initial orientation of wavefronts can change and that false-negative results may be obtained in patients with inferior infarctions [9]. ●There has been a case report of a woman with an acute anterior MI in whom the initial ECG revealed a small R wave in leads V1 and V4 [10]. These R waves were replaced by Q waves after




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There has been a case report of a woman with an acute anterior MI in whom the initial ECG revealed a small R wave in leads V1 and V4 [10]. These R waves were replaced by Q waves after the development of RBBB associated with PR-interval prolongation, suggesting extension of the infarction. However, the Q waves disappeared with resolution of the RBBB.
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ly, primarily in the inferior leads, suggesting that the initial orientation of wavefronts can change and that false-negative results may be obtained in patients with inferior infarctions [9]. ●<span>There has been a case report of a woman with an acute anterior MI in whom the initial ECG revealed a small R wave in leads V1 and V4 [10]. These R waves were replaced by Q waves after the development of RBBB associated with PR-interval prolongation, suggesting extension of the infarction. However, the Q waves disappeared with resolution of the RBBB. ●The coexistence of left anterior fascicular block with or without RBBB can be associated with Q waves suggestive of an acute anterior MI; in this setting, the altered initial vector is




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The coexistence of left anterior fascicular block with or without RBBB can be associated with Q waves suggestive of an acute anterior MI; in this setting, the altered initial vector is attributed to the left anterior fascicular block [11]. These acute Q waves can often be distinguished from nonacute Q-waves by their short duration (0.02 sec versus 0.04 to 0.05 sec with an acute infarction) and their presence in only leads V2 and/or V3.
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eplaced by Q waves after the development of RBBB associated with PR-interval prolongation, suggesting extension of the infarction. However, the Q waves disappeared with resolution of the RBBB. ●<span>The coexistence of left anterior fascicular block with or without RBBB can be associated with Q waves suggestive of an acute anterior MI; in this setting, the altered initial vector is attributed to the left anterior fascicular block [11]. These acute Q waves can often be distinguished from nonacute Q-waves by their short duration (0.02 sec versus 0.04 to 0.05 sec with an acute infarction) and their presence in only leads V2 and/or V3. ●An acute posterior wall infarct in the presence of RBBB might be expected to increase the anterior forces in the right precordial leads, but this has not been systematically studied. ●




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An acute posterior wall infarct in the presence of RBBB might be expected to increase the anterior forces in the right precordial leads, but this has not been systematically studied.
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cute Q waves can often be distinguished from nonacute Q-waves by their short duration (0.02 sec versus 0.04 to 0.05 sec with an acute infarction) and their presence in only leads V2 and/or V3. ●<span>An acute posterior wall infarct in the presence of RBBB might be expected to increase the anterior forces in the right precordial leads, but this has not been systematically studied. ●Note that the Brugada pattern may simulate RBBB with acute or evolving ST-elevation MI. (See "Brugada syndrome: Clinical presentation, diagnosis, and evaluation", section on 'ECG findi




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Note that the Brugada pattern may simulate RBBB with acute or evolving ST-elevation MI.
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d/or V3. ●An acute posterior wall infarct in the presence of RBBB might be expected to increase the anterior forces in the right precordial leads, but this has not been systematically studied. ●<span>Note that the Brugada pattern may simulate RBBB with acute or evolving ST-elevation MI. (See "Brugada syndrome: Clinical presentation, diagnosis, and evaluation", section on 'ECG findings'.) Non-ST-elevation myocardial infarction — There may be some diagnostic difficulties




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Non-ST-elevation myocardial infarction — There may be some diagnostic difficulties in interpreting the ECG in patients with RBBB who have a non-ST-elevation MI. RBBB is typically associated with secondary ST-T changes due to abnormal right ventricular repolarization. Thus, leads with an R' wave (leads V1, V2, and sometimes V3) will show T wave inversions. In contrast, ST depressions or T wave inversions in leads with a terminal S wave (leads V5 and V6) cannot be attributed to the RBBB alone. Such ST-T changes may be due to ischemia, or to other factors such as drug effects (digoxin) or electrolyte abnormalities, such as hypokalemia.
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. ●Note that the Brugada pattern may simulate RBBB with acute or evolving ST-elevation MI. (See "Brugada syndrome: Clinical presentation, diagnosis, and evaluation", section on 'ECG findings'.) <span>Non-ST-elevation myocardial infarction — There may be some diagnostic difficulties in interpreting the ECG in patients with RBBB who have a non-ST-elevation MI. RBBB is typically associated with secondary ST-T changes due to abnormal right ventricular repolarization. Thus, leads with an R' wave (leads V1, V2, and sometimes V3) will show T wave inversions. In contrast, ST depressions or T wave inversions in leads with a terminal S wave (leads V5 and V6) cannot be attributed to the RBBB alone. Such ST-T changes may be due to ischemia, or to other factors such as drug effects (digoxin) or electrolyte abnormalities, such as hypokalemia. LEFT BUNDLE BRANCH BLOCK WITH MI — Left bundle branch block (LBBB) is present in approximately 7 percent of acute infarctions [7]. The diagnosis of acute MI in the presence of LBBB is c




