Overview of the management of chronic mitral regurgitation

Overview of the management of chronic mitral regurgitation

Author
William H Gaasch, MD
Section Editor
Catherine M Otto, MD
Deputy Editor
Susan B Yeon, MD, JD, FACC



Last literature review version 16.2: May 2008 | This topic last updated: April 24, 2008 (More)


INTRODUCTION — Modern management of patients with chronic mitral regurgitation (MR) requires an understanding of multiple factors: These include:

• The pathophysiology and natural history of the disease
• The severity of the valvular lesion
• The development of atrial fibrillation
• The therapeutic potential of chronic vasodilator therapy
• The indications for endocarditis prophylaxis
• The indications for mitral valve repair and mitral valve replacement


While our knowledge of these areas is not yet complete, it is possible to develop a rational plan for the management of patients with chronic MR [1,2] . These management issues will be reviewed here. The management of functional and ischemic MR are addressed elsewhere. (See "Functional mitral regurgitation" and see "Ischemic mitral regurgitation").

PATHOPHYSIOLOGY AND NATURAL HISTORY — An elusive and poorly understood aspect of the pathophysiology of MR is the nature of the transition from the chronic compensated stage to a decompensated stage. This evolution generally occurs over many years, even decades, depending upon the severity of the regurgitant lesion and the cardiovascular response to the regurgitant volume. The etiology of MR also plays a role in the natural history of this process. (See "Natural history of chronic mitral regurgitation in mitral valve prolapse and flail mitral leaflet").

Stages of MR — Left ventricular (LV) chamber size and function have been used to define a compensated, transitional, and decompensated stage in patients with chronic MR (show table 1) [3-9] . (See "Pathophysiology and stages of chronic mitral regurgitation").

• The compensated stage is defined largely on the basis of natural history and other data that indicate a benign prognosis when the end-diastolic dimension is less than 60 mm and the end-systolic dimension is less than 40 mm (as measured by echocardiography).
• The natural history of the transitional stage is not precisely defined, but most published data indicate that a good clinical result can be achieved if surgery is performed at this time.
• The decompensated stage is based upon data derived from patients who have undergone valvular surgery, which indicates that patients who exhibit one or more markers of a decompensated ventricle are at risk for a poor or suboptimal clinical result after valve replacement. These markers include LV end-diastolic dimension greater than 70 mm, LV end-systolic dimension greater than 45 to 47 mm, or a left ventricular ejection fraction (LVEF) less than 50 to 55 percent. (See "Indications for and types of corrective surgery in severe chronic mitral regurgitation", section on Reduced left ventricular function).


While these considerations do not identify the optimal time for mitral valve replacement or repair, they do enable the clinician to predict a poor LV response to corrective surgery and, in this fashion, provide a picture of the options of surgical or nonsurgical treatment. In principle, corrective surgery should be performed during the transition from a compensated to decompensated stage of the disease (ie, before the decompensated stage is established). (See "Mitral valve surgery" below).

Early identification of progression avoids the development of irreversible changes in LV function that may preclude an optimal response to corrective surgery. Patients with chronic MR and severe LV dysfunction (eg, LVEF <40 percent) are at very high risk of a suboptimal postoperative result. Many of these patients exhibit characteristics of a dilated cardiomyopathy with increased LV afterload and depressed myocardial contractility. Their initial management includes aggressive medical therapy with digitalis, diuretics, and vasodilators.

Cardiac catheterization and coronary angiography should be performed in preparation for surgery. Corrective surgery (and continued medical therapy) generally provides symptomatic relief, but chamber enlargement and a low LVEF usually persist despite technically successful surgery.

Etiology of mitral regurgitation — The major causes of MR are primary diseases of the valve leaflets (eg, mitral valve prolapse and, in developing countries, rheumatic heart disease) and secondary MR due to cardiomyopathy or coronary disease. (See "Etiology, clinical features, and evaluation of chronic mitral regurgitation", section on Etiology).

The best natural history data that are currently available have come from studies of patients with mitral valve prolapse and flail mitral valve leaflet. It is generally assumed that these findings may be applied to MR of other causes. (See "Natural history of chronic mitral regurgitation in mitral valve prolapse and flail mitral leaflet").

