Etiology

Mitral regurgitation may be caused by disease or distortion of any component of the mitral valve apparatus—the mitral annulus, leaflets, chordae, and papillary muscles—as well as by alterations in left ventricular (LV) geometry or systolic function (Figure 86-1).² Primary causes of chronic mitral regurgitation include myxomatous valve leaflets (mitral valve prolapse) and rheumatic disease. Chronic secondary mitral regurgitation may be due to dilated cardiomyopathy or to coronary artery disease with regional or global LV dysfunction.

Figure 86-1 Mitral valve anatomy: mitral annulus, anterior and posterior leaflets, chordae tendineae, and papillary muscles. Mitral regurgitation may be due to a disease that primarily affects the valve leaflets (e.g., mitral valve prolapse, rheumatic mitral valve disease) or may result from alterations in function or structure of the left ventricle, such as those induced by ischemic disease or dilated cardiomyopathy.

(From Otto CM. Clinical practice. Evaluation and management of chronic mitral regurgitation. New Engl J Med 2001;345:740-6.)

Acute mitral regurgitation also may be due to involvement of the valve leaflets or the left ventricle. Patients with myxomatous mitral valve disease may develop acute regurgitation due to spontaneous chordal rupture.³ Bacterial endocarditis results in acute mitral regurgitation due to destruction of valve tissue, often with leaflet perforation. Moderate to severe mitral regurgitation due to papillary muscle involvement or regional myocardial dysfunction complicates 12% of acute myocardial infarctions and is associated with an increased risk of heart failure or death.⁴

Clinical Presentation

Although patients with chronic mitral regurgitation may be asymptomatic for many years, the regurgitant lesions impose a volume load on the left ventricle, because an increased total stroke volume is needed to maintain a normal forward cardiac output. Left ventricular volume overload results in progressive LV dilation and may lead to an irreversible decline in ventricular contractility, even in the absence of clinical symptoms. Evaluation of ventricular contractility is problematic in patients with mitral regurgitation, given that measures of ventricular performance are affected by preload and afterload.⁵ However, based on outcomes after mitral valve surgery, the empirical parameters of ventricular end-systolic dimension and ejection fraction can be used to optimize the timing of surgical intervention. Thus, patients with moderate to severe chronic regurgitation undergo periodic echocardiography, with valve repair or replacement recommended when the end-systolic dimension is ≥ 40 mm and the ejection fraction is ≤ 60%.⁶

Chronic mitral regurgitation usually is well tolerated even when there is a superimposed hemodynamic load such as systemic infection, pregnancy, or trauma. However, mitral regurgitant severity may acutely worsen by at least two mechanisms. An increase in afterload, for example with a hypertensive crisis, may increase regurgitant severity due to an increased driving pressure from the left ventricle to the left atrium. Alteration in LV geometry, for example with ventricular dilation due to decompensated heart failure, may change the orientation of the papillary muscles such that leaflet closure is impaired, resulting in a larger regurgitant orifice area.⁷ In this situation, a vicious cycle may ensue where LV dilation worsens mitral regurgitant severity, which increases LV dilation, and so forth.

Acute mitral regurgitation presents with acute pulmonary edema and is a surgical emergency (Figures 86-2 and 86-3). Mitral chordal rupture results in the acute presentation of heart failure, often in patients who were unaware of a diagnosis of mitral valve prolapse. Patients with mitral valve perforation due to endocarditis present with pulmonary edema superimposed on signs and symptoms of endocarditis. Papillary muscle rupture or dysfunction after MI usually presents several days after acute MI; in some cases, the initial presentation is acute pulmonary edema, with the MI being clinically silent.

Figure 86-2 In this 24-year-old man with chronic mitral prolapse, chordal rupture resulted in a flail anterior leaflet, seen in apical four-chamber view (panel A, arrow). Severe mitral regurgitation (MR) was seen with a posterior and laterally directed jet on Doppler color-flow imaging (panel B, arrow). Ao, aorta; LA, left atrium; LV, left ventricle.

Figure 86-3 In the same patient as Figure 86-2, severe mitral regurgitation was recorded with continuous wave Doppler ultrasound (A). The rapid rise in left atrial pressure due to the regurgitant jet entering the left atrium results in a rapid decline in Doppler velocity in late systole—the Doppler equivalent of the v-wave seen on a pulmonary wedge pressure tracing. The continuous-wave Doppler recording of maximum tricuspid regurgitant jet velocity (B) of 4.2 m/sec indicates a right ventricular–to–right atrial pressure difference of 70 mm Hg. The patient’s right atrial pressure was estimated to be 10 mm Hg, based on size and respiratory variation in the inferior vena cava, so the estimated pulmonary systolic pressure is 80 mm Hg.