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Left bundle branch block (LBBB) is present in approximately 7 percent of acute infarctions [7]. The diagnosis of acute MI in the presence of LBBB is considerably more complicated and confusing than that of right bundle branch block (RBBB). The reason is that LBBB alters both the early and the mid to late phases of ventricular depolarization, and also produces secondary ST-T changes (waveform 2A-B).
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he RBBB alone. Such ST-T changes may be due to ischemia, or to other factors such as drug effects (digoxin) or electrolyte abnormalities, such as hypokalemia. LEFT BUNDLE BRANCH BLOCK WITH MI — <span>Left bundle branch block (LBBB) is present in approximately 7 percent of acute infarctions [7]. The diagnosis of acute MI in the presence of LBBB is considerably more complicated and confusing than that of right bundle branch block (RBBB). The reason is that LBBB alters both the early and the mid to late phases of ventricular depolarization, and also produces secondary ST-T changes (waveform 2A-B). Two major issues need to be addressed: the impact of LBBB on the diagnosis of acute MI and the effect on diagnosis of a remote MI [1-4]. There are issues that vary with the site of the




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Two major issues need to be addressed: the impact of LBBB on the diagnosis of acute MI and the effect on diagnosis of a remote MI [1-4]. There are issues that vary with the site of the infarct, and there are changes that are independent of the site of the infarct. Because of these difficulties, careful attention to the strength of the clinical history and confirmation of the diagnosis of an acute MI by cardiac enzyme biomarker elevations are essential.
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ght bundle branch block (RBBB). The reason is that LBBB alters both the early and the mid to late phases of ventricular depolarization, and also produces secondary ST-T changes (waveform 2A-B). <span>Two major issues need to be addressed: the impact of LBBB on the diagnosis of acute MI and the effect on diagnosis of a remote MI [1-4]. There are issues that vary with the site of the infarct, and there are changes that are independent of the site of the infarct. Because of these difficulties, careful attention to the strength of the clinical history and confirmation of the diagnosis of an acute MI by cardiac enzyme biomarker elevations are essential. (See "Diagnosis of acute myocardial infarction".) Acute myocardial infarction — The sequence of repolarization is altered in LBBB, with the ST segment and T wave vectors being directed




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Acute myocardial infarction — The sequence of repolarization is altered in LBBB, with the ST segment and T wave vectors being directed opposite to the main QRS vector. These changes may mask the ST-segment depression and T wave inversion induced by ischemia.
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to the strength of the clinical history and confirmation of the diagnosis of an acute MI by cardiac enzyme biomarker elevations are essential. (See "Diagnosis of acute myocardial infarction".) <span>Acute myocardial infarction — The sequence of repolarization is altered in LBBB, with the ST segment and T wave vectors being directed opposite to the main QRS vector. These changes may mask the ST-segment depression and T wave inversion induced by ischemia. On the other hand, the diagnosis of an acute MI or ischemia can occasionally be made in a patient with underlying LBBB if certain ST-T changes are seen, particularly if the ST-T vectors




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On the other hand, the diagnosis of an acute MI or ischemia can occasionally be made in a patient with underlying LBBB if certain ST-T changes are seen, particularly if the ST-T vectors are in the same direction as the QRS complex as in the Sgarbossa criteria described below.

● The presence of deep T wave inversions in leads with a predominantly negative QRS complex (eg, V1-V3) is highly suggestive of evolving ischemia or MI.

● ST elevations in leads with a predominant R wave (as opposed to QS or rS waves) are also strongly suggestive of acute ischemia [12].

● "Pseudonormalization" of previously inverted T waves is suggestive, however, not diagnostic of ischemia.

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ltered in LBBB, with the ST segment and T wave vectors being directed opposite to the main QRS vector. These changes may mask the ST-segment depression and T wave inversion induced by ischemia. <span>On the other hand, the diagnosis of an acute MI or ischemia can occasionally be made in a patient with underlying LBBB if certain ST-T changes are seen, particularly if the ST-T vectors are in the same direction as the QRS complex as in the Sgarbossa criteria described below. ●The presence of deep T wave inversions in leads with a predominantly negative QRS complex (eg, V1-V3) is highly suggestive of evolving ischemia or MI. ●ST elevations in leads with a predominant R wave (as opposed to QS or rS waves) are also strongly suggestive of acute ischemia [12]. ●"Pseudonormalization" of previously inverted T waves is suggestive, however, not diagnostic of ischemia. The importance of accurate diagnosis in patients with LBBB is illustrated by the following observations: ●The proportion of patients with LBBB and acute chest pain having an acute MI in




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In addition to difficulties in ECG interpretation, approximately one-half of patients with LBBB and an acute MI do not have chest pain [16]. These patients are much less likely to receive appropriate medical therapy (eg, aspirin, beta blockers) or reperfusion therapy than LBBB patients with chest pain [16].
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to 48 percent of patients with LBBB and chest pain but no biochemical evidence of infarction [15]. None of the latter patients satisfied the Sgarbossa criteria described below for an acute MI. ●<span>In addition to difficulties in ECG interpretation, approximately one-half of patients with LBBB and an acute MI do not have chest pain [16]. These patients are much less likely to receive appropriate medical therapy (eg, aspirin, beta blockers) or reperfusion therapy than LBBB patients with chest pain [16]. Attempts to improve ECG diagnosis — Several studies have systematically evaluated the value of different ECG findings of acute MI in LBBB. A 1987 analysis correlated ECG changes in LBBB




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The proportion of patients with LBBB and acute chest pain having an acute MI in different studies has varied considerably (eg, between 13 and 32 percent), with a lower incidence in community-based studies compared with clinical trials [13,14].
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ion" of previously inverted T waves is suggestive, however, not diagnostic of ischemia. The importance of accurate diagnosis in patients with LBBB is illustrated by the following observations: ●<span>The proportion of patients with LBBB and acute chest pain having an acute MI in different studies has varied considerably (eg, between 13 and 32 percent), with a lower incidence in community-based studies compared with clinical trials [13,14]. As a result, inaccurate diagnosis can lead to both undertreatment of patients with an MI and unnecessary overtreatment of patients without an MI [13,15]. In one early report, for exampl




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A 1987 analysis correlated ECG changes in LBBB with localization of the infarct by thallium scintigraphy [2]. The most useful ECG criteria were:

● Serial ECG changes – 67 percent sensitivity.

