Published: August 2010

Mitral Valve Disease:
Stenosis and Regurgitation

Ronan J. Curtin

Brian P. Griffin

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The mitral valve is made up of the annulus, anterior and posterior leaflets, and chordae, which attach the leaflets to their respective papillary muscles. A normally functioning valve allows blood to flow unimpeded from the left atrium to the left ventricle during diastole and prevents regurgitation during systole. Normal mitral valve function is dependent not only on the integrity of the underlying valvular structure, but on that of the adjacent myocardium as well.

This chapter reviews three types of mitral valve disease: mitral stenosis, mitral regurgitation, and mitral valve prolapse. Practice guidelines published jointly by the American College of Cardiology (ACC) and the American Heart Association (AHA) for the management of patients with valvular heart disease are referenced in this chapter.1 Where relevant, we refer in the text to the ACC/AHA evidence grading for diagnostic and therapeutic procedures, as follows:

  • Class I: There is evidence and/or general agreement in favor of a given procedure or treatment.
  • Class II: There is conflicting evidence and/or a divergence of opinion about the efficacy of a given procedure or treatment.
  • Class IIa: The weight of evidence or opinion is in favor of efficacy.
  • Class IIb: Efficacy is less well established by evidence or opinion.
  • Class III: There is evidence and/or general agreement that the procedure or treatment is not useful and in some cases may be harmful.

Mitral stenosis

Definition and Etiology

Mitral stenosis (MS) refers to narrowing of the mitral valve orifice, resulting in impedance of filling of the left ventricle in diastole. It is usually caused by rheumatic heart disease. Less common causes include severe calcification of the mitral annulus, infective endocarditis, systemic lupus erythematosus, rheumatoid arthritis, and carcinoid heart disease.

Prevalence and Risk Factors

Although the incidence of rheumatic heart disease has steeply declined during the past four decades in the United States, it is still a major cause of cardiovascular disease in developing countries. It is estimated that 15.6 million people suffer from rheumatic heart disease worldwide, with approximately 282,000 new cases and 233,000 related deaths each year.2

Pathophysiology and Natural History

Patients with MS typically present more than 20 years after an episode of rheumatic fever. Single or recurrent bouts of rheumatic carditis cause progressive thickening, scarring, and calcification of the mitral leaflets and chordae. Fusion of the commissures and chordae decreases the size of the mitral opening. This obstruction results in the development of a pressure gradient across the valve in diastole and causes an elevation in left atrial and pulmonary venous pressures. Elevated left atrial pressures lead to left atrial enlargement, predisposing the patient to atrial fibrillation and arterial thromboembolism. Elevated pulmonary venous pressure results in pulmonary congestion and pulmonary edema. In advanced mitral stenosis, patients develop pulmonary hypertension and right-sided heart failure.

Signs and Symptoms

Patients with mitral stenosis may present with exertional dyspnea, fatigue, atrial arrhythmias, embolic events, angina-like chest pain, hemoptysis, or even right-sided heart failure. Previously asymptomatic or stable patients may decompensate acutely during exercise, emotional stress, pregnancy, infection, or with uncontrolled atrial fibrillation.

The characteristic findings of MS on auscultation are an accentuated first heart sound, an opening snap, and a mid-diastolic rumble. The first heart sound may be diminished in intensity if the valve is heavily calcified, with limited mobility. If the patient is in sinus rhythm, there is presystolic accentuation of the murmur during atrial contraction. With increasingly severe stenosis, the duration of the murmur increases and the opening snap occurs earlier during diastole as a result of higher left atrial pressure. There is accentuation of P2 when pulmonary hypertension is present. If flow across the mitral valve is reduced because of heart failure, pulmonary hypertension, or aortic stenosis the murmur of mitral stenosis may be reduced in intensity or may be inaudible.

Left atrial myxoma may be distinguished from MS by the presence of a “tumor plop” versus an opening snap in early diastole.

