Medical School · Year 1 · Cardiovascular · includes a quiz and discussion video

Lecture 13: Valvular Heart Disease

Unit 1.7: Cardiovascular System

Learning Objectives

By the end of this lecture, students will be able to:

1. Describe the pathophysiology of valvular stenosis and regurgitation
2. Recognize the clinical features of major valvular lesions
3. Interpret cardiac examination findings in valvular disease
4. Describe the hemodynamic consequences of each lesion
5. Explain the natural history and indications for intervention
6. Describe management options for valvular heart disease

Overview of Valvular Heart Disease

Valvular heart disease encompasses two fundamental types of lesions: stenosis, in which the valve fails to open properly and creates obstruction to forward flow, and regurgitation, in which the valve fails to close properly and allows backward flow. These hemodynamic derangements place chronic stress on the cardiac chambers, triggering compensatory remodeling that eventually becomes maladaptive.

Each cardiac valve has characteristic etiologies. Aortic valve disease most commonly results from degenerative calcification in elderly patients, bicuspid aortic valve in middle-aged adults, or rheumatic disease in developing countries. Mitral valve disease arises from degenerative changes including mitral valve prolapse, rheumatic disease, ischemic injury affecting papillary muscles, or functional dilation of the mitral annulus in heart failure. Tricuspid regurgitation is most often functional, resulting from right ventricular dilation that stretches the tricuspid annulus, though it may also result from endocarditis (particularly in intravenous drug users), rheumatic disease, or congenital abnormalities such as Ebstein anomaly. Pulmonic valve disease is rare in adults and typically results from congenital abnormalities or carcinoid heart disease.

The heart compensates for valvular lesions through ventricular remodeling. Volume overload lesions (regurgitation) trigger eccentric hypertrophy, in which sarcomeres are added in series, causing chamber dilation that allows the ventricle to handle increased volume. Pressure overload lesions (stenosis) trigger concentric hypertrophy, in which sarcomeres are added in parallel, causing wall thickening that normalizes wall stress according to the Law of LaPlace. These compensatory mechanisms maintain function for years to decades but eventually fail, leading to decompensation.

<image>Panel A: Stenotic valve cross-section showing thickened and fused leaflets with restricted opening and obstruction to forward flow. Panel B: Regurgitant valve cross-section showing leaflets that fail to coapt with backward flow through the incompetent valve. Panel C: Eccentric hypertrophy from volume overload showing a dilated chamber with normal wall thickness and sarcomeres added in series, associated with regurgitant lesions. Panel D: Concentric hypertrophy from pressure overload showing thickened wall with normal or small cavity and sarcomeres added in parallel, associated with stenotic lesions.</image>

Aortic Stenosis

Aortic stenosis is the most common valvular lesion requiring surgery in developed countries. The etiology varies by age: degenerative calcification is the predominant cause in patients over 65 years, bicuspid aortic valve (present in 1-2% of the population) causes stenosis in patients aged 50-65 years, and rheumatic disease causes stenosis in younger patients, typically with concomitant mitral valve involvement.

The pathophysiology of aortic stenosis centers on pressure overload of the left ventricle. To generate sufficient pressure to propel blood across the stenotic valve, the left ventricle develops concentric hypertrophy. This compensation maintains stroke volume at the cost of increased wall thickness and decreased compliance. Diastolic dysfunction develops as the stiffened ventricle requires elevated filling pressures. Myocardial oxygen demand increases due to increased muscle mass and wall stress, while oxygen supply may be compromised by compression of intramyocardial vessels during the prolonged systole and by reduced diastolic coronary filling time. This supply-demand mismatch explains why patients develop angina even in the absence of coronary artery disease.

The classic symptomatic triad of aortic stenosis carries important prognostic implications. Angina indicates approximately 50% five-year survival without intervention. Syncope, typically exertional, results from fixed cardiac output and inability to increase output during exercise-induced peripheral vasodilation; it carries approximately 50% three-year survival. Heart failure symptoms indicate approximately 50% two-year survival. Critically, asymptomatic patients with severe aortic stenosis have excellent prognosis, making symptom onset the key determinant of timing for intervention.

Physical examination reveals characteristic findings. The murmur is a crescendo-decrescendo (diamond-shaped) systolic ejection murmur heard best at the right upper sternal border, radiating to the carotids. The carotid upstroke is parvus et tardus—weak and delayed—reflecting the slow ejection of blood across the stenotic valve. The second heart sound may have a soft or absent aortic component because the calcified valve closes poorly. An S4 gallop is common, reflecting atrial contraction against a stiff ventricle. The apical impulse is sustained and forceful.