● ST-segment elevation – 54 percent sensitivity.

● Abnormal Q waves – 31 percent sensitivity.

● Initial positivity in V1 with a Q wave in V6 – 20 percent sensitivity but 100 percent specificity for anteroseptal MI.

● Cabrera sign – 27 percent sensitivity overall, 47 percent for anteroseptal MI.

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usion therapy than LBBB patients with chest pain [16]. Attempts to improve ECG diagnosis — Several studies have systematically evaluated the value of different ECG findings of acute MI in LBBB. <span>A 1987 analysis correlated ECG changes in LBBB with localization of the infarct by thallium scintigraphy [2]. The most useful ECG criteria were: ●Serial ECG changes – 67 percent sensitivity. ●ST-segment elevation – 54 percent sensitivity. ●Abnormal Q waves – 31 percent sensitivity. ●Initial positivity in V1 with a Q wave in V6 – 20 percent sensitivity but 100 percent specificity for anteroseptal MI. ●Cabrera sign – 27 percent sensitivity overall, 47 percent for anteroseptal MI. Note: Cabrera sign refers to prominent (about 0.05 sec in duration) notching in the ascending limb of the S wave in leads V3 and V4; a similar finding is prominent notching of the ascen




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Note: Cabrera sign refers to prominent (about 0.05 sec in duration) notching in the ascending limb of the S wave in leads V3 and V4; a similar finding is prominent notching of the ascending limb of the R wave in lead V5 or V6 (Chapman sign) [2]. These eponymous signs have a specificity that approaches 90 percent. However, there may be a high degree of interobserver variability in their accurate identification and their sensitivity is quite low. Likely, the pathophysiology relates to underlying myocardial scarring and fractionation of depolarization electrograms, reflected on the surface leads as QRS notching in conjunction with LBBB.
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al positivity in V1 with a Q wave in V6 – 20 percent sensitivity but 100 percent specificity for anteroseptal MI. ●Cabrera sign – 27 percent sensitivity overall, 47 percent for anteroseptal MI. <span>Note: Cabrera sign refers to prominent (about 0.05 sec in duration) notching in the ascending limb of the S wave in leads V3 and V4; a similar finding is prominent notching of the ascending limb of the R wave in lead V5 or V6 (Chapman sign) [2]. These eponymous signs have a specificity that approaches 90 percent. However, there may be a high degree of interobserver variability in their accurate identification and their sensitivity is quite low. Likely, the pathophysiology relates to underlying myocardial scarring and fractionation of depolarization electrograms, reflected on the surface leads as QRS notching in conjunction with LBBB. Sgarbossa criteria — A large trial of thrombolytic therapy for acute MI provided an opportunity to revisit the issue of the electrocardiographic diagnosis of evolving acute MI in the pr




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A scoring system, often called the Sgarbossa criteria, was developed from the coefficients assigned by a logistic model for each independent criterion, on a scale of 0 to 5.

The three original ECG criteria with independent value in the diagnosis of acute infarction and the score for each were:

● ST-segment elevation of ≥1 mm in the same direction as the QRS complex (concordant) in any lead: score 5.

● ST-segment depression of ≥1 mm in any lead from V1 to V3: score 3.

● ST-segment elevation of 5 mm or more that is discordant with the QRS complex (ie, associated with a QS or rS complex): score 2. However, prominent J point elevations may occur in V1 to V2 solely due to left ventricular hypertrophy or in other settings. Therefore, a ratio (expressed in absolute units) in any relevant lead of the amplitude of the ST-elevation lead divided by the S wave amplitude in that lead that equals or exceeds 0.25 has been proposed as having greater accuracy than the original (not normalized) Sgarbossa criterion [17]. A higher ratio indicates relatively greater ST elevation. The diagnostic superiority of this modified (STE/S wave) criterion as compared with the original "Sgarbossa rule #3" was supported by the findings of a retrospective case-control study [18].

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graphic diagnosis of evolving acute MI in the presence of LBBB [3]. Among 26,003 North American patients who had a myocardial infarction confirmed by enzyme studies, 131 (0.5 percent) had LBBB. <span>A scoring system, often called the Sgarbossa criteria, was developed from the coefficients assigned by a logistic model for each independent criterion, on a scale of 0 to 5. The three original ECG criteria with independent value in the diagnosis of acute infarction and the score for each were: ●ST-segment elevation of ≥1 mm in the same direction as the QRS complex (concordant) in any lead: score 5. ●ST-segment depression of ≥1 mm in any lead from V1 to V3: score 3. ●ST-segment elevation of 5 mm or more that is discordant with the QRS complex (ie, associated with a QS or rS complex): score 2. However, prominent J point elevations may occur in V1 to V2 solely due to left ventricular hypertrophy or in other settings. Therefore, a ratio (expressed in absolute units) in any relevant lead of the amplitude of the ST-elevation lead divided by the S wave amplitude in that lead that equals or exceeds 0.25 has been proposed as having greater accuracy than the original (not normalized) Sgarbossa criterion [17]. A higher ratio indicates relatively greater ST elevation. The diagnostic superiority of this modified (STE/S wave) criterion as compared with the original "Sgarbossa rule #3" was supported by the findings of a retrospective case-control study [18]. A Sgarbossa score of ≥3 was highly specific (ie, few false positives) but much less sensitive (36 percent) in the validation sample in the original report [3]. Similar findings were not




