Merck & Co., Inc.

The Merck Manual of Geriatrics logo

red line
click here to go to the Contents page of The Merck Manual of Geriatrics
click here to go to the title page of The Merck Manual of Geriatrics
click here to search The Merck Manual of Geriatrics
click here to go to the Index of The Merck Manual of Geriatrics
red line
Section 11. Cardiovascular Disorders
this section includes
Chapter 83. Aging and the Cardiovascular System | Chapter 84. Diagnostic Evaluation | Chapter 85. Hypertension | Chapter 86. Hypotension | Chapter 87. Atherosclerosis | Chapter 88. Coronary Artery Disease | Chapter 89. Valvular Heart Disease | Chapter 90. Infective Endocarditis | Chapter 91. Arrhythmias and Conduction Disturbances | Chapter 92. Heart Failure and Cardiomyopathy | Chapter 93. Peripheral Arterial Disease | Chapter 94. Peripheral Venous Disease | Chapter 95. Aneurysms | Chapter 96. Cardiovascular Surgery and Percutaneous Interventional Techniques

Chapter 89. Valvular Heart Disease

Contributor: Melvin Cheitlin

With age, fibrotic thickening and increased opacity occur in the mitral and aortic valves. The aorta becomes stiffer (increasing systolic blood pressure and stress on the mitral valve), and afterload on the left ventricle increases (increasing myocardial oxygen demand and thus the requirement for myocardial blood flow). These age-related effects influence the development of symptoms and complications in elderly patients with valvular heart disease.

In elderly patients, the predominant causes of valvular heart disease are degenerative calcification, myxomatous degeneration, papillary muscle dysfunction, and infective endocarditis; valvular damage from rheumatic and syphilitic diseases is uncommon. Most often, valvular heart disease is suspected when murmurs are detected during the physical examination. Noninvasive imaging techniques help identify the etiology, establish the diagnosis, and assess disease severity.

Medical management is appropriate for many elderly patients; surgery (see page 947) is indicated when symptoms interfere with daily activities or when hemodynamically significant valvular heart disease cannot be controlled medically. Although age per se is not a contraindication to surgery, comorbid disorders and the overall clinical condition may make surgery inappropriate. Generally, for patients > 75 years, the goal of surgery is to improve the quality of life rather than to prolong life.

Antibiotic prophylaxis for infective endocarditis is recommended before dental, gastrointestinal, gynecologic, and genitourinary procedures. (see Table 90-1)

Aortic Valve Stenosis

Abnormal narrowing of the aortic valve orifice.

The prevalence of aortic valve stenosis, the most clinically significant valvular lesion in the elderly, increases with age. The severity of the stenosis is often underestimated because its progression is so gradual and because symptoms may be attributed to normal aging.

In the elderly, common causes of aortic valve stenosis are calcification of a congenital bicuspid aortic valve and degenerative aortic stenosis. Rheumatic heart disease is the cause in 20%; mitral valve disease often coexists. Regardless of the cause, calcification occurs in patients with aortic valve stenosis by age 65. A congenital bicuspid valve, if present, tends to become calcified in patients aged 45 to 60, and typically, the aortic aspect of the tricuspid semilunar aortic valve is calcified in patients > 75.


In aortic valve stenosis, the systolic gradient across the aortic valve during systole produces turbulence, which results in a systolic ejection murmur. The increased left ventricular systolic pressure leads to concentric left ventricular hypertrophy, and these two changes lead to an increase in myocardial oxygen demand. As the aortic valve narrows to < 0.8 cm2, aortic pressure takes longer to reach its peak, and systolic pressure may decrease. During systole, tissue pressure on the coronary microvasculature increases coronary vascular resistance and decreases blood flow into the midmyocardium and epicardium. These factors decrease myocardial blood flow, especially to the subendocardium, and result in myocardial ischemia, subendocardial fibrosis, angina pectoris, and ventricular arrhythmias. Significant coronary artery disease (CAD) develops in almost 50% of elderly patients.

