Valvular Heart Disease

IV. Valvular Heart Disease
A. Aortic stenosis
1. Etiology
a. Congenital aortic stenosis usually is detected in pediatric patients but occasionally becomes apparent in early adulthood.
b. Senile calcific aortic stenosis occurs when scarring and calcification of a tricuspid aortic valve lead to orifice narrowing in the sixth, seventh, and eighth decades of life. Although once considered a “degenerativeâ€‌ idiopathic disease, it is now clear that the pathology leading up to severe aortic stenosis is due to proliferative and inflammatory changes leading to calcification, similar to the development of the plaque in ASCAD.
c. Bicuspid aortic valve is a common congenital cardiac abnormality. The flow characteristics of the bicuspid valve are more turbulent than those of the normal valve, leading to valve injury, calcification, and stenosis in the fourth and fifth decades of life.
d. Rheumatic aortic stenosis never occurs alone and is always associated with mitral valve disease.
2. Pathophysiology. Aortic valve stenosis produces a pressure overload on the left ventricle due to the greater pressure that must be generated to force blood past the stenotic valve. This commonly leads to compensatory left ventricular hypertrophy.
3. Clinical features
a. Symptoms. Asymptomatic patients with aortic stenosis are at little risk for sudden death. However, this risk increases dramatically when symptoms develop.
(1) Angina occurs in 35%–50% of patients with aortic stenosis.
(a) Fifty percent of patients who develop this symptom die within 5 years of its onset unless aortic valve replacement is performed.
(b) Although the exact mechanism of angina is unknown, current data suggest that coronary blood flow reserve is impaired in the severely hypertrophied left ventricle. Impairment of the coronary blood flow reserve limits oxygen delivery to the myocardium and produces angina during exercise.
(2) Syncope occurs during exercise when total peripheral resistance falls due to local autoregulatory mechanisms [see IX B, C 1 b (2) (b)]. When aortic stenosis is present, cardiac output across the stenotic aortic valve cannot increase during exercise. Because total peripheral resistance falls, blood pressure must also fall, and syncope occurs.
(a) Other causes of syncope in aortic stenosis include a reflex vasodepressor response to high intraventricular pressure, atrial or ventricular arrhythmias, and heart block as a result of conduction system calcification.
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(b) After syncope occurs in patients with aortic stenosis, expected survival is 2–3 years without valve replacement.
(3) Heart failure. Fifty percent of patients who develop heart failure die within 1–2 years of presentation if the stenosis is not corrected. Heart failure occurs because the afterload placed on the myocardium becomes excessive and both contractile dysfunction and diastolic muscle dysfunction occur when the myocardium is exposed to a prolonged, severe pressure overload.
b. Physical signs
(1) Delayed carotid upstroke. In the presence of aortic stenosis, the carotid upstroke typically is delayed in timing and reduced in volume (pulsus parvus et tardus). This finding is the most reliable physical sign in gauging the severity of the disease.
(2) Systolic ejection murmur. A harsh, late-peaking systolic ejection murmur is heard in the aortic area and is transmitted to the carotid arteries. The murmur also may be reflected to the mitral area, producing the false impression that mitral regurgitation also is present (Gallavardin's phenomenon).
(3) Soft, single S2. Because the aortic valve is stenotic, its motion is severely impaired. The reduction in motion of the valve causes the aortic component (A2) of the S2 to be absent. Thus, the only component of the S2 that is heard is the pulmonic component (P2), which is normally soft.
(4) S4. An S4 usually is heard as a result of the reduced left ventricular compliance that occurs in left ventricular hypertrophy.
(5) Sustained, forceful apex beat. The point of maximal cardiac impulse usually is not displaced unless heart failure has occurred. However, the impulse is sustained and forceful throughout systole.