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A Sgarbossa score of ≥3 was highly specific (ie, few false positives) but much less sensitive (36 percent) in the validation sample in the original report [3].
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n. The diagnostic superiority of this modified (STE/S wave) criterion as compared with the original "Sgarbossa rule #3" was supported by the findings of a retrospective case-control study [18]. <span>A Sgarbossa score of ≥3 was highly specific (ie, few false positives) but much less sensitive (36 percent) in the validation sample in the original report [3]. Similar findings were noted in a subsequent meta-analysis of 10 studies of 1614 patients in which a Sgarbossa score of ≥3 had a sensitivity of 20 percent and a specificity of 98 percent




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In patients with RV pacing and signs or symptoms of ischemia, modified versions of the original Sgarbossa criteria can be used to identify acute myocardial ischemia with reasonable accuracy [17,22]. The ECG suggests ischemia in the presence of RV pacing if one or more of the following features are present:

● ST-segment elevation of >1 mm in the same direction as the QRS complex (concordant) in any lead.

● ST-segment depression >1 mm in the same direction as the QRS complex (concordant) in at least one chest lead (ie, V1 to V6).

● ST-elevation (mm) / S-wave amplitude (mm) ratio >0.25 (a measure of discordance) from the lead that generates the greatest ST-elevation/S-wave ratio.

These modified Sgarbossa criteria were validated in a study of patients with RV pacing who presented with signs or symptoms of myocardial ischemia [22]. The diagnosis of acute MI ("occlusion MI") was confirmed by troponin assay values and invasive coronary angiography. The ECG criteria had a sensitivity of 86 percent and a specificity of 83 percent for the diagnosis of acute MI.

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o preexisting LBBB, right ventricular (RV) pacing results in delayed repolarization of the left ventricle that prevents the usual interpretation of ST segment changes in patients with acute MI. <span>In patients with RV pacing and signs or symptoms of ischemia, modified versions of the original Sgarbossa criteria can be used to identify acute myocardial ischemia with reasonable accuracy [17,22]. The ECG suggests ischemia in the presence of RV pacing if one or more of the following features are present: ●ST-segment elevation of >1 mm in the same direction as the QRS complex (concordant) in any lead. ●ST-segment depression >1 mm in the same direction as the QRS complex (concordant) in at least one chest lead (ie, V1 to V6). ●ST-elevation (mm) / S-wave amplitude (mm) ratio >0.25 (a measure of discordance) from the lead that generates the greatest ST-elevation/S-wave ratio. These modified Sgarbossa criteria were validated in a study of patients with RV pacing who presented with signs or symptoms of myocardial ischemia [22]. The diagnosis of acute MI ("occlusion MI") was confirmed by troponin assay values and invasive coronary angiography. The ECG criteria had a sensitivity of 86 percent and a specificity of 83 percent for the diagnosis of acute MI. By comparison, the unweighted "original" Sgarbossa criteria had a lower diagnostic accuracy (sensitivity 56 percent, specificity 90 percent), while the "modified Sgarbossa criteria" had




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Left ventricular free wall — Infarction of the left ventricular free (or lateral) wall ordinarily results in abnormal Q waves in the midprecordial to lateral precordial leads (and selected limb leads). However, the initial septal depolarization forces with LBBB are directed from right to left. These leftward forces produce an initial R wave in the mid to lateral precordial leads, usually masking the loss of potential (Q waves) caused by the infarction. As a result, acute or prior left ventricular free wall infarction by itself will not usually produce diagnostic Q waves in the presence of LBBB.

If, however, the loss of lateral force is sufficiently large, late rightward forces generated by other portions of the left ventricle may predominate, possibly resulting in S waves in I, aVL, and V6. Thus, an anterolateral MI should be suspected in the appropriate clinical setting if new S waves appear in leftward leads in a patient with preexisting common LBBB. This is an old concept that makes electrophysiologic and vectorcardiographic sense; however, it requires further clinical validation.

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equence of depolarization in LBBB can also mask typical findings associated with prior transmural (Q wave) infarctions. Certain ECG patterns, however, may suggest prior infarction despite LBBB. <span>Left ventricular free wall — Infarction of the left ventricular free (or lateral) wall ordinarily results in abnormal Q waves in the midprecordial to lateral precordial leads (and selected limb leads). However, the initial septal depolarization forces with LBBB are directed from right to left. These leftward forces produce an initial R wave in the mid to lateral precordial leads, usually masking the loss of potential (Q waves) caused by the infarction. As a result, acute or prior left ventricular free wall infarction by itself will not usually produce diagnostic Q waves in the presence of LBBB. If, however, the loss of lateral force is sufficiently large, late rightward forces generated by other portions of the left ventricle may predominate, possibly resulting in S waves in I, aVL, and V6. Thus, an anterolateral MI should be suspected in the appropriate clinical setting if new S waves appear in leftward leads in a patient with preexisting common LBBB. This is an old concept that makes electrophysiologic and vectorcardiographic sense; however, it requires further clinical validation. Anteroseptal — The presence of LBBB has a variable effect on the ECG changes that can occur with anteroseptal MI. Perhaps most important, the leftward shift in the initial vector in LBB




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Anteroseptal — The presence of LBBB has a variable effect on the ECG changes that can occur with anteroseptal MI. Perhaps most important, the leftward shift in the initial vector in LBBB causes the loss of normal septal Q waves in the left-right leads, I, aVL, and V6. Furthermore, the leftward and posterior orientation of the initial vector often results in a QS pattern in the anterior leads, V1 and sometimes in V2. These changes can mask the presence of a prior anteroseptal MI.