Diagnosis

On chest radiography, the characteristic findings of mitral stenosis are pulmonary congestion, enlargement of the main pulmonary arteries, and enlargement of the left atrium without cardiomegaly (Fig. 1). An electrocardiogram (ECG) may reveal evidence of left atrial enlargement, atrial fibrillation or, in advanced disease, right ventricular hypertrophy consistent with pulmonary hypertension (Fig. 2).

Two-dimensional (2D) and Doppler echocardiography is indicated for all patients with suspected MS to confirm the diagnosis and determine its severity (Class I indication).1 Characteristic findings of MS include valve thickening, restricted valve opening, anterior leaflet doming, and fusion of the leaflets at the commissures. The mean pressure gradient across the mitral valve on Doppler echocardiography (echo) in MS is at least 5 mm Hg; in severe stenosis, it is usually higher than 10 mm Hg. Because the gradient across the mitral valve is flow dependent, the severity of MS is more accurately defined by the mitral valve area (MVA). The normal valve area is 4 to 5 cm2. In mild mitral stenosis, the MVA is 1.5 to 2 cm2, in moderate stenosis it is 1 to 1.5 cm2, and in severe stenosis it is less than 1 cm2. The valve area may be measured by tracing the mitral valve opening in cross section by 2D echo. Alternatively, the MVA is calculated using the pressure half-time (P × 1/2t), which is the amount of time it takes for the transmitral pressure to fall to one half its initial value (MVA = 220/[P × 1/2t]).

Echocardiography also allows assessment of pulmonary artery pressures, detection of other valve disease, visualization of left atrial thrombus, and identification of important differential diagnoses, such as left atrial myxoma. Transesophageal echo is superior to transthoracic echo at identifying left atrial thrombus in patients who are being considered for percutaneous mitral balloon valvotomy or cardioversion (Class I).1 Stress echocardiography may be helpful if there is a discrepancy between a patient's severity of symptoms and the baseline hemodynamic data. An exercise mean transmitral gradient of more than 15 mm Hg and peak right ventricular systolic pressure of more than 60 mm Hg indicate hemodynamically significant MS (Class I).1

Cardiac catheterization is not necessary in all cases but, like stress echocardiography, may be helpful in characterizing the severity of mitral stenosis when there is a discrepancy between symptoms and findings on echocardiography (Class I).1 A more detailed discussion of the diagnosis of mitral stenosis may be found in the AHA/ACC guidelines.1

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Summary

  • Transthoracic echocardiography is necessary to diagnose and determine the severity of mitral stenosis.
  • Transesophageal echocardiography is indicated in patients before percutaneous mitral balloon valvotomy or cardioversion.
  • Stress echocardiography and cardiac catheterization may be helpful in those cases in which there is a discrepancy between the severity of symptoms and baseline echocardiographic findings.

Treatment

Medical Treatment

Medical therapy has no role in altering the natural history or delaying the need for surgery in patients with MS. Medical treatment is directed toward alleviating pulmonary congestion with diuretics, treating atrial fibrillation, and anticoagulating patients who are at increased risk of arterial embolic events.

Development of atrial fibrillation frequently leads to an acute deterioration in patients with mitral stenosis. The rapid ventricular response results in a decrease in the diastolic filling time. Beta blockers, calcium channel blockers, or digoxin may be used to control ventricular rate. An attempt to restore sinus rhythm with direct current electrical cardioversion or antiarrhythmic drugs may be considered. Anticoagulation with warfarin is indicated to prevent thromboembolism when atrial fibrillation is present, if there is a prior history of thromboembolism, or a thrombus is detected in the left atrium (Class I).1 Although controversial, anticoagulation may also be considered if the left atrium is markedly dilated (5.0-5.5 mm) or if there is spontaneous contrast on echocardiography (Class IIb).1,3,4

Antibiotic therapy is important for the secondary prevention of rheumatic carditis. Patients with a history of rheumatic fever are at high risk of recurrence. Long-term secondary prophylaxis, preferentially with penicillin, is therefore recommended for all patients with a history of rheumatic fever or suspected rheumatic valve disease. The duration of prophylaxis depends on a number of factors, including the time lapsed since the last attack, the age of the patient, the presence or absence of cardiac involvement, and the patient's risk of exposure to streptococcal infections.1,5 Routine antibiotic prophylaxis for endocarditis is no longer recommended for patients with mitral stenosis.6