Diagnosis

A high level of clinical suspicion is needed to make the diagnosis of acute mitral regurgitation (Table 86-2). Acute pulmonary edema often obscures the signs and symptoms of the underlying disease process. The classical finding is a holosystolic murmur at the apex, radiating to the axilla. Although there is some correlation between the loudness of the murmur and regurgitant severity with chronic regurgitation, the murmur may be soft with acute severe mitral regurgitation. In patients with severe mitral regurgitation after MI, a murmur cannot be appreciated at all in up to 50% of patients.

TABLE 86-2 Diagnostic Approach to Acute Valve Dysfunction

Thus, in patients presenting with acute pulmonary edema or cardiogenic shock, prompt echocardiography is essential. Transthoracic images often are diagnostic, allowing identification of the etiology of valve dysfunction, quantitation of regurgitant severity, estimation of pulmonary pressures, and measurement of ventricular size and systolic function. If transthoracic images are nondiagnostic, transesophageal echocardiography (TEE) can be performed at the bedside in the intensive care unit (ICU). TEE provides excellent images of valve anatomy and Doppler evaluation of valve function.

Other diagnostic tests are based on the clinical presentation. Multiple blood cultures should be obtained in febrile patients with systemic or pulmonary edema to exclude the possibility of endocarditis. In patients with an abnormal electrocardiogram (ECG), chest pain, or a history of coronary artery disease, coronary angiography may be needed.

In the patient with acute pulmonary edema or cardiogenic shock after MI, the differential diagnosis includes acute mitral regurgitation, a ventricular septal defect, or a contained rupture of the ventricular free wall. All these possibilities can be diagnosed by echocardiography in an experienced center.

Invasive hemodynamic monitoring with a Swan-Ganz catheter for measurement of pulmonary pressures and cardiac output is needed in the patient with suspected acute mitral regurgitation. At the time of placement, oxygen saturations in the right atrium, right ventricle, and pulmonary artery should be measured. A ventricular septal defect results in a “step-up” in oxygen saturation between the right atrium and ventricle secondary to oxygenated blood from the left ventricle entering the right ventricle. The pulmonary artery balloon-occluded (wedge) pressure tracing should be examined for the presence of a “v-wave,” which supports the diagnosis of acute mitral regurgitation but is not always present.

Management

In patients with chronic mitral regurgitation and heart failure, management is directed at treating the process leading to decompensation and optimizing loading conditions (Table 86-3). For example, in a patient with a systemic infection, treatment of the infection, control of fever and tachycardia, and invasive monitoring to optimize preload and afterload are utilized. Medical therapy typically includes afterload reduction with nitroprusside or other vasodilators and preload reduction with diuretics.^8,9 The goal is to support the patient through the period of decompensation. Typically, hemodynamics return to the baseline compensated state after the acute illness.

TABLE 86-3 Therapeutic Approach to Acute Valve Dysfunction

In contrast, acute severe mitral regurgitation is a surgical emergency. Mortality is extremely high without restoration of valve competence; even with prompt valve surgery, 30-day mortality is 23%.¹⁰ Medical stabilization should occur concurrently with consultation by a cardiac surgeon. Acutely, placement of an intraaortic balloon pump (IABP) provides optimal afterload reduction while improving diastolic coronary blood flow.

The timing and risk of surgical intervention depend on the etiology of acute mitral regurgitation. Spontaneous chordal rupture usually can be treated early with mitral valve repair. Compared to valve replacement, mitral valve repair is associated with a lower operative mortality, improved preservation of LV function, and better long-term survival. In addition, the risks of a prosthetic valve and anticoagulation are avoided.

The timing of surgery for endocarditis depends on the disease course in that individual, but most centers now advocate early surgical intervention in the patient with heart failure or severe valve regurgitation to prevent progressive valve damage and paravalvular abscess formation.^11,12 In a large prospective multicenter study, early surgery was associated with a lower mortality than medical therapy (12% versus 21%).¹³ Valve repair is preferred but may not be possible, depending on the extent of tissue destruction. Early surgery is particularly beneficial in patients with paravalvular complications or systemic embolization.¹⁴

In patients with acute ischemic mitral regurgitation, treatment depends on the exact etiology of valve dysfunction.¹⁵ In patients with acute mitral regurgitation due to a regional wall-motion abnormality, myocardial function may improve after percutaneous revascularization.¹⁶ In these patients, use of an IABP and medical therapy may be advantageous during the acute episode, with weaning of therapy as myocardial function improves.

