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Flashcards in Valvular Heart Disease Deck (49)
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•failure of heart valve to open completely

•almost always due to injury to the tissue of the cusps/leaflets

•usually a chronic process



•insufficiency, incompetence •failure of valve to close completely •may be due to injury to valve cusps/leaflets or injury to the annulus and supporting tissue •may be acute or chronic


functional regurgitation

•regurgitation caused by dilatation of the valvular annulus in the setting of ventricular dilatation •usually in he absence of any abnormality of the valve leaflets •when he valve annulus is dilated, the leaflets are further apart and can't close completely



•abnormal heart sound caused by abnormal blood flow


jet lesion

•focal endocardial fibrosis caused by an abnormal stream ("jet") of blood directed toward that area through a regurgitant valve


causes of aortic stenosis

1. degenerative fibrocalcific ("senile") aortic valve disease 2. congenitally bicuspid aortic valve with degeneration 3. postinflammatory (rheumatic) valve disease


causes of aortic regurgitation

1. diseases that dilate the aorta (aortitis, aortic medial degeneration) 2. congenitally bicuspid aortic valve 3. postinflammatory (rheumatic) valve disease 4. infective endocarditis


causes of mitral stenosis

1. postinflammatory (rheumatic) valve disease (99% of cases of mitral stenosis) 2. radiation valvulopathy (due to radiation therapy to thorax) 3. other rare disorders


causes of mitral regurgitation

1. myxomatous mitral valve degeneration (floppy mitral valve) with mitral valve prolapse 2. postinflammatory (rheumatic) valve disease 3. infective endocarditis 4. papillary muscle rupture (due to myocardial infarction) 5. annular dilatation (due to ischemic heart disease with secondary left ventricular dilation, dilated cardiomyopathy, or other causes of of left ventricular dilatation) 6. annular calcification


degenerative fibrocalcific ("senile") aortic valve disease

•non inflammatory

•aortic valve stenosis

1. age related - >80 yo

2. dystrophic calcification on sinus side of valve

3. minimal to no commissural fusion, mild fibrosis

4. mitral valve is normal or shows annular calcification (in area where there is continuity between the aortic valve annulus and the mitral valve annulus)

5. physiologic consequences: stenosis with or without regurgitation, increased pressure gradient across valve, left ventricular hypertrophy without dilatation due to pressure overload, CHF, sudden cardiac death, increased risk for infective endocarditis


calcific stenosis of bicuspid aortic valve


congenitally bicuspid aortic valve


•aortic stenosis

1. 1-2 % of the population

2. two unequal sided cusps

3. dystrophic calcification on sinus side of valve occurs, very similar to degenerative fibrocalcific aortic valve disease (of a tricuspid aortic valve) but at an accelerated rate, with most patients presenting about a decade sooner (in their 50s)

4. these patients also have a congenital ascending aortopathy (abnormal ascending aorta) and a re prone to developing ascending aortic aneurysms and dissections in addition to developing aortic valvular stenosis

5. physiologic consequences: same as with degenerative fibrocalcific aortic valve disease - stenosis with or without regurgitation, increased pressure gradient across valve, left ventricular hypertrophy without dilatation due to pressure overload, CHF, sudden cardiac death, increased risk for infective endocarditis


mitral valve prolapse

•non inflammatory

•mitral valve regurgitation

1. redundant leaflet tissue balloons back into left atrium during systole

2. affects 5-10 % of population, especially women

3. myxomatous degenration of leaflet tissue, thinning of collagen layer. long chordae

4. common in Marfan syndrome

5. 3% of patients develop complications

-infective endocarditis

-mitral regurgitation

-stroke or systemic infarct, from thrombi that form on surface of redundant leaflets


6. physiologic consequences: regurgitation, left ventricular hypertrophy and dilatation due to volume overload, left atrial dilatation, increased risk for left atrial thrombus formation and systemic embolism, increased risk for atrial and ventricular arrhythmias (due to chamber dilatation), increased risk for infective endocardtitis


•mital valve prolapse

•Fragmentation of the collagen in the valve leaflet

• Deposition of mucopolysaccharides (myxoid or myxomatous degeneration)


mitral valve annular calcification

•mitral regurgitation

*non inflammatory

1. chiefly seen in elderly women

2. no inflammation, valve leaflets mildly affected

3. physiologic consequences: regurgitation, calcific particles may break loose and embolize, increased rsik for infective endocarditis, sudden cardiac death from conduction syste involvement


rheumatic fever 

 •systemic autoimmune disease following group A beta hemolytic streptoccoccal pharyngeal infection

•autoimmune reaction, due to formaion of antibodies to bacterial antigens that cross react with normal tissue antigens

•acute rheumatic fever is a disease of childhood



symptoms of rheumatic fever

•fever, migratory polyarthritis, (one joint after another becomes sore), and sometime cardiac symptoms, occurring a few weeks to a few months after having strep throat