4. Laboratory diagnosis
a. Electrocardiography. The ECG usually shows evidence of left ventricular hypertrophy.
b. Echocardiography can rule out significant aortic stenosis if valve motion is shown to be normal. However, Doppler examination of the aortic outflow tract during echocardiography can accurately measure the pressure gradient across the aortic valve, and can be used to calculate the valve area.
c. Cardiac catheterization. Diagnosis and evaluation of the severity of aortic stenosis may be confirmed by cardiac catheterization, during which the pressure gradient across the valve is measured and the degree of stenosis is calculated.
5. Therapy
a. Palliative therapy
(1) Medical therapy has no definitive role in the treatment of aortic stenosis, but diuretics may temporarily relieve the symptoms of volume overload until mechanical relief of the obstruction is performed.
(2) Insertion and inflation of a large balloon in the aortic valve orifice (balloon valvuloplasty) also may produce a moderate improvement in the amount of obstruction and in the symptoms, but relief from using this technique is usually only temporary. It does not reduce the mortality expected if the disease is left untreated.
b. Curative therapy requires aortic valve replacement, which may be performed using a preserved human homograft valve, a bioprosthetic heterograft valve, a mechanical valve, or a pulmonary autograft.
(1) Homograft valves. The hemodynamic flow pattern is excellent, and patients with homograft valves do not require anticoagulation therapy. Availability of these valves is limited, because most suitable donors are also acceptable for whole heart donation in cardiac transplantation.
(2) Heterograft valves. Patients with heterograft valves do not require anticoagulation therapy, but the durability of the valve is limited, and deterioration after 10 years is common.
(3) Mechanical valves. Patients with mechanical valves do require anticoagulation therapy. However, these valves are more durable than bioprostheses.
(4) Autograft (Ross procedure). In this procedure, the patient's normal pulmonary valve is transplanted into the aortic position, where it has excellent durability and longevity. A
P.20homograft is then inserted into the pulmonary position, where low pressure enhances homograft longevity. In practiced hands, the results of this procedure are excellent.




B. Mitral stenosis
1. Etiology. Almost all cases of mitral stenosis in adults are secondary to rheumatic heart disease. Most cases occur in women.
2. Pathophysiology
a. Mitral valve stenosis impedes left ventricular filling, thereby increasing left atrial pressure as a pressure gradient develops across the mitral valve. Elevated left atrial pressure is referred to the lungs, where it produces pulmonary congestion. As the stenosis becomes more severe, it may significantly reduce forward cardiac output.
b. Because the right ventricle is responsible for filling the left ventricle, the burden of propelling blood across the stenotic mitral valve is borne by the right ventricle. The overload on the right ventricle may be increased further when secondary pulmonary vasoconstriction occurs. Thus, the right ventricle must generate enough force both to overcome the resistance offered by the stenotic valve and to propel blood through constricted pulmonary arteries. Consequently, pulmonary arterial pressure may increase to three to five times normal, eventually resulting in right ventricular failure.
3. Clinical features
a. Symptoms
(1) Left-sided failure. Dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea occur as a result of reduced left ventricular output and increased left atrial pressure. In mitral stenosis, the symptoms of left ventricular failure usually are not attributable to left ventricular dysfunction but, rather, to the mitral stenosis itself.
(2) Right-sided failure. When pulmonary hypertension occurs, the right ventricle may fail, producing edema, ascites, anorexia, and fatigue.
(3) Hemoptysis. The high left atrial pressure produced in mitral stenosis may lead to rupture of small bronchial veins, producing hemoptysis.
(4) Systemic embolism. Stagnation of blood in the enlarged left atrium and left atrial appendage occurs in mitral stenosis, particularly if atrial fibrillation is present. Under these circumstances, a thrombus may form in the left atrium and can become a source of systemic embolism.
(5) Hoarseness may occur in mitral stenosis as the enlarged left atrium impinges on the left recurrent laryngeal nerve (Ortner's syndrome).
b. Physical signs
(1) Atrial fibrillation. Frequently, an irregularly irregular cardiac rhythm indicative of atrial fibrillation is present.