Mitral regurgitation due to partial or complete papillary muscle rupture requires surgical intervention. Although the risk of surgery is high, with an operative mortality rate of about 50%, outcome is even worse with medical therapy, with a mortality of 75% at 24 hours and 95% within 2 weeks after complete papillary muscle rupture.¹⁷ With the use of echocardiography, partial papillary muscle rupture can be recognized; prognosis in these patients depends on the extent of myocardial damage and severity of mitral regurgitation.¹⁸ With partial papillary muscle rupture, some surgeons prefer to stabilize the patient and delay surgery for 6 to 8 weeks after MI to avoid operating on the necrotic myocardial tissue. However, many patients cannot be stabilized, so acute intervention must be considered. Again, valve repair is preferred, but myocardial necrosis may necessitate valve replacement. Risk factors for surgery include older age, female gender, and poor LV systolic function. In some patients, the risk of surgical intervention may be so high as to be futile.

Etiology

Chronic aortic regurgitation most often is due to a congenital bicuspid valve, rheumatic valve disease, or aortic root dilation. There are numerous causes of aortic root dilation, including hypertension, cystic medial necrosis, Marfan syndrome, and a bicuspid aortic valve.¹⁹ The most common causes of acute aortic regurgitation are endocarditis, rupture of a congenital fenestration, and acute aortic dissection.¹ Endocarditis results in aortic regurgitation by destruction of the valve leaflet tissue, with a high percentage of cases also having paravalvular abscess formation. Aortic dissection results in acute aortic regurgitation either due to enlargement of the aortic annulus or to extension of the dissection into the valve region, resulting in a flail aortic valve leaflet.

Clinical Presentation

The acute backflow of blood from the aorta into the left ventricle in diastole results in an acute elevation in LV end-diastolic pressure, with consequent pulmonary edema. Because there has been no time for compensatory LV dilation, forward cardiac output falls abruptly owing to the regurgitant flow across the valve in diastole, so patients with acute aortic regurgitation also may be in cardiogenic shock. Decreased coronary perfusion pressure results in diffuse subendocardial ischemia, further impairing ventricular function.

Diagnosis

The clinical diagnosis of acute aortic regurgitation differs markedly from chronic aortic regurgitation (Figure 86-4). In contrast to the high-pitched diastolic decrescendo murmur of chronic aortic regurgitation, there is a “to-and-fro” murmur across the aortic valve which many clinicians fail to recognize as indicating aortic regurgitation. The pulse pressure is narrow due to the low forward stroke volume, and peripheral signs of aortic regurgitation are not seen. As with acute mitral regurgitation, the physical examination findings often are subtle, so a high index of suspicion and prompt echocardiography are needed to make this diagnosis.

Figure 86-4 Left ventricular (LV) and central aortic (Ao) pressures and corresponding Doppler velocity curves are shown for chronic (purple lines) and acute (green lines) aortic regurgitation. The shape of velocity curve is related to the instantaneous pressure differences across the valve, as stated in the Bernoulli equation. With acute aortic regurgitation (AR), aortic pressures fall more rapidly, and ventricular diastolic pressure rises more rapidly, resulting in a steeper deceleration slope on Doppler curve.

(From Otto CM. Textbook of clinical echocardiography. 4th ed. Philadelphia: Saunders; 2009, p. 303.)

Acute aortic regurgitation should be considered in the patient with signs or symptoms of endocarditis, in patients with a personal or family history of aortic root disease, and in those with a presentation consistent with acute aortic dissection.²⁰

Echocardiography allows imaging of the aortic valve and root and determination of the severity of aortic regurgitation based on a combination of two-dimensional (2D) imaging and pulsed, continuous-wave, and color Doppler modalities²¹ (Figures 86-5, 86-6, and 86-7). The continuous-wave Doppler curve shows a steep diastolic slope corresponding to the rapid equalization of diastolic pressure in the aorta and left ventricle. With severe acute regurgitation, there is no pressure gradient at end-diastole, so cuff diastolic blood pressure is equal to LV end-diastolic pressure. Echocardiography also allows accurate assessment of LV size and systolic function. When the differential diagnosis includes aortic dissection, transthoracic echocardiography is inadequate to exclude this possibility. Instead, TEE or computed tomography (CT) images should be obtained.