Surgery

Three invasive options are available for patients with MS: percutaneous mitral balloon valvotomy (PMBV), surgical mitral commissurotomy, and mitral valve replacement (MVR). In experienced centers, PMBV is the initial procedure of choice and should be considered for (1) symptomatic patients (NYHA functional Classes II to IV) with moderate or severe MS (Class I) and (2) asymptomatic patients with moderate or severe MS and pulmonary hypertension (Class I).1 PMBV is a catheter-based technique in which a balloon is inflated across the stenotic valve to split the fused commissures and increase the valve area. The MVA typically doubles in size, and hemodynamic as well as clinical improvements are seen immediately (Fig. 3).7 The results are comparable with those achieved with open mitral commissurotomy, but it is less invasive and less costly.7,8 The mitral valve morphology is an important predictor of successful balloon valvotomy. Severe valve calcification or significant involvement of the subvalvular apparatus on echocardiography before PMBV is associated with a higher complication rate and a greater risk of recurrence. In addition, balloon valvotomy should not be performed in patients who have left atrial thrombus or more than 2+ (moderate) mitral regurgitation, because the degree of mitral regurgitation usually increases following the procedure. Complications of balloon mitral valvotomy include severe mitral regurgitation (3%), thromboembolism (3%), and residual atrial septal defect with significant shunting (<5%). Mortality with the procedure is lower than 1% in experienced hands. At 7 years after balloon valvotomy, 50% to 69% of patients remain free of cardiovascular events and up to 90% of patients remain free of reintervention.8,9 However, both balloon valvotomy and surgical commissurotomy are palliative procedures and, in most cases, further intervention is eventually required, usually in the form of a mitral valve replacement.

Although closed mitral commissurotomy is still widely used in many developing countries, open mitral commissurotomy is more frequently performed in the United States. It involves the use of cardiopulmonary bypass and the surgical repair of a diseased mitral valve by direct visualization. Open mitral commissurotomy may be considered in the presence of a left atrial thrombus or significant mitral regurgitation if the valve anatomy is suitable. Commissurotomy may also be indicated for patients who have other concomitant valvular disease or coronary artery disease that requires surgery. In patients with calcified valves that cannot be treated by valvotomy or commissurotomy, or in those with significant mitral regurgitation that is not suitable for repair, mitral valve replacement may be necessary. The threshold for mitral valve surgery (commissurotomy or MVR) is higher than for PMBV in patients with mitral stenosis, and commissurotomy or repair is preferable to MVR, if feasible. Surgery for moderate to severe mitral stenosis is indicated for symptomatic patients (New York Heart Association [NYHA] functional Class III or IV) where PMBV is unavailable or contraindicated (Class I).1 MVR may also be considered for patients with severe MS and severe pulmonary hypertension with NYHA functional Classes I or II symptoms who are not candidates for PMBV or mitral valve repair (Class IIa). Both mechanical and biologic prostheses are used for mitral valve replacement; the choice of valve often depends on factors such as age, need for concomitant anticoagulation, and left ventricular (LV) size. Morbidity and mortality are higher with prosthetic valve replacement than with surgical or balloon valvotomy.

A more detailed discussion of the management of mitral stenosis may be found in the AHA/ACC guidelines.1

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Summary

  • Medical therapy in patients with mitral stenosis includes diuretic therapy, rate control of atrial fibrillation, anticoagulation to prevent thromboembolism, and antibiotic prophylaxis against recurrent rheumatic carditis.
  • Invasive therapy should be considered for all patients with symptomatic mitral stenosis. Percutaneous mitral balloon valvotomy and surgical commissurotomy provide equivalent immediate and long-term outcome results and delay the need for mitral valve replacement.

Prevention and Screening

Antibiotic therapy of group A streptococcal tonsillopharyngitis, even delayed 9 days after the onset of symptoms, can prevent rheumatic fever and rheumatic carditis.10 Antibiotic therapy also reduces transmission to contacts. Routine screening or treatment of asymptomatic contacts of persons with group A streptococcal tonsillopharyngitis is not recommended.