(2) Pulmonary rales. Bilateral pulmonary rales occur secondary to elevated left atrial and pulmonary venous pressures.
(3) Increased intensity of the S1. The S1 usually increases in intensity because the transmitral gradient limits spontaneous diastolic mitral valve closure. Thus, the mitral valve remains open until ventricular systole closes it forcibly, resulting in an increase in S1 intensity. Late in the course of the disease, the valve may become so stenotic that it no longer opens or closes, reducing the intensity of S1.
(4) Increased intensity of the P2 component of the S2. The P2 component of the S2 is usually increased in intensity if pulmonary hypertension has developed.
(5) Opening snap. An opening snap is heard following the S2 as the stenotic valve is forced open in diastole by the high left atrial filling pressure. The higher the pressure, the sooner the mitral valve opens. Thus, a short interval (<0.10 second in duration) indicates relatively high left atrial pressure and severe stenosis.
(6) Diastolic rumble. The murmur of mitral stenosis is a low-pitched apical rumble, which begins after the opening snap. If the patient is in sinus rhythm, atrial systole produces a presystolic accentuation of this murmur.
(7) Sternal lift. Enlargement of the right ventricle as a result of pulmonary hypertension produces a systolic lift of the sternum.
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(8) Other symptoms. Neck vein distention, edema, hepatic enlargement, and ascites may be present if right ventricular failure occurs.
4. Laboratory diagnosis
a. Electrocardiography. The ECG may show atrial fibrillation as well as signs of left atrial enlargement and right ventricular hypertrophy.
b. Chest radiography
(1) Straightening of the left heart border and a double density along the right heart border (formed by the right and left atria) occur as a result of left atrial enlargement.
(2) Signs of pulmonary venous hypertension, including an increase in pulmonary vascular markings and Kerley's lines, are likely to be present.
(3) When pulmonary hypertension leads to right ventricular enlargement, the lateral view shows a loss of the retrosternal airspace.
c. Echocardiography usually provides excellent images of the mitral valve.
(1) The echocardiogram shows reduction in the excursion of the valve leaflets and thickening of the valve. Two-dimensional echocardiography can be used to visualize and measure the residual mitral valve orifice. Invariably, left atrial enlargement is present.
(2) Doppler examination of the mitral valve may also help to quantify the severity of the stenosis.
5. Therapy
a. Medical therapy is reserved for patients with mild-to-moderate symptoms of left-sided failure.
(1) Diuretics. The mainstay of treatment, these agents are used to control pulmonary congestion and to limit dyspnea and orthopnea.
(2) Digitalis. Because left ventricular muscle function usually is normal in mitral stenosis, the use of digitalis is of little benefit to patients in sinus rhythm. In patients in atrial fibrillation, however, digitalis is used to slow ventricular rate. A rapid ventricular rate in mitral stenosis shortens diastole, thereby reducing left ventricular filling, which, in turn, further increases left atrial pressure and reduces cardiac output. خ²-Blockers and diltiazem or verapamil may be added to digoxin if further heart rate control is necessary.
(3) Anticoagulants. Patients with mitral stenosis and coexistent atrial fibrillation have a high incidence of systemic embolism. In such patients, anticoagulation therapy (e.g., with warfarin) usually is indicated.
b. Balloon valvuloplasty. Unlike balloon valvuloplasty for aortic stenosis, balloon valvuloplasty for mitral stenosis can offer effective long-term improvement.
(1) Valvuloplasty for mitral stenosis produces a commissurotomy similar to that produced at open heart surgery. During balloon mitral valvuloplasty, transseptal catheterization of the interatrial septum is performed, allowing passage of the balloon catheter from the right atrium to the left atrium. From the left atrium, the balloon catheter is advanced to the mitral valve and is inflated.