There are, however, other changes that can occur that may suggest the presence of a prior anteroseptal or septal MI. The infarct may cause the leftwardly directed initial vector of LBBB to shift to the right, resulting in "pseudonormalization" of the initial vector and the reappearance of q waves in I, aVL and V6. If enough of the septum is infarcted, abnormal QR, QRS, or qrS types of complexes may appear in the mid to lateral precordial leads in conjunction with the LBBB pattern.

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n leftward leads in a patient with preexisting common LBBB. This is an old concept that makes electrophysiologic and vectorcardiographic sense; however, it requires further clinical validation. <span>Anteroseptal — The presence of LBBB has a variable effect on the ECG changes that can occur with anteroseptal MI. Perhaps most important, the leftward shift in the initial vector in LBBB causes the loss of normal septal Q waves in the left-right leads, I, aVL, and V6. Furthermore, the leftward and posterior orientation of the initial vector often results in a QS pattern in the anterior leads, V1 and sometimes in V2. These changes can mask the presence of a prior anteroseptal MI. There are, however, other changes that can occur that may suggest the presence of a prior anteroseptal or septal MI. The infarct may cause the leftwardly directed initial vector of LBBB to shift to the right, resulting in "pseudonormalization" of the initial vector and the reappearance of q waves in I, aVL and V6. If enough of the septum is infarcted, abnormal QR, QRS, or qrS types of complexes may appear in the mid to lateral precordial leads in conjunction with the LBBB pattern. Free wall and septal — Acute or prior infarction involving both the free wall and the septum may produce abnormal Q waves (usually as part of QRS or QrS types of complexes) in leads V4




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Free wall and septal — Acute or prior infarction involving both the free wall and the septum may produce abnormal Q waves (usually as part of QRS or QrS types of complexes) in leads V4 to V6. These initial Q waves probably reflect posterior/lateral and superior forces from the spared basal portion of the septum. Small Q waves (0.03 sec or less) may be seen in leads I and V5 to V6 with uncomplicated LBBB. Thus, wide Q waves (0.04 sec) in one or more of these leads are a more reliable sign of underlying infarction. As an example, wide Q waves (as part of QR complexes) in V6, particularly with an R wave in V1, appear to be a specific, although relatively insensitive, marker of prior anterior infarction [1].
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waves in I, aVL and V6. If enough of the septum is infarcted, abnormal QR, QRS, or qrS types of complexes may appear in the mid to lateral precordial leads in conjunction with the LBBB pattern. <span>Free wall and septal — Acute or prior infarction involving both the free wall and the septum may produce abnormal Q waves (usually as part of QRS or QrS types of complexes) in leads V4 to V6. These initial Q waves probably reflect posterior/lateral and superior forces from the spared basal portion of the septum. Small Q waves (0.03 sec or less) may be seen in leads I and V5 to V6 with uncomplicated LBBB. Thus, wide Q waves (0.04 sec) in one or more of these leads are a more reliable sign of underlying infarction. As an example, wide Q waves (as part of QR complexes) in V6, particularly with an R wave in V1, appear to be a specific, although relatively insensitive, marker of prior anterior infarction [1]. Inferior wall — In a retrospective analysis, 35 patients with LBBB and an unequivocal inferior MI on thallium imaging were compared to 131 patients with LBBB without an inferior wall MI




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Inferior wall — In a retrospective analysis, 35 patients with LBBB and an unequivocal inferior MI on thallium imaging were compared to 131 patients with LBBB without an inferior wall MI [23]. Two ECG findings were most useful for the diagnosis of a prior inferior MI:

● Q or QS wave in lead aVF, found in 29 percent of those with a documented MI versus only 3 percent of those without a prior inferior MI.

● Diagnostic T wave inversion (compete or biphasic with an initial negative deflection), present in 66 percent with and 6 percent without a prior MI.

The presence of either finding was 86 percent sensitive and 91 percent specific for the diagnosis of a prior inferior wall MI.

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s an example, wide Q waves (as part of QR complexes) in V6, particularly with an R wave in V1, appear to be a specific, although relatively insensitive, marker of prior anterior infarction [1]. <span>Inferior wall — In a retrospective analysis, 35 patients with LBBB and an unequivocal inferior MI on thallium imaging were compared to 131 patients with LBBB without an inferior wall MI [23]. Two ECG findings were most useful for the diagnosis of a prior inferior MI: ●Q or QS wave in lead aVF, found in 29 percent of those with a documented MI versus only 3 percent of those without a prior inferior MI. ●Diagnostic T wave inversion (compete or biphasic with an initial negative deflection), present in 66 percent with and 6 percent without a prior MI. The presence of either finding was 86 percent sensitive and 91 percent specific for the diagnosis of a prior inferior wall MI. SUMMARY — The following points summarize the electrocardiographic (ECG) signs of acute and prior myocardial infarction (MI) in the presence of a left bundle branch block (LBBB). ●The or




