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Flashcards in Valvular Heart Disease Deck (57):

What are the semilunar valves?

aortic and pulmonary


What are the AV valves?

mitral and tricuspid


Describe the AV valve structure...

free margins attached to the ventricular wall via chordae tendinae and papillary muscles


What is stenosis?

failure of a valve to open completely– Usually a chronic process affecting a valve cusp


What is insufficiency?

failure to close completely


Causes of insufficiency?

– Functional regurgitation: valvular incompetence due to disruption of supporting structures (Aorta root dilation &Left ventricle dilation)
--Intrinsic disease of valve cusps


Major causes of Vavlular Disease

• Congenital causes– Bicuspid aortic valve (most common)
-Acquired causes–
Aortic valve --Stenosis: senile calcific aortic stenosis & Insufficiency: dilation of ascending aorta related to hypertension and aging
Mitral valve --Stenosis: Rheumatic heart disease & Insufficiency: Myxomatous degeneration


Is stenoses or insufficiency more frequent cause?



What is dystrophic calcification?

Damage caused by wear and tear complicated by deposits of calcium phosphate


Risk factors for dystrophic calcification?

Distinct from atherosclerosis, but shares some risk factors (hyperlipidemia, hypertension, inflammation)


Most common of all valvular abnormalities?

Calcific Aortic Stenosis (AS)


When does AS occur in life?

– 5th/6th decades - bicuspid, unicuspid valves • Occur in 1-2% of population, association w/ Notch mutation
--8th/9th decades – normal valves (“senile”)


What are the clinical effects of AS?

LV: increased pressure causes hypertrophy• Angina, ischemia, & CHF• Syncope (mechanism is not clear)• 50% with CHF will die within two years


Treatment for AS?

valve replacement


Describe the morphology of AS.

Heaped up calcified masses in cusps, primarily at the bases• Free cuspal edges not involved• No fusion of commissures


What is Mitral Annular Calcification?

Degenerative calcific deposits on fibrous ring, at base of valve


Risk factors for mitral annular calcification?

Women > 60 years old • Increased in patients with myxomatous valves or elevated LV pressure


Does mitral annular calcification affect function?

Usually does not affect valve function BUT, calcifications are sites for thrombi/infection


What happens in Myxomatous Degeneration of Mitral Valve (Prolapse)?

Usually no serious complications• One or both leaflets enlarged, hooded, redundant, floppy (myxoid)• Prolapse or balloon back into left atrium during systole (mid-systolic click)


How common and who gets Myxomatous Degeneration of Mitral Valve?

Very common (3% of adults) & Young women


Pathogenesis of Myxomatous Degeneration of Mitral Valve?

Unknown• ? Developmental anomaly of connective tissue
• Feature of Marfan syndrome (fibrillin gene mutation) and other hereditary disordersDeposition of mucoid material in valve


Clinical features of Myxomatous Mitral Valve?

• Asymptomatic - Incidental finding: mid systolic click on auscultation• When regurgitation occurs - Late systolic/holosystolic murmur


Complications of Myxomatous Mitral Valve?

uncommon• Infective endocarditis• Mitral insufficiency• Thrombi on atrial surfaces lead to stroke or other systemic infarcts due to emboli• Arrhythmias -->sudden death• Most often seen with advanced mitral insufficiency


What causes rheumatic fever?

Acute, immunologically mediated, multisystem, inflammatory disease with major cardiac manifestations• Occurs following an episode of group A Streptococcal (pyogenes) pharyngitis


Most important complication of RF?

progression to chronic valvular dysfunction (mitral stenosis)


How does RF affect the heart?

Pancarditis (affects all three layers)
Bread and butter pericarditis
Myocarditis with Aschoff bodies
Endocardium and left sided valves with fibrinoid necrosis and verrucae
Subendocardial (MacCallum) plaques: irregular fibrous thickening of endocardium


What is the classic lesion seen in RF?

Aschoff body – Foci of swollen eosinophilic collagen surrounded by T lymphocytes, plasma cells and plump macrophages –Anitschkow cells, caterpillar cells


Chronic rheumatic heart disease inflammation and fibrosis leads to what?

Thickened valve leaflets– Fusion of commissures (fishmouth or buttonhole deformities)– Fusion/thickening of chordae tendineae


Major effect of of chronic rheumatic heart disease is mitral stenosis which leads to what?

– Leads to left atrial dilatation (sometimes thrombus formation)• Reduced cardiac output (mechanical obstruction prevents filling of LV)– Pulmonary congestion, eventual right ventricular hypertrophy, and right-sided heart failure


What percentage of time does chronic rheumatic heart disease affect the following:mitral valvemitral and aortic vavlestricuspid valvepulmonary valve

• Mitral valve alone in 65 – 70%
Mitral and aortic 25%
Tricuspid less often
Pulmonary rare


Ab cross react after group A strep infection to cause rheumatic heart disease, what's going on?