Severity assessment by echocardiography measures valve area, transvalvular gradient, and peak jet velocity. Severe aortic stenosis is defined by valve area less than 1.0 cm² (normal is 3-4 cm²), mean gradient greater than 40 mmHg, or peak velocity greater than 4.0 m/s. Mild stenosis has valve area greater than 1.5 cm², mean gradient less than 25 mmHg, or peak velocity less than 3.0 m/s.

Treatment is valve replacement for symptomatic severe aortic stenosis. Surgical aortic valve replacement (SAVR) remains the gold standard for low-risk patients. Transcatheter aortic valve replacement (TAVR) is now indicated for patients at all surgical risk levels. Asymptomatic patients with severe aortic stenosis and reduced ejection fraction (below 50%) should also undergo replacement. Medical therapy has not been shown to alter progression; statins do not slow calcific aortic stenosis. Patients should avoid hypotension and dehydration.

<image>Panel A: Pathological aortic valve with calcified immobile leaflets and restricted opening, alongside concentric left ventricular hypertrophy in cross-section with thickened walls. Panel B: Crescendo-decrescendo systolic murmur pattern with timing relative to S1 and S2, heard at the right upper sternal border with radiation to the carotids. Panel C: Carotid pulse waveform comparing normal rapid upstroke to aortic stenosis with slow late peak described as parvus et tardus. Panel D: Severity criteria showing mild, moderate, and severe thresholds for valve area and gradient, with the symptom triad of angina, syncope, and heart failure and corresponding survival statistics.</image>

Aortic Regurgitation

Aortic regurgitation results from either disease of the aortic valve leaflets or dilation of the aortic root that prevents leaflet coaptation. Valvular causes include bicuspid aortic valve, rheumatic heart disease, infective endocarditis, and degenerative disease. Aortic root causes include aortic dissection (a surgical emergency), Marfan syndrome, aortitis from syphilis or Takayasu arteritis, and aortic aneurysm.

The pathophysiology of aortic regurgitation differs fundamentally between acute and chronic presentations. Acute aortic regurgitation, as occurs with endocarditis or aortic dissection, presents as a medical emergency. The left ventricle is suddenly presented with a massive volume load it cannot accommodate. End-diastolic pressure rises rapidly, transmitted backward to the pulmonary veins, causing fulminant pulmonary edema. The forward stroke volume drops, causing hypotension and cardiogenic shock. There is no time for compensatory remodeling.

Chronic aortic regurgitation develops gradually, allowing the left ventricle to adapt through eccentric hypertrophy. The chamber dilates to accommodate the regurgitant volume, and wall thickness increases to normalize wall stress. The result is a large, hyperdynamic ventricle with increased stroke volume (the sum of forward stroke volume and regurgitant volume). Patients may remain asymptomatic for decades while irreversible ventricular dysfunction develops silently.

The hemodynamic signature of chronic aortic regurgitation is wide pulse pressure. The large stroke volume produces elevated systolic pressure, while diastolic runoff into the left ventricle through the incompetent valve produces low diastolic pressure. This wide pulse pressure generates the characteristic peripheral signs named after historical physicians: Corrigan's pulse (waterhammer pulse with rapid collapse), Quincke's sign (visible capillary pulsations in the nail beds), de Musset's sign (head bobbing with each heartbeat), pistol-shot femorals (audible systolic sound over the femoral arteries), and Hill's sign (popliteal systolic pressure exceeding brachial by more than 20 mmHg).

The murmur of aortic regurgitation is a high-pitched, blowing, decrescendo diastolic murmur heard best at the left upper sternal border with the patient sitting forward and in expiration. The Austin Flint murmur is a low-pitched diastolic rumble at the apex caused by the regurgitant jet striking the anterior mitral leaflet, mimicking mitral stenosis.

Severity is assessed by regurgitant volume and fraction. Severe aortic regurgitation has regurgitant volume of 60 mL or greater and regurgitant fraction of 50% or greater. Echocardiographic assessment also evaluates left ventricular size and function.

Treatment is valve replacement for symptomatic severe aortic regurgitation or for asymptomatic patients with left ventricular dysfunction (ejection fraction below 55%) or significant dilation. Vasodilators (nifedipine, ACE inhibitors) may reduce regurgitant volume by lowering afterload but do not replace surgery in severe disease.