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The original and subsequent modifications of the Sgarbossa criteria have high specificity but low sensitivity for acute MI [3,13-15,24]; thus, their presence is highly suggestive of acute infarction, but their absence has little value.
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erior wall MI. SUMMARY — The following points summarize the electrocardiographic (ECG) signs of acute and prior myocardial infarction (MI) in the presence of a left bundle branch block (LBBB). ●<span>The original and subsequent modifications of the Sgarbossa criteria have high specificity but low sensitivity for acute MI [3,13-15,24]; thus, their presence is highly suggestive of acute infarction, but their absence has little value. ●A QS pattern, slow R wave progression, or loss of R waves in the anterior precordial leads or a QS pattern in II, III, aVF, or aVL can occur with uncomplicated LBBB. ●LBBB characterist




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The presence of QR complexes in leads I, V5, or V6, or in II, III, and aVF with LBBB strongly suggests underlying infarction, which may be acute or remote.
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t ST elevations in the lateral leads or ST depression or deep T wave inversions in leads V1 to V3 suggests underlying ischemia [3]. Thus, close attention should be paid to serial ST-T changes. ●<span>The presence of QR complexes in leads I, V5, or V6, or in II, III, and aVF with LBBB strongly suggests underlying infarction, which may be acute or remote. ●An acute anterolateral MI should be suspected if new S waves appear in leftward leads (I, aVL, and V6) in a patient with preexisting common LBBB. ●Prior MI, due to fibrosis and scarrin




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An acute anterolateral MI should be suspected if new S waves appear in leftward leads (I, aVL, and V6) in a patient with preexisting common LBBB.
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uld be paid to serial ST-T changes. ●The presence of QR complexes in leads I, V5, or V6, or in II, III, and aVF with LBBB strongly suggests underlying infarction, which may be acute or remote. ●<span>An acute anterolateral MI should be suspected if new S waves appear in leftward leads (I, aVL, and V6) in a patient with preexisting common LBBB. ●Prior MI, due to fibrosis and scarring, is also suggested by notching of the ascending part of a wide S waves in the midprecordial leads (Cabrera sign), or of the ascending limb of a w




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Prior MI, due to fibrosis and scarring, is also suggested by notching of the ascending part of a wide S waves in the midprecordial leads (Cabrera sign), or of the ascending limb of a wide R wave in V5 or V6 (Chapman sign).
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ing infarction, which may be acute or remote. ●An acute anterolateral MI should be suspected if new S waves appear in leftward leads (I, aVL, and V6) in a patient with preexisting common LBBB. ●<span>Prior MI, due to fibrosis and scarring, is also suggested by notching of the ascending part of a wide S waves in the midprecordial leads (Cabrera sign), or of the ascending limb of a wide R wave in V5 or V6 (Chapman sign). Use of UpToDate is subject to the Terms of Use. REFERENCES Goldberger AL, Goldberger ZA, Shvilkin A. Goldberger's clinical electrocardiography: A simplified approach, 9th Ed, Elsevier/S




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Increased blood concentrations of cTn can also be seen in a variety of other diseases, such as sepsis, atrial fibrillation, heart failure, pulmonary embolism, myocarditis, myocardial contusion, and renal failure. In addition, stable chronic elevation of cardiac troponin may be detectable with high-sensitivity assays in patients with underlying structural (muscle) heart disease.
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ocardial infarction", section on 'Definitions'.) However, troponin is not specific for acute thrombotic occlusion of a coronary artery, the most common precursor to acute myocardial infarction. <span>Increased blood concentrations of cTn can also be seen in a variety of other diseases, such as sepsis, atrial fibrillation, heart failure, pulmonary embolism, myocarditis, myocardial contusion, and renal failure. In addition, stable chronic elevation of cardiac troponin may be detectable with high-sensitivity assays in patients with underlying structural (muscle) heart disease. Analytical false positives or false negatives are rare. Potential causes of troponin elevation unrelated to coronary thrombosis will be reviewed here. Other related topics include: ●(Se




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Cardiac troponins (cTn) are regulatory proteins that control the calcium-mediated interaction of actin and myosin. The troponin complex consists of three subunits: troponin T (cTnT), troponin I (cTnI), and troponin C.
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nt of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department", section on 'Cardiac biomarkers and other laboratory testing'.) CARDIAC TROPONINS — <span>Cardiac troponins (cTn) are regulatory proteins that control the calcium-mediated interaction of actin and myosin. The troponin complex consists of three subunits: troponin T (cTnT), troponin I (cTnI), and troponin C. (See "Excitation-contraction coupling in myocardium", section on 'Role of tropomyosin and troponins'.) The skeletal and cardiac isoforms of cTnT and cTnI are distinct, and skeletal isof




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The skeletal and cardiac isoforms of cTnT and cTnI are distinct, and skeletal isoforms are not detected by the monoclonal antibody-based assays currently in use, except for cTnT in some circumstances of significant skeletal muscle disease [1]. This high specificity for cardiac isoforms is the basis for the clinical utility of cTnT and cTnI assays.
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complex consists of three subunits: troponin T (cTnT), troponin I (cTnI), and troponin C. (See "Excitation-contraction coupling in myocardium", section on 'Role of tropomyosin and troponins'.) <span>The skeletal and cardiac isoforms of cTnT and cTnI are distinct, and skeletal isoforms are not detected by the monoclonal antibody-based assays currently in use, except for cTnT in some circumstances of significant skeletal muscle disease [1]. This high specificity for cardiac isoforms is the basis for the clinical utility of cTnT and cTnI assays. The diagnosis of myocardial infarction requires that cTn must be above the 99th percentile upper reference limit for the assay being used and that there is clinical evidence of myocardi