(2) Echocardiography is essential in predicting immediate and long-term success. Factors influencing the feasibility and success of valvuloplasty include the degrees of mitral regurgitation, valvular thickening, calcification, and mobility, and the degree of subvalvular involvement.
c. Surgical therapy is effective in relieving the symptoms of mitral stenosis and in prolonging life in symptomatic patients. Surgery should be performed prior to the development of pulmonary hypertension, which increases surgical risk. However, if pulmonary hypertension is present and surgery is successful, pulmonary hypertension usually regresses postoperatively.




C. Aortic regurgitation (or aortic insufficiency)
1. Etiology
a. Idiopathic aortic root dilation. Aortic root dilation, a common cause of aortic regurgitation, occurs more frequently in patients with hypertension but correlates best with increasing age. It is also seen more frequently in patients with bicuspid aortic valves.
b. Rheumatic heart disease. Aortic insufficiency usually is present to some degree in most cases of rheumatic heart disease. Mitral stenosis usually predominates, but occasionally aortic insufficiency is the most severe manifestation of rheumatic heart disease.
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c. Infective endocarditis. Infection of the aortic valve may lead to perforation or partial destruction of one or more aortic leaflets, producing aortic insufficiency.
d. Marfan syndrome may produce aortic insufficiency in two ways.
(1) Proximal root dilation. The extreme expansion of the proximal aortic root seen in Marfan syndrome may produce aortic insufficiency.
(2) Aortic root dissection. The advanced cystic medial necrosis present in Marfan syndrome may lead to an intimal tear and dissection of the aorta. If the dissection involves the proximal aortic root, the supporting structures of the aortic valve are disrupted, and the valve is rendered incompetent.
e. Aortic dissection. Any cause of aortic dissection other than Marfan syndrome may lead to aortic insufficiency.
f. Syphilis may produce aortitis, which may extend to the aortic valve and produce aortic incompetence.
g. Collagen vascular disease. Systemic lupus erythematosus (SLE) and ankylosing spondylitis may cause aortic insufficiency.
2. Pathophysiology
a. A portion of the left ventricular stroke volume ejected during systole regurgitates into the left ventricle during diastole. If no compensation occurs, left ventricular forward output decreases. However, chronic regurgitation of blood into the left ventricle produces eccentric cardiac hypertrophy and an increase in end-diastolic volume. The stroke volume (end-diastolic volume minus end-systolic volume) therefore increases, helping to compensate for the volume that is regurgitated. The increase in total stroke volume leads to an increase in pulse pressure and increased systolic pressure. The additional development of concentric hypertrophy compensates this second type of overload. The additional volume and pressure that the left ventricle must generate eventually lead to left ventricular dysfunction and CHF.
b. An additional pathophysiologic consequence of aortic insufficiency is a reduction in systemic diastolic blood pressure.
3. Clinical features
a. Symptoms
(1) Left ventricular failure
(a) Chronic aortic insufficiency may cause left ventricular dysfunction, leading to symptoms of dyspnea, orthopnea, and paroxysmal nocturnal dyspnea.
(b) In acute aortic insufficiency, normal muscle function may coexist with heart failure. In this circumstance, reduced forward output and elevated left ventricular filling pressure occur prior to compensatory left ventricular enlargement.
(2) Syncope. Reduction in diastolic systemic arterial pressure produces a reduction in mean arterial pressure. If the mean arterial pressure is reduced significantly, cerebral perfusion is compromised, and syncope may occur.
(3) Angina occurs less commonly in aortic insufficiency than in aortic stenosis. The cause of angina in aortic insufficiency is reduced coronary blood flow. Coronary blood flow occurs primarily in diastole and is driven by the aortic diastolic blood pressure. This driving pressure is reduced in aortic insufficiency, in turn reducing coronary blood flow.
b. Physical signs
(1) Left ventricular impulse. The PMI is hyperdynamic and is displaced downward and to the left as a result of left ventricular enlargement.