<image>Panel A: Comparison of acute aortic regurgitation with a normal-sized ventricle suddenly receiving regurgitant volume causing pulmonary edema, versus chronic aortic regurgitation with a dilated eccentric hypertrophied ventricle handling compensated volume. Panel B: Wide pulse pressure hemodynamics showing blood pressure waveform with high systolic peak from large stroke volume and low diastolic nadir from regurgitant runoff. Panel C: Peripheral signs including Corrigan's pulse with rapid collapse, Quincke's sign in the nail bed, de Musset's head bobbing, and pistol-shot femorals. Panel D: Decrescendo diastolic murmur pattern at the left upper sternal border and the Austin Flint rumble at the apex.</image>

Mitral Stenosis

Mitral stenosis is almost always caused by rheumatic heart disease, accounting for more than 95% of cases in most series. Rheumatic fever causes inflammation and subsequent fibrosis of the mitral valve, resulting in commissural fusion, leaflet thickening, and chordal shortening. Less common causes include calcification of the mitral annulus (mitral annular calcification) in elderly patients and congenital mitral stenosis.

The pathophysiology of mitral stenosis involves obstruction to left ventricular filling. Unlike aortic stenosis, the pressure load falls on the left atrium rather than the left ventricle. To maintain cardiac output across a stenotic mitral valve, left atrial pressure must rise. This elevated pressure is transmitted backward to the pulmonary veins, causing pulmonary congestion and eventually pulmonary hypertension. The left atrium dilates chronically from pressure overload, predisposing to atrial fibrillation. The combination of atrial fibrillation and left atrial stasis creates high risk for thrombus formation, particularly in the left atrial appendage, and subsequent systemic embolization including stroke.

Symptoms of mitral stenosis reflect pulmonary congestion and reduced cardiac output. Dyspnea on exertion is the cardinal symptom, progressing to orthopnea and paroxysmal nocturnal dyspnea. Hemoptysis may occur from rupture of bronchial veins under high pressure. Ortner syndrome is hoarseness from compression of the recurrent laryngeal nerve by an enlarged left atrium. Importantly, symptoms worsen with conditions that increase heart rate (exercise, fever, atrial fibrillation with rapid ventricular response) because shortened diastole reduces time for blood to cross the stenotic valve.

Physical examination reveals distinctive findings. The murmur is a low-pitched diastolic rumble heard best at the apex with the bell of the stethoscope, with the patient in the left lateral decubitus position. If sinus rhythm is present, presystolic accentuation occurs as atrial contraction provides an additional push across the stenotic valve. An opening snap, a high-pitched sound following S2, indicates sudden opening of the stenotic but still mobile valve; the shorter the S2-opening snap interval, the more severe the stenosis (higher left atrial pressure opens the valve earlier). A loud S1 occurs when the valve leaflets remain mobile.

Severity is defined by valve area and mean gradient. Severe mitral stenosis has valve area less than 1.0 cm² and mean gradient greater than 10 mmHg. Normal mitral valve area is 4-6 cm².

Treatment depends on anatomy and symptoms. Percutaneous mitral balloon commissurotomy (valvuloplasty) is preferred for patients with favorable anatomy (pliable leaflets without significant calcification or subvalvular disease). Surgical repair or replacement is indicated when anatomy is unfavorable. Medical therapy includes diuretics for congestion, rate control for atrial fibrillation (prolonging diastole improves filling), and anticoagulation for atrial fibrillation to prevent stroke.

<image>Panel A: Rheumatic mitral valve with commissural fusion, thickened leaflets, and restricted opening in fish-mouth appearance. Panel B: Hemodynamic consequences showing elevated left atrial pressure, left atrial enlargement, and backward transmission to pulmonary veins leading to pulmonary hypertension. Panel C: Auscultatory findings showing loud S1, opening snap, and low-pitched diastolic rumble with presystolic accentuation, with the S2 to opening snap interval indicating severity. Panel D: Chest X-ray findings of left atrial enlargement including straightening of the left heart border, double density behind the heart, and elevation of the left mainstem bronchus.</image>

Mitral Regurgitation

Mitral regurgitation is classified as primary (organic disease of the valve apparatus) or secondary (functional, due to left ventricular disease). Primary mitral regurgitation results from intrinsic abnormalities of the leaflets or chordae: mitral valve prolapse (myxomatous degeneration causing leaflet redundancy and prolapse), rheumatic disease, infective endocarditis, or ruptured chordae tendineae. Secondary mitral regurgitation results from left ventricular dilation that stretches the mitral annulus and displaces the papillary muscles, preventing leaflet coaptation; this occurs in dilated cardiomyopathy and ischemic cardiomyopathy.