Summarized briefly, the following factors may be useful for stratifying patients into groups that can be managed medically versus those that require surgical intervention. Older age, male gender, and auscultatory evidence of severe MR are prognostic clues that identify patients with mitral valve prolapse who are at a relatively high risk of complications. Echocardiographic evidence of LV enlargement provides further evidence of high risk that requires careful follow-up.

MR due to flail leaflet — Severe MR due to a flail leaflet, an LVEF <60 percent, and presence of symptoms are predictive of excess mortality. The risk of death was reduced by mitral valve surgery (adjusted hazard ratio 0.42, 95% CI 0.21-0.84) in a series of 394 patients of varying baseline symptom status (36 percent with severe symptoms). For asymptomatic patients with flail leaflet and severe MR (as for other asymptomatic patients with severe MR), surgical correction should be considered early in the course of the disease if valve repair is feasible with a >90 percent likelihood of success. (See "Natural history of chronic mitral regurgitation in mitral valve prolapse and flail mitral leaflet" and see "Mitral valve surgery" below).

Effect of pregnancy — Chronic MR is usually well tolerated during pregnancy. The normal fall in systemic vascular resistance tends to reduce the degree of regurgitation. Issues related to the management of mitral regurgitation during pregnancy are discussed separately. (See "Natural history of chronic mitral regurgitation in mitral valve prolapse and flail mitral leaflet", section on Effect of pregnancy).

SEVERITY OF MR — In addition to the stage of MR (show table 1), decisions regarding the timing of surgery depend upon the severity of MR. This can be assessed by both clinical and echocardiographic criteria. (See "Indications for and types of corrective surgery in severe chronic mitral regurgitation")

Symptoms — Patients with severe chronic MR often experience exercise intolerance, dyspnea, or fatigue during the transition from a compensated to a decompensated stage. Because of the importance of identifying such a transition, a careful history is important to establish an estimate of baseline exercise tolerance [1] . (See "Etiology, clinical features, and evaluation of chronic mitral regurgitation", section on Clinical manifestations).

Most experts and the ACC/AHA guidelines recommend that patients with chronic MR who become symptomatic are candidates for corrective mitral surgery, even if the symptoms improve with medical therapy or the left ventricle appears to be compensated (show table 2) [1,2] . If there is uncertainty about the presence or absence of symptoms, exercise testing may provide objective information that may not be available from the medical history alone. (See "Indications" below).

There has traditionally been reluctance to treat asymptomatic patients with chronic MR surgery. With nothing to gain in the way of symptomatic improvement, early surgery exposes the patient to perioperative morbidity and mortality as well as the long-term complications of a prosthetic valve if a valve repair procedure cannot be performed. (See "Complications of prosthetic heart valves").

On the other hand, there may be benefit from surgery prior to the onset of symptoms. As an example, left ventricular decompensation may develop in the setting of severe MR despite the absence of symptoms. Thus, waiting for the patient to experience dyspnea or exercise intolerance may allow time for the development of irreversible depression of LV function. For this reason, it is important to have an objective measure of LV function in patients with asymptomatic MR.

Echocardiography — The severity of MR can be assessed semiquantitatively by Doppler echocardiography; the results of these two methods correlate highly in grading MR [1,10] . Transthoracic echocardiography usually provides the desired information and is preferred to routine transesophageal echocardiography because it is noninvasive (show table 3 and show table 4).

Based upon the 2003 American Society of Echocardiography guidelines [11] , the following findings, in order or priority, are consistent with severe MR (show table 5):

• A vena contracta width ≥7 mm
• A regurgitant orifice area ≥0.40 cm2
• A regurgitant volume ≥60 mL
• A regurgitant fraction ≥50 percent
• A jet area >40 percent of left atrial area, but this is not so reproducible and less often used

These values are based on an average adult size and may need to be adjusted for body size in small or large patients; however, there is no specific formula for making this adjustment. (See "Etiology, clinical features, and evaluation of chronic mitral regurgitation", section on Severity of MR).

Regardless of echo-Doppler grading, severe chronic MR does NOT exist (with rare exceptions) without clear evidence of left atrial or left ventricular enlargement. If the left ventricular end-diastolic dimension (by echocardiography) is less than 60 mm (approximately 35 mm/m2), the diagnosis of severe chronic MR should be seriously questioned. Left atrial size may reflect the "history" (severity and duration) of chronic MR [12] .

Cardiac catheterization is primarily indicated when echocardiography does not provide diagnostic information or the echocardiographic findings are discrepant from the clinical features (show table 6) [1] .