Special Populations

Patients with asymptomatic moderate to severe mitral stenosis may decompensate during periods of increased physiologic stress, such as pregnancy or surgery. Surgical intervention, preferably percutaneous valvotomy, should be considered before a planned pregnancy or surgical procedure in these patients. Balloon valvotomy can also be performed with abdominal or pelvic shielding during pregnancy if symptomatic mitral stenosis does not respond to medical therapy.

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Mitral regurgitation

Definition and Causes

Mitral regurgitation (MR) is leakage of blood from the left ventricle into the left atrium during systole. It is caused by various mechanisms related to structural or functional abnormalities of the mitral apparatus, adjacent myocardium, or both. The most common causes of mitral regurgitation in the United States are myxomatous degeneration, chordal rupture, rheumatic heart disease, infective endocarditis, coronary artery disease, and cardiomyopathy.

Prevalence and Risk Factors

Significant mitral valve regurgitation occurs in about 2% of the population with a similar prevalence in males and females.11 Myxomatous disease is the most common cause of nonischemic mitral regurgitation in the United States (Fig. 4).

Pathophysiology and Natural History

Significant MR leads to volume overload of the left ventricle, because it has to accommodate both the stroke volume and regurgitant volume with each heartbeat. To compensate, the left ventricle dilates and becomes hyperdynamic. In acute severe MR, the left atrial and pulmonary venous pressures increase quickly, leading to pulmonary congestion and pulmonary edema. In chronic MR, a gradual increase in left atrial size and compliance compensate so that left atrial and pulmonary venous pressures do not increase until late in the course of the disease. Progressive left ventricular dilation eventually leads to an increase in afterload, contractile dysfunction, and heart failure. Left atrial enlargement predisposes the patient to atrial fibrillation and arterial thromboembolism. In long-standing MR, patients may develop pulmonary hypertension and right-sided heart failure.

Signs and Symptoms

Patients with chronic, severe mitral regurgitation may remain asymptomatic for years because the regurgitant volume load is well tolerated as a result of compensatory ventricular and atrial dilation. When symptoms do develop, the most common are dyspnea, fatigue, orthopnea, paroxysmal nocturnal dyspnea, and palpitations caused by atrial fibrillation. Acute severe MR, as occurs with chordal rupture or papillary muscle rupture, is almost always symptomatic because the sudden regurgitant volume load in the nondilated left ventricle and atrium leads to pulmonary venous hypertension and congestion.

The characteristic finding in a patient with MR is a blowing holosystolic murmur heard best at the cardiac apex. When ventricular enlargement is present, the apical impulse may be diffuse and laterally displaced, and a third heart sound may be heard.

Diagnosis

The chest radiograph demonstrates left atrial enlargement and cardiomegaly. Two-dimensional and Doppler echocardiography is indicated for all patients with suspected mitral regurgitation to confirm its presence and determine its severity (Class I).1 Two-dimensional echocardiography usually reveals the cause (e.g., the presence of myxomatous mitral valve disease and leaflet prolapse or evidence of underlying dilated cardiomyopathy). Evaluation of the severity of mitral regurgitation on echocardiography requires an integrated assessment of several parameters, including regurgitant jet size by color Doppler, regurgitant jet density by continuous-wave (CW) Doppler, and pulmonary vein and mitral valve inflow by pulse-wave (PW) Doppler.12 Newer applications of Doppler echocardiography allow quantitative measurement of mitral regurgitation, including the regurgitant volume and the regurgitant orifice area (ROA)—that is, the area through which the valve leaks in systole. In asymptomatic patients with significant mitral regurgitation, serial echocardiography every 6 to 12 months to assess LV size and systolic function is important for optimal timing of surgery (Class I).1 Transesophageal echocardiography is indicated for patients who are not adequately imaged by transthoracic echocardiography and before surgery to assess feasibility for repair (Class I).1 Stress echocardiography may be useful to assess exercise tolerance and the response of mitral regurgitation severity, pulmonary pressure, and contractile reserve to exercise in asymptomatic patients with significant MR (Class IIa).1,13