(2) Diastolic murmur. The murmur of aortic insufficiency is a high-pitched, diastolic blowing murmur heard along the left sternal border. Often the murmur is heard best when the patient is sitting up and leaning forward.
(3) Austin Flint murmur. A low-pitched diastolic rumble similar to that heard in mitral stenosis may be present in patients with aortic insufficiency. The Austin Flint murmur usually indicates moderate-to-severe insufficiency. The murmur is believed to be caused by reverberation of the regurgitant flow against the mitral valve, although the exact mechanism is unclear.
(4) Total stroke volume and consequently, pulse pressure, increases in chronic aortic insufficiency. The increased stroke volume and pulse pressure lead to many physical signs, some of which are included in the following.
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(a) Corrigan's pulse. The carotid pulse has a rapid rise and full upstroke with a rapid fall in diastole.
(b) Hill's sign refers to a disproportionate increase of systolic blood pressure (i.e., >30 mm Hg) when measured in the leg, as compared with the systolic blood pressure measured in the arm. This sign suggests severe aortic insufficiency.
(c) Pistol-shot femoral pulses. Auscultation over the femoral arteries reveals a pulse that sounds like a pistol shot.
(d) Duroziez's sign. A stethoscope is placed over the femoral artery with enough pressure to produce a systolic bruit. The concomitant occurrence of a diastolic bruit constitutes Duroziez's sign.
(e) de Musset's sign refers to a bobbing movement of the head caused by the increased stroke volume and pulse pressure.
(f) Quincke's pulse is systolic blushing and diastolic blanching of the nail bed when gentle pressure is placed on the nail.
(5) Acute aortic insufficiency. The preceding signs are usually absent in acute aortic insufficiency because compensatory increases in end-diastolic volume and stroke volume have not yet occurred. In fact, the clinical picture of acute severe aortic insufficiency is remarkably bland. The apical impulse is not enlarged. S1 is soft because increased left ventricular end-diastolic pressure closes the mitral valve before systole. This finding marks a poor prognosis for patients treated without valve replacement.
4. Diagnosis
a. Electrocardiography. The ECG usually shows left ventricular hypertrophy. In endocarditis, a prolonged PR interval may indicate abscess formation involving the conduction system.
b. Chest radiography. Unless the aortic insufficiency is mild or acute, cardiac enlargement is usually present, and often the proximal aorta is dilated. The absence of cardiac enlargement is evidence against the diagnosis of severe chronic aortic insufficiency.
c. Echocardiography. Evidence of an enlarged left ventricular cavity is usually present in aortic insufficiency. Frequently, diastolic vibration of the mitral valve is present, produced by the regurgitant flow striking the valve. Doppler examination of the aortic outflow tract reveals abnormal diastolic flow from the aorta to the left ventricle, which may be analyzed quantitatively.
d. Cardiac catheterization. Aortography may be performed at the time of cardiac catheterization. This is useful if noninvasive testing is not diagnostic or discordant with clinical findings.
5. Therapy. If aortic insufficiency is severe, eventual aortic valve replacement is necessary.
a. Timing of surgery is difficult, however, because the lesion may be tolerated for several years. Careful follow-up is required to detect early signs of decompensation; at this time, valve replacement is advisable. In most cases, valve replacement should be performed before the left ventricular echocardiographic end-systolic dimension exceeds 55 mm and the ejection fraction falls below 55%.
b. For those who do not yet meet the criteria for surgery, vasodilator therapy with dihydropyridine calcium channel blockers or ACE inhibitors can improve hemodynamics and may delay onset of left ventricular dysfunction and the need for surgery.




D. Mitral regurgitation (or mitral insufficiency)
1. Etiology
a. Mitral valve prolapse is characterized by redundant mitral valve leaflets or chordae that permit systolic prolapse of the mitral valve into the left atrium with resultant mitral regurgitation.