During exercise, systemic vascular resistance decreases normally. If stroke volume cannot increase, systolic blood pressure can decrease. This drop in blood pressure plus transient and rapid ventricular arrhythmias can result in exertional syncope.

Symptoms and Signs

Most patients with aortic valve stenosis are asymptomatic. Those with symptoms have an extremely poor prognosis without valve replacement. Chest discomfort, which is usually characteristic of angina pectoris, is an early symptom. During exertion, presyncope (transient alteration of consciousness) or syncope occurs in about one third of symptomatic patients. Exertional dyspnea may progress to pulmonary edema, or pulmonary edema may occur suddenly without previous symptoms. If aortic valve stenosis is severe, the left ventricle becomes stiff, and the left atrium may become dilated, resulting in atrial fibrillation. Absence of an atrial contraction markedly decreases the late filling of the noncompliant left ventricle, and stroke volume may decrease, resulting in a marked worsening of symptoms and in heart failure. Heart failure develops in about one half of elderly patients with severe aortic valve stenosis. Because of vascular stiffening, systolic hypertension may coexist with severe aortic stenosis in elderly patients. About one fourth of deaths due to aortic stenosis occur suddenly.

Physical findings may include a narrow pulse pressure, especially when stroke volume decreases, and a slow-rising, small-volume carotid pulse. However, the poorly compliant arterial wall may mask these abnormalities, so that the carotid pulse appears relatively normal. The cardiac apex impulse is forceful and sustained, but this finding may be masked by kyphosis (in which the anteroposterior diameter of the chest is increased). The first heart sound is soft. The aortic component of the second heart sound is also soft; it may be inaudible when stenosis is severe and the valve is heavily calcified. Reverse splitting of the second heart sound may occur in patients with left ventricular failure. A fourth heart sound is common but disappears in the one fourth of elderly patients who develop atrial fibrillation. Ejection sounds are rare because the valve cusps are immobile.

A harsh, loud crescendo-decrescendo systolic murmur, often associated with a thrill, is maximal at the upper right sternal border. The murmur peaks in mid to late systole and often radiates throughout the precordium and into the neck. This late peaking is often the best clue to severe aortic stenosis. The murmur's high-frequency components are often transmitted to the lower left sternal border and the cardiac apex during most of systole and may resemble the murmur of mitral regurgitation. In patients with heavily calcified aortic valves, the murmur sometimes has a musical high-pitched quality (termed seagull murmur). The murmur's intensity does not correlate with the severity of the obstruction. Basal diastolic murmurs of aortic regurgitation are heard in more than one half of patients with aortic valve stenosis.

The ECG shows evidence of left ventricular hypertrophy, but hyperinflated lungs may mask increased left ventricular voltage. Even when left ventricular hypertrophy is severe, heart size often remains normal until heart failure develops; the heart then enlarges. Poststenotic aortic dilation is common.


Dense calcification of the aortic valve, best seen on a lateral chest x-ray, suggests hemodynamically significant aortic stenosis. If calcification is not seen on the chest x-ray or echocardiogram, the diagnosis of critical (very severe) aortic valve stenosis is virtually excluded.

Two-dimensional echocardiography is used to assess cardiac chamber size, wall thickness, wall motion, valve leaflet motion, valve orifice size, and valvular calcification. Doppler echocardiography is used to measure intracardiac blood velocity, from which the severity of valvular regurgitation or obstruction can be calculated. Serial measurements can determine progression of the disorder. If the anteroposterior diameter of the chest is increased, the echocardiographic views of the heart may be limited, and the technician may have to spend a long time getting the maximum jet velocity to reflect the maximum aortic systolic gradient. For this reason, the severity of aortic stenosis can be underestimated in the elderly.

Frequently, the severity of aortic stenosis can be determined on the basis of Doppler-echocardiographic findings. However, if surgery is being considered for an elderly patient, catheterization is usually performed to determine whether CAD is present and, if present, how severe it is. Stress testing to the level of the patient's ordinary activity with ECG monitoring may be used to check for ischemic changes and arrhythmias, especially in patients with moderate aortic stenosis. (see page 827) However, if severe aortic stenosis is suspected, exercise testing is contraindicated because exercise-related syncope and death are risks.