The pathophysiology of mitral regurgitation differs between acute and chronic presentations. Acute mitral regurgitation, as occurs with papillary muscle rupture following myocardial infarction or chordal rupture in endocarditis, produces hemodynamic catastrophe. The left atrium, with normal compliance, cannot accommodate the sudden volume load, and left atrial pressure rises abruptly, causing severe pulmonary edema. Chronic mitral regurgitation develops gradually, and the left atrium dilates and becomes more compliant, accommodating the regurgitant volume at lower pressures. The left ventricle receives increased total volume (forward cardiac output plus regurgitant volume) and develops eccentric hypertrophy. Because the ventricle can eject into the low-pressure left atrium, ejection fraction may appear normal or supranormal even when intrinsic contractility is impaired.

Physical examination in mitral regurgitation reveals a holosystolic (pansystolic) murmur heard best at the apex and radiating to the axilla. The intensity reflects the volume of regurgitation. An S3 gallop indicates rapid ventricular filling from volume overload. S1 is often soft. The point of maximal impulse is displaced laterally if the left ventricle is dilated. In mitral valve prolapse, a mid-systolic click may precede a late systolic murmur; the click occurs when the redundant leaflet prolapses into the left atrium during systole.

Severity assessment measures effective regurgitant orifice area (EROA), regurgitant volume, and regurgitant fraction. Severe mitral regurgitation has EROA of 0.4 cm² or greater, regurgitant volume of 60 mL or greater, and regurgitant fraction of 50% or greater.

Treatment differs between primary and secondary mitral regurgitation. For primary mitral regurgitation, surgical repair is preferred over replacement because it preserves the native valve apparatus and left ventricular geometry. Repair is indicated for symptomatic severe mitral regurgitation and for asymptomatic patients with left ventricular dysfunction (ejection fraction below 60% or end-systolic dimension above 40 mm). Repair at experienced centers has excellent outcomes. For secondary mitral regurgitation, the underlying cardiomyopathy should be treated with guideline-directed medical therapy. Percutaneous edge-to-edge repair (MitraClip) may benefit selected patients with secondary mitral regurgitation who remain symptomatic despite optimal medical therapy.

<image>Panel A: Primary mitral regurgitation showing mitral valve prolapse with a redundant prolapsing leaflet and regurgitant jet into the left atrium, and flail leaflet from ruptured chordae. Panel B: Secondary mitral regurgitation showing a dilated left ventricle with displaced papillary muscles causing incomplete leaflet closure despite structurally normal leaflets. Panel C: Holosystolic murmur pattern at the apex radiating to the axilla, with physical findings of severe MR including S3 and displaced point of maximal impulse. Panel D: Mitral valve prolapse findings showing mid-systolic click with late systolic murmur that increases with standing and decreases with squatting.</image>

Tricuspid Valve Disease

Tricuspid regurgitation is far more common than tricuspid stenosis. Secondary (functional) tricuspid regurgitation results from right ventricular dilation that stretches the tricuspid annulus, a consequence of any cause of pulmonary hypertension or right ventricular failure. Left heart disease leading to pulmonary hypertension is the most common underlying cause. Primary tricuspid regurgitation results from infective endocarditis (particularly in intravenous drug users, who develop right-sided endocarditis from injection of contaminated material), carcinoid heart disease (which causes valve thickening), rheumatic disease (almost always with mitral involvement), or Ebstein anomaly (a congenital malformation with apical displacement of the tricuspid valve).

Physical examination reveals a holosystolic murmur at the left lower sternal border that increases with inspiration (Carvallo sign)—the augmentation with inspiration distinguishes tricuspid from mitral murmurs. The jugular venous pressure is elevated with prominent v waves (systolic venous pulsation from regurgitation into the venous system). Hepatomegaly with pulsatile liver occurs as regurgitant waves are transmitted to the hepatic veins. Peripheral edema and ascites develop in severe right heart failure.