Serial monitoring — In addition to the initial evaluation, serial monitoring is warranted in patients with chronic MR. The goals of monitoring are to assess changes in clinical status by history and physical examination and to assess changes in left ventricular function, which can occur in the absence of symptoms, by echocardiography.

The 2006 ACC/AHA guidelines included recommendations for clinical and transthoracic echocardiographic monitoring in asymptomatic patients with chronic MR (show table 3) [1] . Echocardiography is performed to assess the left ventricular ejection fraction and end-systolic dimension.

The recommendations varied with the severity of MR:

• Patients with mild MR and no evidence of left ventricular enlargement, left ventricular dysfunction, or pulmonary hypertension should be seen yearly for history and physical examination with instructions to contact the physician if symptoms occur. Repeat echocardiography at these visits is not necessary in the absence of clinical evidence of worsening MR.
• Patients with moderate MR should be seen yearly or sooner if symptoms occur. Repeat transthoracic echocardiography should be obtained at these visits.
• Patients with severe MR should be seen every 6 to 12 months or sooner if symptoms occur. Repeat transthoracic echocardiography should be obtained at these visits. The six month interval is preferred if stability has not been documented, there is evidence of progression, or measurements are close to the echocardiographic cutoff values for mitral valve surgery (show table 2). (See "Indications for and types of corrective surgery in severe chronic mitral regurgitation").


Exercise stress testing may add objective evidence about symptoms and a change in exercise tolerance; it may be particularly useful if a good history of exercise capacity is difficult to obtain. Measurement of MR severity and pulmonary artery pressure during exercise also may be helpful.

Transesophageal echocardiography is NOT ndicated for routine follow-up (show table 4). It does, however, have a role in preoperative and intraoperative evaluation when mitral valve surgery is being considered.

A separate issue, the indications for repeat echocardiography in patients with mitral valve prolapse independent of MR, is discussed elsewhere. (See "Natural history of chronic mitral regurgitation in mitral valve prolapse and flail mitral leaflet", section on Monitoring).

PHYSICAL ACTIVITY AND EXERCISE — Exercise has a variable effect on the regurgitant fraction in patients with chronic MR [13] . The reduction in systemic vascular resistance may result in no change or a mild reduction in the regurgitant fraction. On the other hand, an elevation in blood pressure, as occurs with static exercise, can lead to marked increases in regurgitant volume and pulmonary capillary pressure.

The 2006 ACC/AHA guidelines concluded that there are no exercise restrictions in asymptomatic patients who are in sinus rhythm and have normal left ventricular and left atrial dimensions and a normal pulmonary artery pressure [1] . Specific recommendations for participation in competitive sports in patients with MR were made by the 36th Bethesda Conference [13] , which also included a classification of sports (show table 7) [14] :

• Patients with mild to moderate MR who are in sinus rhythm, have normal left ventricular size and function, and normal pulmonary artery pressures can participate in all competitive sports.
• Patients with mild to moderate MR who are in sinus rhythm, have normal left ventricular systolic function at rest, and mild left ventricular enlargement can participate in low and moderate static and all dynamic competitive sports (class IA, IB, IIA, IIB, and IIC) (show table 7).
• Patients with severe MR and definite left ventricular enlargement, pulmonary hypertension, or any reduction in left ventricular systolic function at rest should not participate in any competitive sports.
• Patients with atrial fibrillation or a history of atrial fibrillation who are treated with long-term anticoagulation therapy should not engage in sports with any for bodily contact or risk of trauma (show table 7).


Recommendations for exercise after mitral repair for chronic MR are described below. (See "Exercise after valve repair" below).

ATRIAL ENLARGEMENT AND FIBRILLATION — Chronic MR is often complicated by the development of left atrial enlargement and atrial fibrillation (AF), both of which can have an impact on patient outcome.

Atrial fibrillation — If the ventricle is compensated and the heart rate is not excessive, the patient with AF merely notices palpitations. There is little or no disability in these cases except for an increased risk of stroke or other sign of systemic embolization. These patients are candidates for direct current cardioversion and antiarrhythmic drug therapy to maintain sinus rhythm. (See "Restoration of sinus rhythm in atrial fibrillation: Recommendations" and see "Antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation: Recommendations").

It can be argued, however, that mitral valve surgery should be performed before AF is persistent or resistant to cardioversion. This notion is based upon the observation that persistent AF after surgery places the patient at particularly high risk for atrial thrombus and arterial embolism.