Two-dimensional echocardiography and Doppler studies help differentiate aortic valve stenosis from benign aortic sclerosis, which occurs in one third to one half of elderly persons. Benign aortic sclerosis typically produces no symptoms and is not hemodynamically significant; the basal systolic murmur is short and peaks early, and the carotid pulse is normal.

Because the chest discomfort of aortic valve stenosis is due to myocardial ischemia, aortic valve stenosis cannot be distinguished from angina pectoris due to CAD on the basis of symptoms. Syncope due to aortic valve stenosis must be distinguished from that due to atrioventricular block or tachyarrhythmias, both common among elderly patients. Ventricular tachyarrhythmias may be due to CAD or to ischemia produced by severe aortic valve stenosis. Severe aortic valve stenosis should be suspected and ruled out in all elderly patients with heart failure and a systolic ejection murmur, especially if they have unexplained left ventricular hypertrophy.

Prognosis and Treatment

Elderly patients with noncritical aortic valve stenosis require serial surveillance because stenosis often progresses at an unpredictable pace.

Asymptomatic elderly patients with severe aortic stenosis can usually be managed medically; surgery is justified only if the risk of perioperative mortality is less than that of sudden death. However, a detailed history is very important for verifying that the patient is active and asymptomatic before concluding that the patient can be safely managed medically.

Aortic valve replacement is indicated for symptomatic patients with hemodynamically significant aortic valve stenosis, (see page 947) because their expected life span is reduced. The 3-year mortality rate for untreated symptomatic patients is about 50%; life span is shorter for such patients if they have heart failure and longer if they have angina pectoris. Elderly patients with severe aortic stenosis may have a worse prognosis. In one series, the mortality rate was 50% at 1 year and 65% at 2 years.

Percutaneous balloon valvuloplasty is used only for symptomatic palliation of severely ill patients who are not candidates for surgery, because valvuloplasty has high rates of restenosis and mortality after hospital discharge. (see page 949) Ultrasonic debridement of calcium is no longer performed.

Acute Aortic Regurgitation

Sudden development of retrograde blood flow through an incompetent aortic valve into the left ventricle during ventricular diastole.

Trauma, infective endocarditis, or aortic dissection may cause acute aortic regurgitation.

Symptoms and Signs

Frequently, patients present with acute severe pulmonary edema and tachycardia; often, hypotension also occurs. Heart failure is precipitated by abrupt ventricular volume overload within a noncompliant left ventricle and pericardial sac; compensatory hypertrophy or dilation does not have time to occur. Because myocardial oxygen demand increases and subendocardial coronary blood flow decreases, myocardial ischemia and its complications, including sudden death, may occur early in the course of the disorder.

The carotid pulse has a collapsing quality, like that of the left ventricle pressure curve, because of rapid runoff back into the left ventricle. In acute aortic regurgitation compared with the chronic form, the collapsing quality is less pronounced, aortic diastolic pressure cannot decrease as low (because of the rapid elevation of left ventricular filling pressure), and systolic pressure does not increase as much (because of the smaller stroke volume). Therefore, pulse pressure is not as wide, and many of the peripheral signs of severe chronic aortic regurgitation are absent.

The rapid increase in left ventricular filling pressure causes the mitral valve to close late in diastole, making the first heart sound soft. Because pressure in the aorta and left ventricle equilibrates early in diastole, the diastolic murmur along the left sternal border can be harsh and short. In patients with tachycardia and a short diastole, the diastolic murmur can be so short that it is difficult to hear, or it may be absent.

Diagnosis and Treatment

Acute aortic regurgitation should be considered in patients with acute heart failure or pulmonary edema. Echocardiography helps confirm the diagnosis. The ECG may be normal initially. Echocardiography often shows early mitral valve closure.