Cardiac catheterization is no longer routinely performed to evaluate mitral regurgitation severity, but it is indicated for those patients in whom noninvasive test results are inconclusive, and also to detect concomitant coronary artery disease in patients undergoing mitral valve surgery (Class I).1 A more detailed discussion of the diagnosis of mitral regurgitation may be found in the AHA/ACC guidelines.1

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Summary

  • Determining the severity of mitral regurgitation requires an integrated assessment of several parameters on echocardiography.
  • Serial echocardiography with measurement of LV size and function is important for timing surgical intervention in asymptomatic patients.
  • Transesophageal echocardiography is necessary before surgery to assess feasibility for repair, as well as for patients who are not adequately imaged by transthoracic echocardiography.

Treatment

Medical Treatment

In patients with acute severe MR, afterload reduction with intravenous nitroprusside and nitroglycerin reduces the regurgitant fraction and pulmonary pressures. Placement of an intra-aortic balloon pump also helps stabilize these patients. However, these are temporary measures before urgent mitral valve repair or replacement. In patients with chronic asymptomatic mitral regurgitation caused by primary valve disease, there is no evidence for the routine use of medication in delaying the need for surgery or preventing left ventricular dysfunction.14 The management of these patients is focused on deciding on the appropriate timing of surgery, before the development of irreversible left ventricular dysfunction. Patients should be followed up every 6 to 12 months to assess for symptoms and to measure left ventricular size, function, and severity of MR by echocardiography (Class I).1

In patients with ischemic heart disease or dilated cardiomyopathy, mitral regurgitation indicates a poor prognosis.15 MR in these patients is called functional mitral regurgitation and is caused by global or regional changes in left ventricular geometry as well as annular dilation. Functional MR is primarily treated medically with antihypertensive therapy, angiotensin-converting enzyme (ACE) inhibitors, beta blockers, diuretics, and antianginal therapies when mitral regurgitation is worsened by acute ischemia.16 Biventricular pacing has also been shown to decrease the degree of mitral regurgitation in dilated cardiomyopathy.17

Routine antibiotic prophylaxis for endocarditis is no longer recommended for patients with mitral regurgitation.6

Surgery

Surgery is indicated for symptomatic patients with severe primary MR (Class I) and asymptomatic patients with severe primary MR and evidence of LV dysfunction (Class I).1 Optimal timing of mitral valve surgery is challenging in asymptomatic patients because the actual contractile function of the left ventricle is difficult to measure. The standard indications for surgery in asymptomatic patients is an LV end-systolic dimension of more than 4.0 cm and a resting LV ejection fraction of less than 60% (Class I).1 Other indications in asymptomatic patients include pulmonary hypertension or development of atrial fibrillation (Class IIa).1 In addition, mitral valve repair may be undertaken in experienced surgical centers for asymptomatic patients with severe MR, but without evidence of LV dilation or dysfunction, for whom the likelihood of a successful repair is greater than 90% (Class IIa). Most asymptomatic patients with severe MR develop symptoms, LV dysfunction, or both over long-term follow-up. One retrospective study showed an increased risk of cardiac death (4%/year) in patients with severe mitral regurgitation based on an ROA of more than 0.4 cm2.18 However, another recent prospective study has shown that careful follow-up of patients with severe MR and timing of surgery based on symptoms, LV dysfunction, development of atrial fibrillation, or pulmonary hypertension is associated with an excellent patient outcome.19

In patients with severe functional mitral regurgitation, surgery may be considered for severe symptoms despite medical therapy. Patients with ischemic MR may improve with coronary bypass surgery if significant ischemia or myocardial viability is present. In many coronary bypass patients with MR, concomitant mitral valve repair with an undersized annuloplasty ring is performed. Patients with severe left ventricular dysfunction and significant MR were once believed to be poor surgical candidates, but recent studies have shown an acceptable operative risk. Symptoms usually improve, although a survival benefit has not been demonstrated.