Figure 86-5 Endocarditis resulting in acute severe aortic regurgitation. In a long-axis view of the aortic valve (A), a flail aortic valve leaflet is seen (arrow), with the leaflet (arrow) prolapsing into the left ventricular (LV) outflow tract in diastole. Color-flow Doppler imaging (B) in the same view shows a broad jet of diastolic flow filling the outflow tract, consistent with severe regurgitation. Ao, aorta; LA, left atrium; LV, left ventricle.

Figure 86-6 Same patient as Figure 86-5. Pulsed Doppler flow in the proximal abdominal aorta (Ao) shows normal forward flow in systole (S), with abnormal reversed flow in diastole (D) that extends throughout diastole. This finding is highly specific for severe aortic regurgitation and can be helpful in the acute setting.

Figure 86-7 Same patient as Figure 86-5. Continuous-wave Doppler recording of flow across the aortic valve shows an increased antegrade velocity in systole (S) consistent with a high transaortic stroke volume. In diastole (D), a dense signal of retrograde flow is seen, with a steep deceleration slope (arrow) consistent with equalization of pressures between the aorta and left ventricle in diastole.

Management

Acute aortic regurgitation is a surgical emergency.¹ Preoperative management is supportive, with ventilatory support and invasive hemodynamic monitoring. While the diagnosis is being made, therapy may include the use of diuretics, inotropic agents, and nitroprusside or other vasodilators in an attempt to stabilize hemodynamics.^1,9 However, an IABP is contraindicated, as inflation of the balloon in the descending thoracic aorta in diastole will increase the amount of backflow across the aortic valve.

If acute aortic regurgitation is due to aortic dissection, acute surgical intervention is needed. The surgical approach may be replacement of the ascending aorta and valve with a combined prosthetic valve and fabric tube. When the valve leaflets are normal, some centers will preserve the native valve by resuspension of the leaflets in the prosthetic conduit (called the David procedure).

When acute aortic regurgitation is due to endocarditis, surgical options include a mechanical valve, a heterograft tissue valve such as a porcine aortic valve or bovine pericardial valve, or a cryopreserved homograft aorta valve. Rarely, the patient may undergo valve repair if there is a simple perforation with adjacent normal leaflet tissue.

Etiology and Clinical Presentation

Mitral stenosis is nearly always due to rheumatic disease, with only rare cases of calcific mitral stenosis seen in the elderly. Rheumatic mitral stenosis is a slowly progressive disease with an insidious decline in exercise tolerance and symptom onset over many years.²² However, in the asymptomatic patient with compensated moderate or severe mitral stenosis, acute decompensation can occur in the setting of increased systemic hemodynamic demands. Because mitral stenosis is more common in women (80% of cases) and occurs during the reproductive years, the most common emergency presentation of mitral stenosis is a pregnant woman with heart failure. Many of these patients are unaware of underlying valve disease and are initially diagnosed during pregnancy. The clinical presentation may also be due to or exacerbated by the onset of atrial fibrillation.

A large atrial myxoma may mimic the clinical presentation of mitral stenosis, presenting with acute hemodynamic compromise due to obstruction of the mitral valve orifice by the tumor mass.

Diagnosis

The apical diastolic rumble and opening snap of mitral stenosis is challenging to appreciate even in a quiet room with optimal patient positioning and frequently is inaudible in the ICU setting. However, the diagnosis is easily made by transthoracic echocardiography, with the mitral leaflet showing the characteristic findings of rheumatic disease: commissural fusion, chordal shortening and fusion, and restriction of the diastolic opening of the leaflets (Figure 86-8).²³ Mitral stenosis severity can be quantitated by calculation of valve area by 2D planimetry or by the Doppler pressure half-time method, with moderate to severe stenosis defined as a valve area less than 1.5 cm² (Figure 86-9). Transthoracic echocardiography also provides information on LV size and systolic function, left atrial size, pulmonary pressures, and any associated valve lesions. If evaluation for left atrial thrombus is needed, TEE has a sensitivity of only 60% compared to a sensitivity of nearly 100% from the transthoracic approach.

Figure 86-8 In a patient with mitral stenosis the long axis view (A) demonstrates the classic findings of diastolic doming of leaflets (arrows) due to commissural fusion, with thickening predominantly at the leaflet tips. In the short-axis view (B), the restricted mitral orifice with fusion of the commissures is visualized, providing accurate measurement of valve area by direct planimetry. In this case, the valve area of 0.7 cm² indicates severe valve obstruction. Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.