•diagnosis established by Jones criteria: evidence of streptococcal infection and presence of sufficient major and minor criteria

•less than 1% of patients die acutley

•disease is reactivated with each new strep infection

•heart failure occurs decades later

•decreased in US, but making a comeback, globally 15-20 millionnew cases/year


•Marfan's syndrome

•mitral valve prolapse


acute rheumatic heart disease - "pancarditis"

1. myocarditis with Aschoff bodies

2. pericarditis, usually fibrinous

3. endocarditis, with small non-infectios vegetations (verrucae)


•pathognomonic of rheumatic heart disease

•giant cells (Aschoff giant cells), histiocytes (Anitschkow cells), lymphocytes and plasma cells, surrounding a focus of fibrinoid necrosis, it heals as a nonspecific scar

•degenerated collagen surrounded by lynphocytes, plasma cells, and characteristic Anitschkow cells and Aschoff cells


• Derived from cardiac macrophages.

• Characterized by a prominent central chromatin bar

• Cut in cross section, the nuclei have an "owl eye" appearance (red arrows)

• Cut longitudinally, the nuclei look like "caterpillars" (black arrows)

•acute rheumatic disease


• Multinucleated forms of Anitschkow cells, analogous to the giant cells of granulomatous inflammation.

•acute rheumatic disease


• Inflammation of the endocardium leads to fibrinoid necrosis in foci along the valve leaflets or chordae.

• Overlying these areas of necrosis are small vegetations, usually along the lines of closure of left-sided valves

• Not clinically significant

•acute rheumatic heart disease


chronic rheumatic heart disease

•deforming fibrosis, especially of valves

1.mitral valve is almost always involved

2. isolated mitral valve disease is seen in 70% of cases

3. combined mitral and aortic valve disease is seen in 25% of cases

4. tricuspid involvement is uncommon, and pulmomary valve involvement is rare

• Repeated episodes of valvulitis and scarring produce with each subsequent exposure to the bacteria result in cumulative damage to the valves

• Ultimately, after many years (decades), the valve disease is severe enough to manifest clinically – Typically 30-50 years of age – Mitral valve is always involved, +/- aortic valve – Most common cause of mitral stenosis


pathology of rheumatic mitral vlave disease

1. diffuse fibrosis of mitral valve, often with calcification (looks like it's coated in candle wax, with a deformed configuration that looks like a fish mouth - the fish mouth deformity)

2. commissural and chordal fusion

3. physiologic consequences: usually stenosis but sometimes regurgitation or both, severley dilated left atrium, without left ventricualr hypertrophy or dilatation, atrial arrhythmias, increased rsik for left atrial thrombus formation and systemic embolism, increased risk for infective endocarditis


• Most cases are result of chronic rheumatic fever

• Valve deformity as a result of scarring:

– Leaflets thicken and retract

– Commissures fuse

– Chordae thicken and shorten, may fuse

– “fishmouth” or “buttonhole” appearance

• Subsequently, the valve may calcify into a rigid and fixed structure


consequences of mitral stenosis:

•Left ventricular Dilated Left Atrium failure

• Dilation of LA

– Risks: thrombosis/embolism; arrhythmias

• Increased pulmonary pressures

– Pulmonary edema

– RV hypertrophy, failure LV


infective endocarditis

•colonization or invasion of heart valves or mural endocardium by a microbiologic organism. Vegetations are masses of fibrin and inflammatory cells that form on the endocardial surface at teh site of infection, and often contain numerous microorganisms


• Infection of endocardial surface, usually a valve

– Left > right

– Mitral>aortic

– Native> prosthetic

• Pathogenesis:

1. Bacteremia

2. Adherence of circulating organisms either directly to endothelium or to microthrombi on the endothelium


predisposing factors for infective endocarditis

1. preexisting valve disease

2. congenital heatr disease

3. immunodeficiency

4. any endocardial injury

•microbes reach the valve during an episode of silent transient bactoremia: after dental work trivial injuries, catheters, needle sticks, IV drug abuse etc...

•left sided valves are most commonly affected, except in IV drug abusers, where right sided valves are most commonly affected

– Tricuspid is nearly always involved

– 50% of cases also involve the left side • Involved valves are usually structurally normal

• Organisms with high virulence (S. aureus is the most common) – S. epidermidis and fungi also


complications of infective endocarditis

1. valve dysfunction - reguritation due to leaflet/cusp perforations or chordal rupture; stenosis if vegetation is large or blocks valve orifice

2. anuular or myocardial abscess - if infection spreads into wall of adjacent valve

3. systemic or pulmonary emboli - infarction and secondary infection of distal organs

4. glomerulonephritis - due to immune complex disease and/or emboli


• Erosion into the myocardium (ring abscess)

• Septic thromboemboli – Heart – Brain – Kidney

• Septic shock

Valve stenosis or regurgitation

• Congestive heart failure

• Septic shock