The two available surgical options are mitral valve repair (Fig. 5) and mitral valve replacement. Mitral valve repair is the procedure of choice in the surgical management of MR caused by degenerative valve disease and in some cases of MR caused by infective endocarditis and ischemic heart disease. Repair offers several advantages over replacement, including lower operative and long-term mortality, better preservation of LV function, a lower risk of subsequent infective endocarditis, and no need for long-term anticoagulation. Reoperation rates for mitral valve repair and replacement are similar, occurring at a rate of 1% to 2% per year. On the other hand, repair is technically more difficult than replacement, and many cases of mitral regurgitation are not amenable to valve repair. Percutaneous mitral valve repair is currently being investigated. The techniques involved include a clip that joins the mitral leaflets at their midpoint and an annuloplasty ring delivered via the coronary sinus.20,21

A more detailed discussion of the management of mitral regurgitation may be found in the AHA/ACC guidelines.1

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Summary

  • Medical therapy has no role in the treatment of patients with primary mitral regurgitation but is the mainstay of treatment in patients with functional mitral regurgitation.
  • In patients with primary mitral regurgitation, surgery is indicated in the presence of symptoms or, in asymptomatic patients, if there is evidence of secondary LV dysfunction.
  • Mitral valve repair is the procedure of choice for the surgical management of mitral regurgitation and is associated with lower mortality and better preservation of LV function.

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Mitral valve prolapse

Definition and Causes

Mitral valve prolapse (MVP) is the systolic billowing of one or both mitral leaflets into the left atrium during systole.22 It may occur in the setting of myxomatous valve disease or in persons with normal mitral valve leaflets.

Prevalence and Risk Factors

MVP is the most common valvular disorder in the United States, occurring in 2.4% of the general population. There is a similar prevalence in men and women, with a greater risk of complications in men.23

Pathophysiology and Natural History

Many patients with MVP have normal mitral leaflets, with little or no mitral regurgitation, and a benign prognosis. Survival rates among affected patients are similar to those of age- and gender-matched individuals without MVP.24 In other patients, MVP is caused by myxomatous valve disease, with typical findings of elongated and thickened leaflets, interchordal hooding, and chordal elongation (see Fig. 4). Patients with myxomatous MVP are at increased risk for cardiovascular complications, particularly when prolapse is associated with at least moderate mitral regurgitation or LV dysfunction. Although most patients with MVP do not develop severe mitral regurgitation, MVP is a common underlying cause of progressive mitral regurgitation, often necessitating mitral valve repair or replacement.25

The causes of myxomatous mitral valve disease are not certain, but appear to involve dysregulation of extracellular matrix proteins. Myxomatous mitral valve disease usually occurs sporadically, although there are well-described cases of familial clustering that involve an autosomal dominant mode of inheritance.22 Three genetic loci for autosomal dominant myxomatous mitral valve disease have been described, but the precise genes and mutations have not yet been identified. Myxomatous MVP also may occur in conjunction with certain connective tissue disorders, such as Marfan syndrome and Ehlers-Danlos syndrome.

Signs and Symptoms

Most patients with MVP are asymptomatic. In the past, multiple nonspecific symptoms (atypical chest pain, dyspnea, palpitations, anxiety, and syncope) and clinical findings (low body weight, low blood pressure, and pectus excavatum) were associated with MVP and termed mitral valve prolapse syndrome. Prospective testing has failed to confirm most of these associations.23 The classic findings of MVP on physical examination are a midsystolic click, with a late systolic murmur, heard best at the cardiac apex.

Diagnosis

Two-dimensional echocardiography is the most important test for diagnosing MVP (Class I).1 The diagnosis is made when there is displacement of one or both mitral leaflets by 2 mm or more into the left atrium during systole (Fig. 6). Because the mitral annulus is known to have a saddle shape, a normal mitral valve can appear to prolapse in certain echocardiographic views, most notably in the apical two- and four-chamber views. Therefore, the diagnosis of MVP should be based on a long-axis parasternal or apical three-chamber view. In patients with MVP, echocardiography is also useful in determining the presence and severity of MR and assessing left atrial and ventricular chamber size, LV function, and leaflet thickening and redundancy. Unless severe mitral regurgitation is present, findings on the chest radiograph and ECG typically are unremarkable. A more detailed discussion of the diagnosis of mitral valve prolapse may be found in the AHA/ACC guidelines.1

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Summary

  • Mitral valve prolapse is present if there is more than 2 mm displacement of the mitral valve leaflets into the left atrium during systole in a parasternal long-axis or apical three-chamber view on echocardiography.