(1) This syndrome usually is benign, but in some cases it may be associated with significant mitral regurgitation. Additional complications include atypical chest pain, cardiac arrhythmias, and an increased risk of endocarditis. Most clinically important sequelae occur in those patients whose mitral valves are clearly thickened and echocardiographically abnormal.
(2) A midsystolic click and a late systolic murmur typically are heard on physical examination.
b. Coronary artery disease may lead to ischemia or infarction of the papillary muscles to which the mitral valve is tethered, thereby producing mitral incompetence.
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c. Rheumatic heart disease. Scarring and retraction of the mitral leaflets as a result of rheumatic heart disease cause mitral regurgitation.
d. Ruptured chordae tendineae. Spontaneous rupture of the chordae tendineae may occur in otherwise healthy individuals. Chordal rupture permits prolapse of a portion of a mitral valve leaflet into the left atrium, rendering the valve incompetent.
e. Infective endocarditis. Infection of the mitral valve may cause its destruction with subsequent regurgitation.
2. Pathophysiology. Mitral regurgitation permits a portion of the left ventricular stroke volume to be pumped backward into the left atrium instead of forward into the aorta, resulting in increased left atrial pressure and decreased forward cardiac output. Preload is increased by the volume overload, and afterload is initially decreased as the left ventricle empties a portion of its contents into the relatively (i.e., compared with the aorta) low-pressure left atrium. This augments ejection performance and helps compensate for the regurgitation.
a. Initially, compliance of the left atrium is low, and the regurgitant volume produces high left atrial pressure with resultant congestive symptoms.
b. With time, the left atrial compliance and volume increase, allowing accommodation of the regurgitant volume at more physiologic filling pressures.
c. The development of left ventricular eccentric cardiac hypertrophy restores forward stroke volume.
d. After a prolonged period of compensation, left ventricular muscle dysfunction eventually occurs, resulting in a fall in ejection fraction from supranormal to normal or even subnormal values.
3. Clinical features
a. Symptoms. Characteristics include those of left ventricular failure (i.e., dyspnea, orthopnea, and paroxysmal nocturnal dyspnea).
(1) If mitral regurgitation is severe and chronic, pulmonary hypertension and symptoms of right-sided failure also may occur.
(2) Patients in atrial fibrillation may experience symptoms of systemic embolization. The risk of embolization appears to be less in patients with mitral regurgitation than in those with mitral stenosis, although this is debatable.
b. Physical signs
(1) Left ventricular impulse. As with aortic regurgitation, the PMI is hyperdynamic and displaced downward and to the left.
(2) Murmur. The murmur of mitral regurgitation is a holosystolic apical murmur that radiates to the axilla. It does not vary in intensity with variation in R-R interval.
(3) An S3 usually is heard in mitral regurgitation and may occur even in the absence of overt heart failure. The S3 is caused by the rapid filling of the left ventricle by the large volume of blood accumulated in the left atrium during systole.
4. Diagnosis
a. Electrocardiography. The ECG shows signs of left ventricular hypertrophy and left atrial enlargement.
b. Chest radiography shows cardiac enlargement. Vascular congestion indicates heart failure.
c. Echocardiography
(1) In cases of a ruptured chorda or mitral valve prolapse, the mitral valve can be seen extending into the left atrium during systole.
(2) When the mitral valve has been damaged by endocarditis, vegetations on the mitral leaflets frequently are demonstrated. Transesophageal echocardiography is better than transthoracic echocardiography for detecting vegetations.
(3) Regardless of the cause of the mitral regurgitation, left atrial and left ventricular enlargement occur if the condition is both chronic and severe.
(4) Doppler examination reveals abnormal systolic flow from the left ventricle into the left atrium. Quantitative doppler techniques can accurately assess the regurgitant orifice area and the regurgitant volume, both of which are important in determining severity.
d. Cardiac catheterization. Right-heart catheterization yields a pulmonary capillary wedge tracing that often displays a large v wave representative of the systolic volume overload on
P.25the left atrium. Left ventriculography demonstrates systolic regurgitation of contrast material into the left atrium.
