on 12-May-2016 (Thu)

Pathology of Aortic stenosis:
-congenital bicuspid valve
-degenerative (Ca & fibrosis restricts valve opening)

• calcific (wear & tear)
• ​rheumatic

Progression of aortic stenosis:
-50% reduction in valve orifice results in minimal pressure gradient
-Increments beyond this produce exponential increases in gradient
-Progression is variable between individuals
-Careful, frequent follow-up is important

Syncope:
-Classically exertional
---Cardiac output is fixed and cannot rise with exercise
---Vasodilation occurs during exercise → Blood pressure & cerebral perfusion fall

-May also be from arrhythmia
---Tachycardia (ventricular or atrial)
---Bradycardia (heart block)

-Medical therapy for Aortic stenosis is basically non-existent
-Mechanical problem = mechanical treatment
-Afterload-reducing drugs are contraindicated
---BP = CO x resistance (by reducing resistance, BP will shoot down b/c CO can't increase to compensate)
-Mild to moderate asymptomatic aortic stenosis:
---Close follow up: history, exam, echocardiogram
---Warn re: endocarditis risk
---Treat associated atherosclerotic risk factors

Chronic severe aortic regurgitation will eventually result in left ventricular fibrosis and systolic dysfunction

As the ventricle dilates further, wall tension and filling pressure rise

Ejection fraction falls, reducing stroke volume and forward output

Irreversible structural changes may occur prior to the development of symptoms
-one of the insidious features of regurgitation is that by the time sx's occur, you're already in big trouble

Aortic stenosis → pressure overload
--“Concentric hypertrophy”
--Operate for symptoms

Aortic regurgitation → volume overload
--“Eccentric hypertrophy”
--Operate for adverse ventricular remodeling

Etiology of mitral stenosis

Rare causes: Calcified mitral annulus, Atrial myxoma, Endocarditis, Carcinoid valvulopathy, Congenital

Pathophysiology of mitral stenosis:

-A pulmonary capillary wedge pressure of 25mmHg causes transudation of fluid into alveoli, resulting in dyspnea

-Increases in pulmonary venous and capillary pressures raise pulmonary artery systolic pressure (pulm HTN)

Complications of mitral stenosis:

-Pulmonary edema & hemoptysis
-Atrial fibrillation and cardioembolism
-Right heart failure
-Endocarditis

New York Heart Association (NYHA) functional class:

I - no limitation
II - slight limitation, symptoms with ordinary activity
III - marked limitation, symptoms with less than ordinary activity
IV - symptoms at rest or any activity

Indications for Intervention in mitral stenosis:

-Definite
---NYHA III-IV & valve area < 1.5 cm^2

-Very Probable
---Severe mitral stenosis (< 1.0 cm^2 ) & severe pulmonary hypertension (pulmonary artery pressure > 60-80 mmHg) & NYHA I-II

-Probable
---Asymptomatic patients with moderate or worse mitral stenosis (< 1.5 cm^2 ) with new onset atrial fibrillation

Surgery for Mitral Stenosis

-Mechanical vs. bioprosthetic valves
---durability vs. anti-coagulation

-Mechanical valve thromboembolic complication rate ~ 3%/year

- ~30% of bioprosthetic mitral valves fail at 10 years

-mitral prostheses tend to last less than aortic ones b/c thrombotic rate is higher

Etiology of mitral regurg:

-Leaflets/chordae
---Myxomatous (becomes progressively floppy), Rheumatic, Endocarditis (gets chewed up), Congenital

-Annulus
---Left ventricular dilation (cardiomyopathy)

-Papillary muscles
---Ischemia or infarction

Pathophysiology of chronic mitral regurg

-A state of left ventricular and left atrial volume overload

-Left ventricular systolic function may remain normal for years until fibrosis and progressive dilation herald a decline in ejection fraction

-The low-pressure left atrial “outlet” is a form of afterload reduction - and may mask clinical deterioration
---Left ventricular ejection fraction may be normal despite impaired contractile function

Pathophysiology of chronic mitral regurg:

-Reduced left ventricular ejection fraction in mitral regurgitation is serious... and indicates a poor prognosis regardless of treatment!

-When ejection fraction declines, diastolic filling pressures, left atrial & pulmonary pressures rise, Causing the left ventricle to dilate, increasing afterload further... creating more mitral regurgitation

Clinical Features of mitral regurg:
-Fatigue
-Exertional dyspnea
-Orthopnea
-Edema
-Paroxysmal nocturnal dyspnea
-Palpitations

Medical Therapy of mitral regurg:

-Treat the underlying cause (if possible)
-Afterload reduction e.g. ACE inhibitors
---however, little if any benefit in delaying surgery (fundamental rx is surgery)
-Preload reduction: diuretics & nitrates
-Endocarditis recognition and treatment
-Anti-arrhythmics and anti-coagulants (for complications)

Surgical Therapy (mitral regurg)

-Valve repair:
---for myxomatous degeneration / prolapse; less successful in other etiologies
---good outcomes in selected patients
---preferable

-Valve replacement: Mechanical vs. bioprosthetic

Mitral stenosis → Lt ventricular underfilling, pulm edema
-Balloon or surgery for symptoms

Mitral regurgitation → Left ventricular volume overload
-Operate for adverse ventricular remodeling or symptoms

Transient Bacteremia (exposure) + Predisposing Cardiac Lesion (diathesis) (abn leaky flow, turbulent flow, etc) = Infective Endocarditis

Treatment of Endocarditis:

-Targeted parenteral animicrobial therapy
---Narrow-spectrum, intensive, synergistic
---Depends on culture and sensitivity!
-Eliminate portal of entry (if possible)
-Valve surgery
---For hemodynamic compromise
---For recurrent embolism
---For large and highly mobile vegetations
---For prosthetic valve endocarditis
---For fungal endocarditis

. A Baixa Idade Média: A Idade Média – séculos V ao XV – é marcada pelo sistema social feudal na

a burguesia. Esta não tem o poder sobre o Estado, mas terá grande influência junto a este.