Figure 86-9 Same patient as Figure 86-10. Apical four-chamber view (A) shows severe left atrial enlargement due to mitral obstruction, with thickened valve leaflets (arrow). Haziness in left atrium is due to stasis of blood flow, with spontaneous contrast on echocardiography. Continuous-wave Doppler recording of flow across mitral valve shows increased velocity corresponding to transvalvular pressure gradient. Pressure half-time (T1/2) can be used to accurately calculate mitral valve area (0.7 cm²).

Management

Most patients with mitral stenosis and acute decompensation can be managed conservatively with treatment of the superimposed illness.⁹ Efforts should be directed towards decreasing overall metabolic demand and increasing oxygen delivery by controlling fever, maintaining a normal hemoglobin level, and providing supplemental oxygen. If atrial fibrillation is present, rate control is essential, preferably with conversion back to sinus rhythm. Even when sinus rhythm is present, beta-blockers may improve ventricular diastolic filling by prolonging the duration of diastole as heart rate is decreased.²⁴ Invasive hemodynamic monitoring and ventilatory support may be needed when severe heart failure is present.

In patients who do not respond to conservative therapy, emergency intervention should be considered. The optimal intervention is percutaneous balloon mitral valvotomy (PBMV), which typically results in an increase in mitral valve area to more than 1.5 cm².^25–27 PBMV can be safely performed even during pregnancy.^28–30 Patients with a left atrial thrombus, coexisting moderate to severe mitral regurgitation, or heavily calcified and deformed mitral valves are not candidates for PBMV; in theses patients, surgical mitral valve replacement may be needed.

Etiology and Clinical Presentation

Valvular aortic stenosis in adults is most often due to calcification of a normal trileaflet or congenital bicuspid valve (Figure 86-10). Rheumatic aortic stenosis is less common and is invariably accompanied by mitral valve involvement. In younger adults, congenital aortic stenosis may be encountered; some of these patients have restenosis after prior commissurotomy in childhood.

Figure 86-10 In this 26-year-old pregnant woman with a loud systolic murmur, the long-axis view shows doming of the aortic valve in systole (arrow). Short axis images confirmed a unicuspid aortic valve. Ao, aorta; LA, left atrium; LV, left ventricle.

Like mitral stenosis, aortic valve stenosis is a chronic, slowly progressive disease that presents acutely only in patients who have not been receiving regular medical care.^31–33 As in mitral stenosis, acute decompensation may occur with a superimposed systemic condition. Young women with congenital aortic stenosis may present with angina or heart failure during pregnancy. In older adults, asymptomatic patients with moderate to severe valve obstruction may present with heart failure in the setting of pneumonia, anemia, or other condition with increased metabolic demands.

Diagnosis

The classic physical examination findings for aortic stenosis include a delayed and decreased carotid upstroke, a narrow pulse pressure, a single second heart sound (S₂), and a systolic ejection murmur at the aortic region that radiates to the carotids. However, while a grade 4 murmur (palpable thrill) with a single S₂ and diminished carotids is specific for severe stenosis, these findings are very insensitive for the diagnosis.³⁴ Particularly when the patient is decompensated, the murmur may be soft, and carotid upstrokes may be altered by coexisting vascular disease or loading conditions.

Echocardiography provides reliable evaluation of aortic stenosis severity based on the maximum velocity through the narrowed orifice and valve area, calculated with the continuity equation (Figure 86-11). Disease severity is a continuum, and velocities may be relatively low despite severe stenosis when cardiac output in reduced. In general, stenosis can be graded as severe (valve area <1.0 cm² or jet velocity >4 m/sec), moderate (valve area 1.0-1.5 cm² or jet velocity 3-4 m/sec) or mild (valve area >1.5 cm² or jet velocity <3 m/sec). Echocardiography also allows evaluation of ventricular systolic and diastolic function and any associated valve disease.²³

Figure 86-11 Continuous-wave Doppler examination of the aortic valve (same patient as Figure 86-8) demonstrates a high-velocity signal consistent with severe aortic stenosis. The maximum velocity of 4.2 m/sec corresponds to a maximum transaortic pressure gradient of 69 mm Hg and a mean gradient of 41 mm Hg. Valve area, calculated by the continuity equation, was 0.8 cm².