5. Therapy
a. Medical treatment. The goal of medical therapy is to relieve symptoms by increasing forward cardiac output and reducing pulmonary venous hypertension.
(1) Digitalis. When atrial fibrillation occurs, digitalis is useful in controlling heart rate. In chronic mitral regurgitation with muscle dysfunction, this agent may be useful in increasing the inotropic state. In cases of acute mitral regurgitation when no inotropic deficit exists, it is not indicated.
(2) Diuretics are used to reduce central volume overload, which in turn reduces pulmonary venous hypertension and congestion.
(3) Vasodilators. Arteriolar vasodilators are particularly useful in managing acute mitral regurgitation. These agents reduce resistance to aortic outflow, thereby preferentially increasing forward output while reducing the amount of regurgitation. Vasodilators also reduce left ventricular size, which helps to reestablish mitral competence.
(4) Anticoagulants. Patients with mitral regurgitation and atrial fibrillation are at some risk for systemic embolism; therefore, anticoagulants usually are indicated.
b. Surgical treatment. Mitral valve replacement or repair is indicated for chronic mitral regurgitation, even if symptoms are mild, if there is evidence of ventricular dysfunction.
(1) Valve replacement must be performed prior to the onset of significant muscle dysfunction, which limits the success of operative intervention. To help ensure preservation of ventricular function, surgery should occur before the ejection fraction falls below 60% or the end-systolic dimension exceeds 40 mm.
(2) Valve repair offers several advantages over replacement, including eliminating the introduction of a prosthesis and decreasing the need for anticoagulation therapy. Furthermore, repairing, rather than replacing, the valve helps preserve left ventricular function because the mitral valve apparatus, which plays an important role in ventricular contraction is preserved.








E. Tricuspid regurgitation
1. Etiology
a. Infective endocarditis. In drug abusers who inject drugs under septic conditions, infective endocarditis is a common cause of tricuspid regurgitation.
b. Right ventricular failure. Sustained pressure or volume overload on the right ventricle leads to right ventricular dilation and improper alignment of the papillary muscles, which produces tricuspid regurgitation.
c. Rheumatic heart disease. In rheumatic heart disease, tricuspid regurgitation may occur, secondary to right ventricular pressure overload from left-sided valvular lesions. Tricuspid regurgitation also may occur as a result of primary rheumatic involvement of the tricuspid valve.
2. Pathophysiology. During systole, the dysfunctioning tricuspid valve allows blood to flow backward into the right atrium, leading to systemic venous congestion and venous hypertension.
3. Clinical features
a. Symptoms. Right-sided failure (i.e., edema, ascites) occurs. In severe and acute cases, hepatic congestion may be sufficiently extensive to produce right upper quadrant pain. Passive hepatic congestion also may lead to hepatocellular damage and jaundice.
b. Physical signs
(1) Right ventricular lift. The enlarged right ventricle may be palpated as a systolic lift of the sternum.
(2) Murmur. A holosystolic murmur that increases with inspiration is heard along the left sternal border.
(3) Jugular venous pulsation. A large v wave is seen in jugular veins during systole.
(4) Pulsatile liver. Systolic expansion of the liver frequently is present.
4. Diagnosis
a. Chest radiography shows right ventricular enlargement as an obliteration of the retrosternal airspace on the lateral view.
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b. Echocardiography demonstrates enlargement of the right atrium and right ventricle. Doppler examination is highly effective in demonstrating tricuspid regurgitation.
5. Therapy. Left-sided failure frequently is the cause of right-sided failure and tricuspid regurgitation. Effective treatment of left-sided failure reduces right ventricular pressure overload, which may decrease right ventricular size, thereby restoring valvular competence. If tricuspid regurgitation is caused by organic valvular disease, surgical repair or replacement of the tricuspid valve may be necessary.