Preoperative variables that are associated with the persistence of AF after surgery are a prolonged duration of the arrhythmia (exceeding one year) and moderate to severe left atrial enlargement [12,15,16] . When the preoperative left atrial size exceeds 50 mm (by echocardiography), fewer than one-half of the patients return to normal sinus rhythm after surgery; in contrast, when left atrial dimension is normal, 85 percent of patients return to normal sinus rhythm [15] .

These data and anecdotal clinical experience support the concept that, if postoperative AF and its complications are to be minimized, corrective surgery should be considered within months of the development of AF or before substantial left atrial enlargement is present. The 2006 ACC/AHA guidelines concluded that the weight of evidence was in favor of the efficacy of mitral valve surgery in asymptomatic patients with severe chronic MR and preserved left ventricular function who have new onset AF (show table 2) [1] . The 2007 ESC guidelines thought that this was a debatable point [2] .

Although AF is not necessarily an indication for surgery in an asymptomatic patient with preserved left ventricular function, the burden of this arrhythmia in a patient with borderline left ventricular function (LVEF 55 to 60 percent) might be used as an indication for surgery, especially if the risk of surgery is low and the valve appears to be amenable to repair. (See "Mitral valve replacement versus repair" below).

The use of the maze procedure or radiofrequency or cryoablation as an adjunct to mitral valve repair or replacement is an effective approach to reduce the incidence of postoperative AF. (See "Surgical approaches to prevent recurrent atrial fibrillation").

Left atrial enlargement — Left atrial enlargement itself, in the absence of AF, may be a risk factor for an adverse outcome following mitral valve surgery. In one study, for example, measures of left ventricular systolic function and left atrial size were equally important in predicting postoperative cardiac-related mortality in patients with symptomatic chronic MR [12] . The authors concluded that left atrial size may reflect the "history" (severity and duration) of MR. This observation again supports the notion that surgery should be considered prior to the development of significant left atrial enlargement.

USE OF VASODILATORS — The indications for vasodilator therapy in patients with chronic MR depend upon the presence or absence of symptoms and the functional state of the left ventricle. These issues are discussed in detail elsewhere and will be briefly reviewed here. (See "Vasodilator therapy in chronic mitral regurgitation").

Asymptomatic patients — There are no published studies that support the hypothesis that vasodilator therapy is beneficial in asymptomatic patients with chronic MR. In addition, the administration of vasodilators in patients with normal LV function might limit the development of symptoms due to increasing LV dysfunction, thereby masking an indication for surgery. Thus, with some exceptions (eg, the hypertensive patient), vasodilators are not recommended for use in asymptomatic patients with chronic MR due to primary valve disease [1,2] .

Symptomatic patients — Several studies confirm a beneficial effect of acute vasodilator therapy in patients with chronic MR. Intravenous nitroprusside, for example, decreases left ventricular end-diastolic pressure and volume while increasing forward stroke volume and cardiac index. Hydralazine has similar salutary effects. In contrast, the acute effect of angiotensin converting enzyme (ACE) inhibitors or nitrates is usually a decrease or no change in the cardiac index.

Data regarding the chronic effect of vasodilators are less impressive. Chronic therapy provides the most benefit for patients with the largest hearts, the poorest systolic function, and the most disabling symptoms. When combined with digitalis and diuretics, for example, hydralazine can produce substantial symptomatic and hemodynamic improvement in patients who are in NYHA functional class II-IV [17] . ACE inhibitors may also be beneficial in this setting [18] . However, because of the substantial improvement in outcome associated with surgery in patients with symptomatic MR, chronic vasodilator therapy is only indicated in those who are not surgical candidates.

In patients for whom chronic vasodilator therapy is warranted, the following recommendations can be made based upon the etiology of MR and whether or not the patient is a candidate for surgery. (See "Vasodilator therapy in chronic mitral regurgitation").