Treatment focuses on the underlying cause. Diuretics reduce venous congestion. Surgical intervention is considered for severe tricuspid regurgitation with symptoms or progressive right ventricular dilation, but outcomes are less favorable than for left-sided valve surgery.

Tricuspid stenosis is rare, usually rheumatic in origin, and almost always occurs with mitral stenosis. The diastolic rumble at the left lower sternal border increases with inspiration. The jugular venous pressure shows a slow y descent due to impaired right atrial emptying.

<image>Panel A: Mechanism of secondary tricuspid regurgitation showing a dilated right ventricle with stretched tricuspid annulus preventing leaflet coaptation, caused by pulmonary hypertension. Panel B: Physical examination findings showing holosystolic murmur at the left lower sternal border with inspiratory augmentation known as Carvallo sign. Panel C: Additional examination findings including elevated JVP with prominent v wave, pulsatile hepatomegaly, and peripheral edema. Panel D: Primary tricuspid regurgitation causes including vegetation on the valve in endocarditis, thickened fibrotic valve in carcinoid disease, and apically displaced valve in Ebstein anomaly.</image>

Prosthetic Valves and Endocarditis

When native valves cannot be repaired, prosthetic valve replacement is necessary. Mechanical valves, typically bileaflet designs, offer excellent durability lasting the patient's lifetime. However, the thrombogenic surfaces require lifelong anticoagulation with warfarin (direct oral anticoagulants are contraindicated with mechanical valves). Target INR is 2.5 (range 2.0-3.0) for mechanical aortic valves and 3.0 (range 2.5-3.5) for mechanical mitral valves. Bioprosthetic valves, made from porcine valve tissue or bovine pericardium, do not require anticoagulation beyond the first three months (when aspirin alone is often used). However, bioprosthetic valves undergo structural deterioration over 10-20 years and eventually require replacement. Younger patients may outlive their bioprosthetic valves, while older patients may have acceptable durability. Transcatheter valves (TAVR) are delivered percutaneously and are increasingly used for aortic valve replacement; they are bioprosthetic in composition.

Prosthetic valve complications include thrombosis (causing valve dysfunction or embolism), endocarditis (with higher mortality than native valve endocarditis), structural deterioration (in bioprostheses), paravalvular leak (regurgitation around the sewing ring), hemolysis (from mechanical trauma to red blood cells), and patient-prosthesis mismatch (when the effective orifice area is too small for the patient's body size, creating persistent obstruction).

Infective endocarditis is infection of the endocardial surface, typically involving cardiac valves. Risk factors include prosthetic valves, prior endocarditis, structural heart disease (including bicuspid aortic valve), intravenous drug use, poor dental hygiene, and immunosuppression. Staphylococcus aureus is the most common causative organism, particularly in acute, aggressive presentations. Viridans group streptococci cause more indolent infections. Prosthetic valve endocarditis in the first year after surgery is often caused by coagulase-negative staphylococci or Staphylococcus aureus; late prosthetic valve endocarditis resembles native valve endocarditis. Culture-negative endocarditis may result from prior antibiotic therapy or fastidious organisms (HACEK group, Coxiella, Bartonella).

The modified Duke criteria provide a framework for diagnosis. Major criteria include positive blood cultures with typical organisms (or positive serology for Coxiella) and echocardiographic evidence of endocarditis (vegetation, abscess, new dehiscence of prosthetic valve, new valvular regurgitation). Minor criteria include predisposing heart condition or intravenous drug use, fever, vascular phenomena (septic emboli, mycotic aneurysms, intracranial hemorrhage, Janeway lesions), immunologic phenomena (glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor), and positive blood cultures not meeting major criteria. Definite endocarditis requires two major criteria, one major plus three minor, or five minor criteria.

Treatment involves prolonged intravenous antibiotics (typically four to six weeks) tailored to culture results. Surgical intervention is indicated for heart failure due to valve dysfunction, uncontrolled infection despite appropriate antibiotics, prosthetic valve endocarditis with complications, embolic events despite therapy, or large vegetations at high embolic risk.