Treatment

Medical Treatment

Asymptomatic patients require no specific treatment and they should be reassured of their excellent prognosis. Although antibiotic prophylaxis for endocarditis was once advocated for certain patients with MVP, more recent guidelines do not recommend antibiotic prophylaxis in this group of patients.1,6 Beta blockers are useful for alleviating symptoms of palpitations, anxiety, and chest pain in certain patients.

MVP patients without mitral regurgitation should be evaluated every 3 to 5 years. Echocardiography should be performed if the patient has new cardiovascular symptoms or if the physical examination suggests that significant mitral regurgitation has developed. Patients with severe mitral regurgitation or high-risk features should be reviewed with an echocardiogram yearly or more often if their clinical condition warrants it.

Surgery

In MVP patients with severe mitral regurgitation, the indications for mitral valve surgery are similar to those for patients with other causes of severe regurgitation. When surgery is required, mitral valve repair is usually feasible (Fig. 7). Repair is characterized by low mortality and long-lasting durability; the 10-year reoperation-free survival rate ranges between 93% and 96%.26 A more detailed discussion of the management of mitral valve prolapse may be found in the AHA/ACC guidelines.1

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Summary

  • Mitral valve prolapse is a benign condition in most cases.
  • Indications for surgery are the same as those for patients with other causes of primary mitral regurgitation.