Acute aortic regurgitation must be differentiated from other causes of acute severe heart failure (eg, myocardial infarction with papillary muscle, chordal, or septal rupture). Pulmonary edema may be erroneously attributed to myocardial infarction because the heart is not enlarged, the wide pulse pressure may be absent, and the murmur may not be detected. Doppler echocardiography and ECG are the most helpful procedures in differential diagnosis.

If the cause is aortic dissection involving the ascending aorta, (see page 938) urgent aortic valve replacement (see page 947) or resuspension of the valve is indicated. For all patients who have signs of acute aortic regurgitation due to other etiologies, even those who do not have obvious pulmonary edema, urgent aortic valve replacement should be performed because clinical deterioration of these patients is rapid and sudden death is possible. If the cause is infective endocarditis, appropriate antibiotics should be given for 12 to 24 hours before aortic valve replacement. (see page 882)

Chronic Aortic Regurgitation

Long-standing retrograde blood flow through an incompetent aortic valve into the left ventricle during ventricular diastole.

Chronic aortic regurgitation may be caused by disease of the aortic valve leaflets (due to congenital or rheumatic heart disease, myxomatous degeneration, or infective endocarditis) or by aortic annular root dilation or ascending aortic disease (eg, as occurs in syphilis, rheumatoid spondylitis, Marfan's syndrome, ascending aortic aneurysm, aortic dissection, and various types of aortitis).


The regurgitant volume increases the left ventricular end-diastolic volume. If the left ventricular end-diastolic volume increases gradually, eccentric hypertrophy (hypertrophy with dilation) of the left ventricle results; ie, the ventricle enlarges so that it can accommodate the increased left ventricular end-diastolic volume without an increase in left ventricular filling pressure. Left ventricular stroke volume increases sufficiently to maintain a normal aortic forward effective stroke volume and to accommodate the regurgitant volume. With the increased stroke volume, systolic aortic pressure and runoff into the left ventricle are increased, and diastolic pressure is decreased, increasing pulse pressure.

The enlarged ventricle and increased left ventricular systolic pressure increases myocardial oxygen demand, and the low diastolic aortic pressure limits subendocardial blood flow. Consequently, myocardial ischemia and its complications occur, usually late in the course of the disorder.

Symptoms, Signs, and Diagnosis

Most often, mild to moderate aortic regurgitation produces no symptoms for many years, and exercise tolerance is preserved.

Rheumatic aortic regurgitation, which occurs predominantly in men, often produces no symptoms, even in old age. A short, soft basal diastolic murmur is characteristic and may be accentuated by hypertension. Syphilitic aortic regurgitation is more severe, and the prognosis is worse, often because of an associated aortic aneurysm or coronary ostial involvement. A long, loud decrescendo basal diastolic murmur, often with a short basal systolic ejection murmur, is characteristic of hemodynamically severe aortic regurgitation. Because left ventricular stroke volume is increased, the systolic ejection murmur can be loud and long, sounding like that of aortic valve stenosis. The peripheral signs of severe aortic regurgitation distinguish predominant aortic regurgitation from predominant aortic valve stenosis.

Effort intolerance and dyspnea may develop and may progress to heart failure. Chest pain is often due to associated coronary atherosclerosis but can be due to myocardial ischemia. Usually, palpitations are not due to arrhythmias but to the forceful ejection of blood.

The findings of severe regurgitation include bounding peripheral arterial pulses, a wide pulse pressure, and a hyperactive precordium with a rocking motion. Occasionally, a bisferious pulse (pulsus bisferiens) is present. The high-pitched diastolic murmur is best heard at the cardiac base. It is louder at the upper right sternal border in aortic root disease and is more prominent along the left sternal border in aortic valve leaflet disease. An associated diastolic thrill and a systolic murmur of increased aortic outflow may be heard. Third and fourth heart sounds and an apical diastolic rumble (Austin Flint murmur) are common. If the femoral artery is compressed over the groin with the bell of a stethoscope, a to-and-fro diastolic bruit (Duroziez's murmur) can be heard because there is retrograde flow of blood across the compressed artery during diastole.