Hypersensitivity reaction induced by group A Streptococci• Antibodies against M protein cross react with glycoprotein antigens in the heart, joints and other tissues– Specific antigen not yet definitively identified• ? Glycoprotein in heart valves• ? Protein in sarcolemma of myocyte


JONES criteria?

2 major or 1 major and 2 minor:
major- joints, heart, subQ nodules, erythema marginatum, sydenham chorea
minor- fever, arthralgia and elevated acute phase reactants


Prognosis of acute RF?

good for primary attack; increased vulnerability to reactivation


Course and prognosis of chronic rheumatic carditis?

– Years or decades after initial episode– Valvular disease (valvulitis)– Prognosis: surgical repair of valves improves outlook


What are the two basic forms of infective endocarditis?

– Acute: • Highly virulent organism, normal valve, 50% mortality • Necrotizing ulcerative invasive infection, requiring surgery
--Subacute: • Low virulence , deformed valve • Less destructive lesions, respond to antibiotics


Risk factors for infective endocarditis?

More common in patients with cardiovascular abnormalities, neutropenia, immunodeficiency, malignancy, diabetes, alcoholics and IV drug users


Causes 50-60% of infective endocarditis for deformed valves?

Strep viridans for deformed valves


Causes 10-20% of infective endocarditis overall?

Staph aureus


Describe acute infective endocarditis?

Friable, large bulky destructive vegetations– Fibrin, inflammatory cells and bacteria (less often fungi)– Mitral valve and aortic valve most common sites – Tricuspid valve in IV drug users – May erode myocardium --> ring abscess


Describe subacute infective endocarditis.

Less valvular destruction, fibrosis and granulation tissue reaction at the base of vegetation


What are the Duke Criteria for bacterial endocarditis?

Major Positive blood cultures Echocardiographic findings (valve-related mass/abscess) New valvular regurgitation (new murmur on auscultation)
Minor  Predisposing heart lesion or IVDA Fever Uncommon findings resulting from septic emboli: petechiae, splinter hemorrhages, Janeway lesions (palms, soles hemorrhagic lesions), Osler nodes (digits), Roth spots (retina)


Complications of bacterial endocarditis?

Valvular insufficiency or stenosis and possible heart failure– Myocardial abscesses and possible perforation– Vegetations break off  embolic complications• Brain, kidneys, spleen, etc.– Glomerulonephritis (immune complexes)


Treatment of bacterial endocarditis?

– IV antibiotics, valve replacement if necessary– Prophylactic antibiotics after valve damage


What can cause nonbacterial thrombotic endocarditis?

– Hypercoagulable states– Associated with mucin producing adenocarcinomas (DVTs & Trousseau syndrome)– Endocardial trauma - Swan-Ganz catheter


What is nonbacterial thrombotic endocarditis?

Depositions of small masses of fibrin, platelets and other blood products on leaflets


Endocarditis associated with Systemic lupus erythematosus:– Mitral & tricuspid valves involved– Antiphospholipid antibodies presentWhat is it?

Libman-Sacks Endocarditis


Carcinoid tumors produce what?

serotonin, kallikrein, bradykinin, histamine, prostaglandins, and tachykinins


Symptoms of carcinoid syndrome?

flushing, cramps, nausea, vomiting, diarrhea


Serotonin and bradykinin inactivated by what?

MAO in pulmonary vasculature AND also inactivated by passage through functioning liver


What is carcinoid heart disease?

In 50% of patients with carcinoid syndrome -plaque-like fibrosis of right-heart endocardium and valves


Where does carcinoid heart disease usually occur?

Usually occurs on right side of heart (not left) because of inactivation of mediators by MAO in lung


What is the cause of carcinoid heart disease?

Exact cause is unknown; believed to be related to endothelial injury caused by vasoactive agents


What happens when pt has GI carcinoids with hepatic mets?

Normally, bioactive proteins are inactivated by liver• With mets to liver, secretion occurs directly into the hepatic vein & reaches right-side of heart


What happens when pt has carcinoids outside of the portal system of venous drainage?

Direct secretion into systemic circulation – Example: carcinoids arising in ovary, testes• Very high blood levels may prevent complete inactivation by the lung MAO– Example: primary lung carcinoid


Which valves are usually involved in carcinoid heart disease?

– Tricuspid and pulmonic valves equally affected• Usually tricuspid insufficiency or pulmonic stenosis


Complications with mechanical valves?

Thromboembolic complications &Infective endocarditis


Complications with bioprothesis artificial valves?

• Structural deterioration - 50% need replacement by 15 years • Infective endocarditis