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References

  1. Bonow RO, Carabello BA, Chatterjee K, et al: 2006 Writing Committee Members; American College of Cardiology/American Heart Association Task Force. 2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease). Circulation. 2008, 118: e523-e661.
  2. Carapetis JR, Steer AC, Mulholland EK, et al: The global burden of group A streptococcal diseases. Lancet Infect Dis. 2005, 5: 685-694.
  3. Salem DN, Stein PD, Al-Ahmad A, et al: Antithrombotic therapy in valvular heart disease—native and prosthetic: The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004, 126: 457S-482S.
  4. Vahanian A, Baumgartner H, Bax J, et al: Guidelines on the management of valvular heart disease: The Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology. Eur Heart J. 2007, 28: 230-268.
  5. Dajani A, Taubert K, Ferrieri P, et al: Treatment of acute streptococcal pharyngitis and prevention of rheumatic fever: a statement for health professionals: Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young, the American Heart Association. Pediatrics. 1995, 96: 758-764.
  6. Wilson W, Taubert KA, Gewitz M, et al: Prevention of infective endocarditis. Guidelines from the American Heart Association. A guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 2007, 116: 1736-1754.
  7. Reyes VP, Raju BS, Wynne J, et al: Percutaneous balloon valvuloplasty compared with open surgical commissurotomy for mitral stenosis. N Engl J Med. 1994, 331: 961-967.
  8. Ben Farhat M, Ayari M, Maatouk F, et al: Percutaneous balloon versus surgical closed and open mitral commissurotomy: Seven-year follow-up results of a randomized trial. Circulation. 1998, 97: 245-250.
  9. Hernandez R, Banuelos C, Alfonso F, et al: Long-term clinical and echocardiographic follow-up after percutaneous mitral valvuloplasty with the Inoue balloon. Circulation. 1999, 99: 1580-1586.
  10. Catanzaro FJ, Stetson CA, Morris AJ, et al: The role of the streptococcus in the pathogenesis of rheumatic fever. Am J Med. 1954, 17: 749-756.
  11. Jones EC, Devereux RB, Roman MJ, et al: Prevalence and correlates of mitral regurgitation in a population-based sample (the Strong Heart study). Am J Cardiol. 2001, 87: 298-304.
  12. Zoghbi WA, Enriquez-Sarano M, Foster E, et al: Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr. 2003, 16: 777-802.
  13. Lee R, Haluska B, Leung DY, et al: Functional and prognostic implications of left ventricular contractile reserve in patients with asymptomatic severe mitral regurgitation. Heart. 2005, 91: 1407-1412.
  14. Levine HJ, Gaasch WH. Vasoactive drugs in chronic regurgitant lesions of the mitral and aortic valves. J Am Coll Cardiol. 1996, 28: 1083-1091.
  15. Blondheim DS, Jacobs LE, Kotler MN, et al: Dilated cardiomyopathy with mitral regurgitation: Decreased survival despite a low frequency of left ventricular thrombus. Am Heart J. 1991, 122: 763-771.
  16. Rosario LB, Stevenson LW, Solomon SD, et al: The mechanism of decrease in dynamic mitral regurgitation during heart failure treatment: Importance of reduction in the regurgitant orifice size. J Am Coll Cardiol. 1998, 32: 1819-1824.
  17. Sutton MG, Plappert T, Hilpisch KE, et al: Sustained reverse left ventricular structural remodeling with cardiac resynchronization at one year is a function of etiology: Quantitative Doppler echocardiographic evidence from the MulticenterInSync Randomized Clinical Evaluation (MIRACLE). Circulation. 2006, 113: 266-272.
  18. Enriquez-Sarano M, Avierinos JF, Messika-Zeitoun D, et al: Quantitative determinants of the outcome of asymptomatic mitral regurgitation. N Engl J Med. 2005, 352: 875-883.
  19. Rosenhek R, Rader F, Klaar U, et al: Outcome of watchful waiting in asymptomatic severe mitral regurgitation. Circulation. 2006, 113: 2238-2244.
  20. Feldman T, Wasserman HS, Herrmann HC, et al: Percutaneous mitral valve repair using the edge-to-edge technique: Six-month results of the EVEREST Phase I Clinical Trial. J Am Coll Cardiol. 2005, 46: 2134-2140.
  21. Daimon M, Shiota T, Gillinov AM, et al: Percutaneous mitral valve repair for chronic ischemic mitral regurgitation: A real-time three-dimensional echocardiographic study in an ovine model. Circulation. 2005, 111: 2183-2189.
  22. Hayek E, Gring CN, Griffin BP. Mitral valve prolapse. Lancet. 2005, 365: 507-518.
  23. Freed LA, Levy D, Levine RA, et al: Prevalence and clinical outcome of mitral-valve prolapse. N Engl J Med. 1999, 341: 1-7.
  24. Nishimura RA, McGoon MD, Shub C, et al: Echocardiographically documented mitral-valve prolapse. Long-term follow-up of 237 patients. N Engl J Med. 1985, 313: 1305-1309.
  25. Avierinos JF, Gersh BJ, Melton LJ 3rd, et al: Natural history of asymptomatic mitral valve prolapse in the community. Circulation. 2002, 106: 1355-1361.
  26. Gillinov AM, Cosgrove DM, Blackstone EH, et al: Durability of mitral valve repair for degenerative disease. J Thorac Cardiovasc Surg. 1998, 116: 734-743.

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Suggested Readings

  • Avierinos JF, Gersh BJ, Melton LJ 3rd, et al: Natural history of asymptomatic mitral valve prolapse in the community. Circulation. 2002, 106: 1355-1361.
  • Ben Farhat M, Ayari M, Maatouk F, et al: Percutaneous balloon versus surgical closed and open mitral commissurotomy: Seven-year follow-up results of a randomized trial. Circulation. 1998, 97: 245-250.
  • Bonow RO, Carabello B, Chatterjee K, et al: ACC/AHA 2006 Guidelines for the management of patients with valvular heart disease: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Valvular Heart Disease). Circulation. 2006, 114: e84-e231.
  • Dajani A, Taubert K, Ferrieri P, et al: Treatment of acute streptococcal pharyngitis and prevention of rheumatic fever: A statement for health professionals: Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young, the American Heart Association. Pediatrics. 1995, 96: 758-764.
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