Chest x-ray shows characteristic cardiac enlargement with a dilated aorta. Occasionally, an ascending aortic aneurysm is seen. Linear calcification of the ascending aorta is typical in syphilitic aortic regurgitation; in contrast, calcification in aortic atherosclerosis is patchy and frequently denser and thicker. The ECG shows left ventricular hypertrophy. The echocardiogram shows an enlarged left ventricular cavity, often with early diastolic fluttering of the anterior mitral valve leaflet. Doppler echocardiography can be used to estimate the severity of aortic regurgitation.


Patients with left ventricular failure and severe chronic aortic regurgitation should be stabilized medically even if the valve is to be replaced. (see page 947) Patients with heart failure are treated with a diuretic, an angiotensin-converting enzyme (ACE) inhibitor, and digoxin before valve replacement. Asymptomatic patients with moderate to severe aortic regurgitation and good left ventricular function should receive an ACE inhibitor, a vasodilating calcium channel blocker, or hydralazine to reduce afterload. Afterload reduction can slow progression of left ventricular dilation and even postpone the onset of symptoms that warrant valve replacement. Drugs that cause bradycardia should be avoided, because relative diastolic prolongation can increase regurgitation and accentuate symptoms.

Patients who have left ventricular failure, even if they become asymptomatic with medical management, and patients who remain symptomatic after receiving optimal medical therapy should be considered for aortic valve replacement, preferably with bioprosthetic valves. However, because these patients commonly have severe underlying ventricular dysfunction, the results are less satisfactory than those for patients with aortic valve stenosis. Because decreasing myocardial contractility is manifested by a decreasing ability to eject a large stroke volume, a progressive increase in left ventricular end-diastolic and end-systolic dimensions with a decreasing left ventricular ejection fraction (detected by echocardiography or radionuclide angiography) is an indication for aortic valve replacement. Most patients become symptomatic before these changes occur.

Mitral Stenosis

Abnormal narrowing of the mitral valve orifice.

Mitral stenosis is usually identified before patients reach old age. Most patients with severe mitral stenosis have surgery or die before reaching the age of 65; thus, elderly patients with mitral stenosis have a mild to moderate form of disease that has become severe because the valve has become heavily calcified in late life.

Mitral stenosis is due almost exclusively to rheumatic heart disease. Rheumatic fever, although its incidence has markedly decreased in the USA, was still prevalent when the elderly were children or adolescents. Also, in developing countries, the incidence of rheumatic heart disease is still high. A much less common cause of mitral stenosis is progressive extension of mitral annular calcification, which results in moderate mitral stenosis. One third of patients > 70 have calcium deposits in the mitral or aortic valve.


Acute rheumatic fever results in commissural fusion and fibrosis. Later, the chordae tendineae fuse and the valve calcifies. Some degree of mitral regurgitation often coexists.

As the mitral orifice narrows to < 2 cm2 during diastole, blood flow through the valve is progressively obstructed, resulting in an increase in left atrial pressure and a diastolic gradient across the mitral valve. As left atrial pressure increases, pulmonary capillary pressure increases and right ventricular and pulmonary artery systolic pressures passively increase, leading to pulmonary hypertension. In 10 to 15% of patients, pulmonary arteriolar vasoconstriction is marked, pulmonary vascular resistance is greatly increased, and pulmonary hypertension is severe. Because afterload on the right ventricle is increased, right ventricular hypertrophy, dilation, and failure develop.

Increased pulmonary venous pressure results in collateral runoff to the bronchial veins; if they rupture, hemoptysis results. Dilation of the left atrium results in early atrial fibrillation and stasis of blood. Atrial fibrillation results in thromboembolic events and may cause heart failure.

Symptoms, Signs, and Diagnosis

Most elderly patients with mild to moderate mitral stenosis have few or no symptoms and are in sinus rhythm. If mitral stenosis is moderate (especially if atrial fibrillation develops) or is severe, exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and pulmonary edema can occur. Later, with the development of pulmonary hypertension, right ventricular failure supervenes.