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The diagnosis of myocardial infarction requires that cTn must be above the 99th percentile upper reference limit for the assay being used and that there is clinical evidence of myocardial ischemia.
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use, except for cTnT in some circumstances of significant skeletal muscle disease [1]. This high specificity for cardiac isoforms is the basis for the clinical utility of cTnT and cTnI assays. <span>The diagnosis of myocardial infarction requires that cTn must be above the 99th percentile upper reference limit for the assay being used and that there is clinical evidence of myocardial ischemia. The 99th percentile reference limit has also been shown to differ between men and women when measured with high-sensitivity assays for cardiac troponin [2]. (See "Troponin testing: Anal




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Data suggest that brief periods of ischemia, sudden increases in preload, and physiological challenges like tachycardia and catecholamines can lead to the release of cTn [4,5]. In the first two situations, cTn release has been attributed to apoptosis.
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LULAR MECHANISMS — With prolonged ischemia, myocytes are irreversibly damaged (necrosis). The cell membrane degrades, followed by the gradual release of myofibril-bound cytosolic complexes [3]. <span>Data suggest that brief periods of ischemia, sudden increases in preload, and physiological challenges like tachycardia and catecholamines can lead to the release of cTn [4,5]. In the first two situations, cTn release has been attributed to apoptosis. However, it is possible that cardiac troponins can also be released into the circulation without cell death: ●Increased myocyte membrane permeability – It is thought that myocardial dep




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Increased myocyte membrane permeability – It is thought that myocardial depressive factors (released in the setting of sepsis and other inflammatory states) cause degradation of free troponin to lower-molecular-weight fragments [6]. With increased membrane permeability, those smaller troponin fragments could be released into the systemic circulation. In this setting, troponin may be elevated, although myocyte cell death may not have occurred. This hypothesis is also supported by the clinical observation that myocardial depression during sepsis is a fully reversible process in most surviving patients [7].
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n [4,5]. In the first two situations, cTn release has been attributed to apoptosis. However, it is possible that cardiac troponins can also be released into the circulation without cell death: ●<span>Increased myocyte membrane permeability – It is thought that myocardial depressive factors (released in the setting of sepsis and other inflammatory states) cause degradation of free troponin to lower-molecular-weight fragments [6]. With increased membrane permeability, those smaller troponin fragments could be released into the systemic circulation. In this setting, troponin may be elevated, although myocyte cell death may not have occurred. This hypothesis is also supported by the clinical observation that myocardial depression during sepsis is a fully reversible process in most surviving patients [7]. ●Normal turnover of myocardial cells – Cell turnover could lead to release of cTn degradation products through the formation and release of membranous blebs [8], although this has not y




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Normal turnover of myocardial cells – Cell turnover could lead to release of cTn degradation products through the formation and release of membranous blebs [8], although this has not yet been shown.
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eath may not have occurred. This hypothesis is also supported by the clinical observation that myocardial depression during sepsis is a fully reversible process in most surviving patients [7]. ●<span>Normal turnover of myocardial cells – Cell turnover could lead to release of cTn degradation products through the formation and release of membranous blebs [8], although this has not yet been shown. DEMAND ISCHEMIA — The concept of "demand ischemia" refers to a mismatch between myocardial oxygen demand and supply. The term was originally applied to patients with evidence of ischemi




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Myocardial oxygen supply is reduced (and serum troponins may be increased) in a number of clinical settings: sepsis, septic shock, and the systemic inflammatory response syndrome [10,11]; hypotension or hypovolemia [12]; noncardiac critically ill patients presented to the emergency department [13]; and atrial fibrillation or other tachyarrhythmias [14,15].
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I) refers to a Type 2 MI when the event is secondary to ischemia due to either an increased oxygen demand or a decreased supply in the absence of an acute primary coronary thrombotic event [9]. <span>Myocardial oxygen supply is reduced (and serum troponins may be increased) in a number of clinical settings: sepsis, septic shock, and the systemic inflammatory response syndrome [10,11]; hypotension or hypovolemia [12]; noncardiac critically ill patients presented to the emergency department [13]; and atrial fibrillation or other tachyarrhythmias [14,15]. (See 'Non-MI causes of an elevated troponin' below.) In these settings, increased myocardial demand can be due to: ●Tachycardia ●Changes in cardiac loading conditions ●Increases in card




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In these settings, increased myocardial demand can be due to:

● Tachycardia

● Changes in cardiac loading conditions

● Increases in cardiac output to accommodate increased systemic oxygen consumption

● Myocardial depression

Simultaneously, myocardial oxygen delivery may be reduced due to the following:

● Reduced coronary perfusion due to both tachycardia, which reduces diastolic time, during which coronary flow occurs, and reduced perfusion pressure in the setting of hypotension and increased cardiac filling pressures.

● Decreased oxygen delivery to the heart.