<image>Panel A: Bileaflet mechanical valve with metallic semicircular occluders showing thrombogenic surfaces requiring lifelong warfarin anticoagulation. Panel B: Bioprosthetic valve with tissue leaflets mounted on a frame, without anticoagulation need but with limited durability showing structural deterioration over 10-20 years. Panel C: Infective endocarditis showing a vegetation on a valve leaflet with peripheral manifestations including Janeway lesions, Osler nodes, splinter hemorrhages, and Roth spots. Panel D: Modified Duke criteria summarized with major criteria including positive blood cultures and echocardiographic evidence, and minor criteria including predisposing conditions, fever, and vascular and immunologic phenomena.</image>

Clinical Approach to Murmurs

Cardiac murmurs result from turbulent blood flow and may indicate valvular pathology, though many murmurs are innocent. Systematic assessment of murmur characteristics guides diagnosis.

Timing is the first distinction. Systolic murmurs occur between S1 and S2 and include ejection murmurs (aortic stenosis, pulmonic stenosis, flow murmurs) and regurgitant murmurs (mitral regurgitation, tricuspid regurgitation). Diastolic murmurs occur between S2 and S1 and include regurgitant murmurs (aortic regurgitation, pulmonic regurgitation) and filling murmurs (mitral stenosis, tricuspid stenosis). Continuous murmurs extend through systole and diastole (patent ductus arteriosus, arteriovenous fistula).

Location indicates the valve of origin. Aortic valve murmurs are heard at the right upper sternal border. Pulmonic valve murmurs are heard at the left upper sternal border. Tricuspid valve murmurs are heard at the left lower sternal border. Mitral valve murmurs are heard at the apex. Radiation follows the direction of flow: aortic stenosis radiates to the carotids, mitral regurgitation radiates to the axilla.

Intensity is graded on a six-point scale. Grade 1 is very faint, heard only with concentration. Grade 2 is faint but readily audible. Grade 3 is moderately loud without thrill. Grade 4 is loud with palpable thrill. Grade 5 is very loud, audible with the stethoscope edge on the chest. Grade 6 is audible with the stethoscope off the chest.

Dynamic maneuvers help differentiate murmurs. Valsalva strain reduces preload, decreasing most murmurs but increasing hypertrophic cardiomyopathy (HCM) and mitral valve prolapse murmurs. Handgrip increases afterload, increasing mitral regurgitation and aortic regurgitation while decreasing aortic stenosis and HCM. Standing reduces preload, similar to Valsalva. Squatting increases both preload and afterload, decreasing HCM and MVP. Inspiration increases right heart filling, augmenting right-sided murmurs.

<image>Panel A: Murmur timing patterns relative to the cardiac cycle including ejection systolic crescendo-decrescendo, holosystolic constant intensity, early diastolic decrescendo, mid-diastolic rumble, and continuous murmur. Panel B: Anterior chest with four traditional auscultation areas labeled: aortic at right upper sternal border, pulmonic at left upper sternal border, tricuspid at left lower sternal border, and mitral at apex. Panel C: Radiation patterns showing aortic stenosis radiating to the carotids and mitral regurgitation radiating to the axilla. Panel D: Dynamic maneuver effects table showing Valsalva, handgrip, standing, squatting, and inspiration with their effects on preload and afterload and which murmurs increase or decrease.</image>

Summary

Valvular heart disease includes stenosis (obstruction to forward flow) and regurgitation (backward flow). Each lesion produces characteristic hemodynamic effects and compensatory ventricular remodeling.

Aortic stenosis causes pressure overload and concentric left ventricular hypertrophy. The symptom triad of angina, syncope, and heart failure heralds poor prognosis without intervention. The crescendo-decrescendo systolic murmur at the right upper sternal border with parvus et tardus carotid pulse is diagnostic. Valve replacement is indicated for symptomatic severe disease.

Aortic regurgitation causes volume overload and eccentric left ventricular hypertrophy. Wide pulse pressure produces characteristic peripheral signs. The decrescendo diastolic murmur is heard at the left upper sternal border. Acute aortic regurgitation is a surgical emergency.

Mitral stenosis is almost always rheumatic and causes left atrial pressure overload, atrial fibrillation, and pulmonary hypertension. The diastolic rumble with opening snap is heard at the apex. Percutaneous commissurotomy or surgical intervention is indicated for symptomatic disease.

Mitral regurgitation may be primary (valve disease) or secondary (ventricular disease). The holosystolic murmur is heard at the apex radiating to the axilla. Repair is preferred over replacement for primary mitral regurgitation.

Prosthetic valves require anticoagulation (mechanical) or have limited durability (bioprosthetic). Infective endocarditis is diagnosed by Duke criteria and requires prolonged antibiotics with surgery for complications.

Key Terms

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