Clinical features, comparable to those in younger patients, include a loud first heart sound, an apical diastolic rumble with presystolic accentuation, and an opening snap. The first heart sound and opening snap may soften or disappear if valvular calcification is present. The diastolic murmur may become softer, especially when stroke volume is decreased (as in heart failure) and when dilation of the right ventricle pushes the left ventricle away from the chest wall. A right ventricular parasternal impulse is often palpable, and venous pressure may be elevated. Atrial fibrillation and arterial embolism are more common among elderly patients. Atrial fibrillation often precipitates clinical deterioration; it sometimes causes pulmonary edema, peripheral arterial embolism, and stroke.

Left atrial enlargement is often seen on chest x-ray. ECG evidence of right ventricular hypertrophy is common when the stenosis is severe. Doppler echocardiography can document mitral stenosis and help estimate its severity. Left atrial myxoma, which may mimic mitral stenosis, can be differentiated by echocardiography.


Most elderly patients with mild to moderate mitral stenosis respond well to medical therapy. If atrial fibrillation develops, digoxin, verapamil, or a beta-blocker can slow the ventricular response rate and reduce symptoms. Pharmacologic or electrical cardioversion to sinus rhythm may relieve symptoms, especially if the patient can be maintained in sinus rhythm by antiarrhythmic drugs.

Although elderly patients are at increased risk of bleeding, anticoagulants are recommended. The risk of peripheral arterial embolism and of embolic stroke is much higher than the risk of complications from anticoagulant therapy. (see pages 697-700) Prolongation of the international normalized ratio (INR) to 2 to 3 is optimal.

Valve replacement (see page 947) is warranted for symptomatic patients with progressively severe mitral stenosis, because the calcified valve is rarely amenable to commissurotomy. Embolization without symptomatic hemodynamically severe mitral stenosis is not an indication for valve replacement. For the few patients who have uncalcified or minimally calcified valves, flexible valve leaflets, and mild mitral regurgitation, percutaneous balloon valvuloplasty is the procedure of choice.

Acute Mitral Regurgitation

Sudden development of retrograde blood flow from the left ventricle into the left atrium through an incompetent mitral valve during systole.

Acute, often massive mitral regurgitation in elderly patients is commonly due to chordal rupture or development of a flail mitral valve. The underlying disorder may be myocardial infarction, papillary muscle rupture, infective endocarditis, trauma, or mucoid degeneration of the valve cusps. Chordal rupture, common among the elderly, may be idiopathic and often results in life-threatening heart failure.


With sudden valvular incompetence, a large regurgitant volume enters the left atrium, suddenly increasing the volume of the left atrium during systole. During diastole, this increased volume enters and suddenly dilates the left ventricle; left ventricular filling pressure increases sharply because the normal pericardial sac is relatively noncompliant. Left ventricular dilation produces compression of the right ventricle during diastole, increasing right ventricular filling pressure and leading to right-sided heart failure.

Symptoms and Signs

Typically, patients have symptoms of pulmonary edema or acute pulmonary congestion, both of which often develop rapidly. Sinus tachycardia and a harsh, early systolic apical murmur, often with a thrill, are characteristic. The murmur ends early, when the noncompliant left atrium can no longer accept additional volume. The first heart sound is soft, and the accentuated pulmonic component of the second heart sound reflects acute pulmonary hypertension. An early diastolic sound (S3) is characteristic, and an atrial gallop (S4) may be present. Severe acute mitral regurgitation often leads to right ventricular failure. The ECG and chest x-ray may be normal initially but soon show pulmonary venous congestion.

Diagnosis and Treatment

Echocardiography confirms the diagnosis and often suggests the etiology. It can differentiate acute mitral regurgitation due to papillary muscle dysfunction or rupture from interventricular septal rupture and can detect the valvular vegetations of infective endocarditis. Transesophageal echocardiography, a safe procedure, allows the valve to be evaluated in greater detail, thus helping to determine whether the valve can be repaired or must be replaced.