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]; noncardiac critically ill patients presented to the emergency department [13]; and atrial fibrillation or other tachyarrhythmias [14,15]. (See 'Non-MI causes of an elevated troponin' below.) <span>In these settings, increased myocardial demand can be due to: ●Tachycardia ●Changes in cardiac loading conditions ●Increases in cardiac output to accommodate increased systemic oxygen consumption ●Myocardial depression Simultaneously, myocardial oxygen delivery may be reduced due to the following: ●Reduced coronary perfusion due to both tachycardia, which reduces diastolic time, during which coronary flow occurs, and reduced perfusion pressure in the setting of hypotension and increased cardiac filling pressures. ●Decreased oxygen delivery to the heart. Ultimately, these forces combine to create mismatch in myocardial oxygen supply and demand, resulting in ischemia and the release of troponin into the systemic circulation. However, thi




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In many patients, there are direct effects related to catecholamines or in sepsis to heat shock proteins and tissue necrosis factor. Such increases in cardiac troponin are deemed as myocardial injury rather than Type 2 myocardial infarction [16]. Thus, it should not be assumed that all elevations where one sees hemodynamic perturbations are due solely to supply-demand imbalance [17].
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emand, resulting in ischemia and the release of troponin into the systemic circulation. However, this does not imply that all elevations in these individuals are due to supply-demand imbalance. <span>In many patients, there are direct effects related to catecholamines or in sepsis to heat shock proteins and tissue necrosis factor. Such increases in cardiac troponin are deemed as myocardial injury rather than Type 2 myocardial infarction [16]. Thus, it should not be assumed that all elevations where one sees hemodynamic perturbations are due solely to supply-demand imbalance [17]. OUR APPROACH — We agree with the 2018 Joint European Society of Cardiology/American College of Cardiology/American Heart Association/World Health Federation task force for the Fourth Un




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, which recommends that an elevated value of cardiac troponin, in the absence of clinical evidence of ischemia, should prompt a search for other causes of myocardial necrosis [16].

Some causes require immediate medical attention: myocarditis, pulmonary embolism, heart failure, sepsis, or renal failure.

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pean Society of Cardiology/American College of Cardiology/American Heart Association/World Health Federation task force for the Fourth Universal Definition of Myocardial Infarction (MI) document<span>, which recommends that an elevated value of cardiac troponin, in the absence of clinical evidence of ischemia, should prompt a search for other causes of myocardial necrosis [16]. Some causes require immediate medical attention: myocarditis, pulmonary embolism, heart failure, sepsis, or renal failure. While an elevated troponin is generally associated with a worse prognosis, there is insufficient evidence at present to conclude that screening the general population (with troponin) is




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Troponin elevations have been reported in a variety of clinical scenarios (other than an acute thrombotic occlusion of the coronary artery), which is the most common cause of an elevated troponin (table 1).
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there is uncertainty as to which individuals with an elevated troponin need additional testing. Consideration should be given to screening for structural heart disease on a case-by-case basis. <span>Troponin elevations have been reported in a variety of clinical scenarios (other than an acute thrombotic occlusion of the coronary artery), which is the most common cause of an elevated troponin (table 1). These clinical scenarios are often acute medical problems or serious chronic illnesses. There are three major categories: myocardial damage related to supply-demand mismatch, myocardial




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There are three major categories: myocardial damage related to supply-demand mismatch, myocardial damage related to non-ischemic causes (eg, myocarditis or direct trauma), and myocardial injury that is multifactorial or of indeterminate cause [ 46].
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otic occlusion of the coronary artery), which is the most common cause of an elevated troponin (table 1). These clinical scenarios are often acute medical problems or serious chronic illnesses. <span>There are three major categories: myocardial damage related to supply-demand mismatch, myocardial damage related to non-ischemic causes (eg, myocarditis or direct trauma), and myocardial injury that is multifactorial or of indeterminate cause [46]. (See 'Cellular mechanisms' above.) Below is a list of some of the causes for the elevation of troponin. In some circumstances, these potential categories of causes may be overlapping or




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In one series of 21 patients with elevated troponin levels and a normal coronary angiogram, the following etiologies for troponin elevations were suggested [14]:

● Tachycardia – 28 percent

● Pericarditis – 10 percent

● Heart failure – 5 percent

● Strenuous exercise – 10 percent

● No clear precipitating event – 47 percent

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uding surgery, ablation, pacing, implantable cardioverter-defibrillator shocks, cardioversion, endomyocardial biopsy, cardiac surgery, following interventional closure of atrial septal defects. <span>In one series of 21 patients with elevated troponin levels and a normal coronary angiogram, the following etiologies for troponin elevations were suggested [14]: ●Tachycardia – 28 percent ●Pericarditis – 10 percent ●Heart failure – 5 percent ●Strenuous exercise – 10 percent ●No clear precipitating event – 47 percent Coronavirus disease 2019 (COVID-19) — Elevated troponin in patients with or suspected of COVID-19 infection is discussed separately. (See "COVID-19: Evaluation and management of cardiac




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Thus, troponin elevation among patients with sepsis and SIRS is common. Affected patients often have no evidence of significant CHD. In this setting, troponin elevation is associated with a worse prognosis (see 'Prognosis' below), but it is unclear whether any cardiovascular intervention could improve outcomes. Although a causal relationship has yet to be established, inflammatory mediators in conjunction with a myocardial oxygen demand-supply mismatch are potential explanations for this phenomenon.
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and C-reactive protein levels were significantly higher in patients with elevated troponin levels. ●Significant coronary artery disease was excluded in 72 percent of troponin-positive patients. <span>Thus, troponin elevation among patients with sepsis and SIRS is common. Affected patients often have no evidence of significant CHD. In this setting, troponin elevation is associated with a worse prognosis (see 'Prognosis' below), but it is unclear whether any cardiovascular intervention could improve outcomes. Although a causal relationship has yet to be established, inflammatory mediators in conjunction with a myocardial oxygen demand-supply mismatch are potential explanations for this phenomenon. Troponin elevations suggestive of demand ischemia have also been described in a broader range of critically ill patients. In a review of 20 observational studies involving 3278 critical