Management

As with mitral stenosis, most patients with decompensated aortic stenosis can be managed conservatively by (1) treating the underlying disease process that led to decompensation and (2) restoring the patient’s normal loading conditions. However, in the patient who has denied symptoms or has not been receiving medical care, the first presentation of aortic stenosis may be syncope or pulmonary edema. In these patients, aortic stenosis is the cause of decompensation, as evidenced by very severe valve obstruction, often with a low ejection fraction. Treatment is urgent aortic valve replacement. Some centers advocate the use of balloon aortic valvuloplasty in these patients, but the magnitude and duration of benefit is limited. Cautious use of nitroprusside may improve hemodynamics prior to valve replacement in severe decompensated aortic stenosis if mean arterial pressure is above 60 mm Hg,^35,36 and some patients can be managed with careful diuresis. However, in unstable patients who are surgical candidates, it is more prudent to proceed promptly to valve replacement. Transcatheter aortic valve implantation is currently in clinical trials for high-risk patients with severe aortic stenosis and may become an option for acutely ill patients in the future.³⁷

Mechanical Valves

Prosthetic mechanical heart valves are very durable, with complications most often due to valve thrombosis or paravalvular regurgitation.⁴⁰ Valve thrombosis occurs in the setting of inadequate anticoagulation and may result in functional valve stenosis if movement of the valve occluder is restricted, or valve regurgitation if the clot prevents full closure of the valve. The clinical presentation of valve thrombosis is similar to that of native valve stenosis or regurgitation. Again, echocardiography provides key information on the presence and severity of valve dysfunction (Figure 86-12).⁴¹ TEE is especially important with mitral prosthetic valves; the valve itself blocks ultrasound penetration from a transthoracic approach.

Figure 86-12 Acute prosthetic mitral valve thrombosis in an 82-year-old man 29 years after valve replacement. Patient presented acutely with pulmonary edema and a right upper extremity thrombotic occlusion after anticoagulation was temporarily discontinued owing to a gastrointestinal bleed. Color Doppler imaging (A) shows only narrow jets (arrows) of flow antegrade across the mitral valve replacement (MVR), and continuous-wave Doppler signal (B) shows a high gradient and very prolonged deceleration slope, consistent with severe obstruction to flow. After careful discussion, given his high risk for surgery, he was treated with thrombolytic therapy, which resulted in normalization of his mitral valve Doppler flows and resolution of pulmonary edema.

Treatment of prosthetic valve thrombosis is controversial. When only a small thrombus and mild hemodynamic compromise are present, conservative therapy with full-dose intravenous anticoagulation for several days may be adequate. With severe hemodynamic compromise, surgical intervention with repeat valve replacement may be necessary, although operative mortality is reported to be high, ranging from 17% to 40%.⁶ Systemic thrombolytic therapy can restore valve function in about 80% of patients but is associated with death in 20%, systemic embolism due to fragmentation of the valve thrombosis in 16%, and the need for emergency surgery in 20%.⁶ The duration of thrombolytic therapy is based on the resolution of Doppler echocardiographic evidence of resolution of thrombus and valve dysfunction (see Figure 86-12). Current guidelines recommend emergency operation for left-sided valve thrombosis and severe symptoms or a large clot burden, except in patients with excessively high surgical risk. Fibrinolytic therapy is reasonable for right-sided valve thrombosis, for left-sided thrombosis with mild obstruction or a small clot burden, and for patients who are not surgical candidates.^6,42,43

Paravalvular regurgitation early after valve replacement may be related to suture dehiscence at a site of annular calcification. Paravalvular regurgitation may be associated with hemolytic anemia, which can be treated conservatively if mild but may require reoperation if severe recurrent anemia is present. The new onset of paravalvular regurgitation should prompt careful evaluation for endocarditis (see Chapter 87).

Tissue Valves

Tissue valves are subject to degeneration of the leaflets, with superimposed calcification that may result in stenosis or regurgitation. Usually this is a slowly progressive process with presentation 10 to 15 years after valve implantation.⁴⁴ As with native valve disease, acute decompensation may occur in patients with chronic prosthetic valve dysfunction if there is a superimposed hemodynamic stress.

Acute regurgitation of a tissue valve can result from endocarditis or from a leaflet tear due to tissue degeneration. Tears in the valve leaflet typically occur adjacent to an area of calcification secondary to the increased stress on the normal leaflet tissue. As with mechanical valves, both transthoracic and transesophageal imaging are needed for full evaluation of suspected prosthetic tissue valve dysfunction. Treatment is similar to that for native valves, with medical stabilization followed by surgery for repeat valve replacement.

Key Points