Acute pulmonary edema due to acute mitral regurgitation is managed in the same way as that due to other cardiac disorders. Patients with hemodynamic instability, characterized by hypotension with pulmonary edema, require intra-aortic balloon counterpulsation to allow cardiac catheterization and the subsequent induction of anesthesia for surgery. Patients with infective endocarditis require treatment with appropriate antibiotics. (see page 882)

Patients with acute massive mitral regurgitation and clinical deterioration typically require urgent valve surgery. (see page 947)

Chronic Mitral Regurgitation

Long-standing retrograde blood flow from the left ventricle into the left atrium through an incompetent mitral valve during ventricular systole, with eccentric left ventricular hypertrophy.

Chronic rather than acute mitral regurgitation is the most common type of mitral valve disease in the elderly. About half of patients with rheumatic mitral regurgitation have associated aortic valve disease, usually aortic regurgitation.

In the elderly, isolated chronic mitral regurgitation often results from papillary muscle dysfunction after myocardial infarction. Chronic mitral regurgitation may also be due to mitral annular calcification, myxomatous valve degeneration (with mitral valve prolapse), chordal rupture, or rheumatic heart disease. Mitral annular calcification occurs in about 6% of persons > 60, predominantly women. The incidence of myxomatous valvular degeneration increases with age.


In chronic mitral regurgitation, the regurgitant volume gradually increases, increasing the volume of the left atrium during systole and that of the left ventricle during diastole. Enlargement of the left ventricle results in eccentric hypertrophy. Eventually, stretching of the left atrium results in atrial fibrillation, and the left ventricle can no longer maintain a normal effective forward stroke volume because of decreased myocardial contractility. Left ventricular failure develops, leading to increased pulmonary artery and right ventricular systolic pressure. Thus, right ventricular failure develops very late in the course of the disorder.

Mitral regurgitation due to mitral annular calcification prevents annular systolic contraction and may limit valve leaflet closure. It is rarely hemodynamically significant; however, calcification may involve the conduction system, causing various degrees of atrioventricular block, and may double the risk of stroke.

Symptoms, Signs, and Diagnosis

Patients may be asymptomatic or present with only a pansystolic apical murmur or a decrease in exercise tolerance with easy fatigability. Atrial fibrillation may occur later than it does in patients with mitral stenosis. Atrial fibrillation may precipitate hemodynamic deterioration, with an apical holosystolic murmur engulfing the first heart sound, and symptoms and signs of left-sided heart failure. Systemic embolism occurs predominantly when atrial fibrillation or heart failure is present but is less common among patients with chronic mitral regurgitation than among those with mitral stenosis.

If the cause is mitral valve prolapse, presenting symptoms and signs may include atypical chest pain, palpitations or syncope due to arrhythmia, and heart failure (more common among men). A midsystolic click or clicks and a late systolic or holosystolic murmur may be heard. The mitral regurgitant murmur predominates in elderly patients, whereas clicks and late crescendo systolic murmurs predominate in younger patients. An ECG often shows ST-T wave changes, but when mitral regurgitation is severe, it may show left ventricular hypertrophy. Ventricular arrhythmias are common, even in patients with normal ventricular function. With severe mitral regurgitation, the onset of atrial fibrillation may accentuate mitral and tricuspid valve prolapse and often precipitates hemodynamic deterioration. Systemic embolism and sudden death may occur.

Doppler echocardiography can be used to determine the magnitude of the mitral regurgitation and to assess overall ventricular size and function. It can sometimes determine the etiology of the mitral insufficiency. For example, vegetations suggest infective endocarditis; prolapse and thickening of the leaflets suggest myxomatous degeneration; flail mitral valve suggests chordal rupture; and thickened retracted leaflets and chordal fusion suggest rheumatic heart disease. Doppler echocardiography can differentiate mitral valve prolapse from other causes of mitral regurgitation. A ringlike calcification in the area of the mitral valve on a chest x-ray and dense horseshoe-shaped calcifications on an echocardiogram indicate mitral annular calcification.

Coronary arteriography may be needed to differentiate the chest pain due to mitral valve prolapse from that due to coronary atherosclerosis.


Atrial fibrillation and heart failure are managed with standard therapy. (see pages 890 and 904) Anticoagulants are given to prevent systemic embolism. Most symptomatic elderly patients with chronic mitral regurgitation respond readily to medical therapy.

Surgery (see page 947) is indicated when medical therapy does not control symptoms and/or when ventricular function deteriorates, as indicated by a progressive increase in left ventricular end-diastolic and end-systolic volumes and a decrease in ejection fraction. The ejection fraction should not be allowed to decrease below 55%. Elderly men with mitral valve prolapse are more likely to require surgery than are elderly women. If high-degree atrioventricular block occurs, a pacemaker should be placed. (see page 899)

For patients with papillary muscle dysfunction due to CAD, an annuloplasty ring placed during coronary artery bypass grafting can reduce the degree of regurgitation.

Tricuspid Regurgitation

Retrograde blood flow from the right ventricle into the right atrium caused by inadequate closure of the tricuspid valve orifice during ventricular systole.

In the elderly, tricuspid regurgitation is most often caused by a dilated valve ring secondary to right ventricular failure, which usually results from left-sided heart failure or pulmonary hypertension related to primary pulmonary disease. Infective endocarditis is a less common cause. Tricuspid regurgitation may be silent, or a short ejection or holosystolic murmur may be present.

The diagnosis is made by finding the characteristic systolic murmur, usually heard in the third or fourth intercostal space at the left sternal border. The murmur increases in intensity with inspiration (Carvallo's sign) in about 50% of patients. If tricuspid regurgitation is severe, a prominent large V wave may be seen in the jugular venous pulse. The diagnosis is confirmed by Doppler echocardiography.

Medical treatment of heart failure ameliorates tricuspid regurgitation. Surgery is rarely necessary.

Tricuspid Stenosis

Abnormal narrowing of the tricuspid valve orifice.

Tricuspid stenosis is rare and is most often due to multivalvular rheumatic heart disease or the carcinoid syndrome. Patients with isolated tricuspid stenosis have signs of right-sided heart failure with elevated cervical venous pressure, hepatomegaly, edema, and ascites; dyspnea and orthopnea are often absent. Commonly, exercise tolerance decreases because of low cardiac output. Hepatomegaly is present without other signs of left-sided heart failure.

The lower left sternal border diastolic rumble increases during inspiration. A low-pitched murmur is heard in the third or fourth intercostal space at the left sternal border; it frequently becomes louder with inspiration. A prominent A wave with poor or absent Y descent is seen in the jugular venous pulse. The diagnosis is made by finding the characteristic murmur and jugular venous pulse.

Medical therapy is indicated for mild disease. Although surgical repair is rarely required, balloon valvotomy is the treatment of choice for patients with signs of right-sided heart failure or with markedly decreased exercise tolerance due to inability to increase cardiac output. If the valve is calcified (a rare finding), valve replacement is necessary.

Pulmonic Valve Regurgitation

Retrograde blood flow from the pulmonary artery into the right ventricle through an incompetent pulmonary valve.

Among the elderly, pulmonic valve regurgitation is rarely due to primary pulmonic valve disease. It is almost always a sequela of pulmonary hypertension, usually due to left-sided heart failure or to primary pulmonary disease. It is characterized by a high-pitched, blowing decrescendo diastolic murmur in the second and third intercostal space to the left of the sternum. Often, this murmur cannot be distinguished from the murmur of aortic regurgitation. Doppler echocardiography can help distinguish the two disorders.

Treatment is aimed at managing the underlying disorder and attempting to lower pulmonary artery pressure.

Copyright © 2009-2010 Merck Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc., Whitehouse Station, N.J., U.S.A.  Privacy  Terms of Use  Sitemap