• In symptomatic patients with primary MR (eg, myxomatous or rheumatic), there is little potential to induce a change in the regurgitant orifice area via preload reduction and the therapeutic goal should be a reduction in systolic pressure. Thus, a beta blocker, diuretic, hydralazine, or calcium channel blocker should be used. However, medical therapy is not a substitute for surgical intervention in patients with chronic symptomatic MR.
• Chronic vasodilator therapy is indicated in symptomatic patients who are not candidates for surgery. The evidence of benefit is best in patients with secondary (functional) MR due to left ventricular dysfunction. Treatment of such patients should consist of optimal medical therapy of heart failure and, in appropriate patients, cardiac resynchronization therapy. With respect to ACE inhibitors and/or angiotensin II receptor blockers, the dose titration and monitoring schedules are the same as for heart failure due to left ventricular systolic dysfunction in the absence of moderate to severe MR. (See "Functional mitral regurgitation" and see "Overview of the therapy of heart failure due to systolic dysfunction" and see "ACE inhibitors in heart failure due to systolic dysfunction: Therapeutic use").


CARDIAC RESYNCHRONIZATION — In selected patients with functional MR, cardiac resynchronization therapy (CRT) with biventricular pacing may be helpful. At this time, however, standard indications for CRT in patients with heart failure are based upon left ventricular (LV) function, functional class, and measures of LV dyssynchrony. (See "Functional mitral regurgitation", section on Cardiac resynchronization therapy, and see "Cardiac resynchronization therapy (biventricular pacing) in heart failure")

ANTICOAGULATION — The risk of an embolic event is increased in patients with rheumatic or nonrheumatic MR, particularly when atrial fibrillation is also present. The presence of mitral annular calcification, which if often associated with MR, also increases the risk of embolism, even in the absence of atrial fibrillation. It was estimated by the Framingham Heart Study that the risk of stroke associated with mitral annular calcification was 2.1-fold greater compared to the absence of mitral valve calcification [19] . (See "Antithrombotic therapy to prevent embolization in nonvalvular atrial fibrillation" and see "Echocardiography in detection of intracardiac sources of embolism", section on Mitral annular calcification).

The Seventh ACCP Consensus Conference on Antithrombotic Therapy published in 2004 included the following recommendations for anticoagulation in patients with chronic MR [20] . These recommendations are essentially the same as for patients without mitral valve disease who have atrial fibrillation and/or systemic embolic events:

Rheumatic MR — Anticoagulation with warfarin (target INR 2.5, range 2.0 to 3.0) is indicated in patients with rheumatic MR who have a history of systemic embolism, intermittent (paroxysmal) or persistent (chronic) atrial fibrillation, or sinus rhythm with a left atrial diameter greater than 5.5 cm. Since the risk of embolism may be increased in other patients with MR who are in sinus rhythm, a decision about the use of warfarin should also be based on comorbid risk factors, including age and the hemodynamic severity of the lesion.

If recurrent systemic embolism occurs despite adequate anticoagulation, aspirin (75 to 100 mg/day) should be added. For patients unable to take aspirin, alternative therapies are dipyridamole (400 mg/day) or clopidogrel (75 mg per day).

Nonrheumatic MR/mitral annular calcification — Long-term anticoagulation with warfarin (target INR 2.5, range 2.0 to 3.0) is recommended in patients with nonrheumatic MR who have atrial fibrillation or a history of systemic embolism and in patients with mitral annular calcification complicated by systemic embolism.

Mitral valve prolapse — The 2006 ACC/AHA guidelines on the management of valvular heart disease included recommendations for aspirin and warfarin therapy in patients with mitral valve prolapse (show table 8) [1] . When warfarin is given, the target INR is usually 2.5 (range 2.0 to 3.0). (See "Nonarrhythmic complications of mitral valve prolapse").

ENDOCARDITIS PROPHYLAXIS — The 2007 American Heart Association guidelines on infective endocarditis revised prior recommendations for patients with acquired valvular disease, including those with chronic MR [21] . As a result, antibiotic prophylaxis is no longer recommended when such patients undergo dental or other invasive procedures that produce significant bacteremia with organisms associated with endocarditis. (See "Antimicrobial prophylaxis for bacterial endocarditis").

MITRAL VALVE SURGERY — Two issues must be addressed when considering mitral valve surgery in patients with chronic MR: the indications for intervention; and the choice of procedure. These issues are discussed in detail separately but will be briefly reviewed here. (See "Indications for and types of corrective surgery in severe chronic mitral regurgitation").

This discussion will be limited to chronic MR due to primary valve disease. The management of functional and ischemic MR are reviewed elsewhere. (See "Functional mitral regurgitation" and see "Ischemic mitral regurgitation").

Indications — Among patients with severe chronic MR, surgery is indicated in patients with symptoms and in asymptomatic patients with abnormalities in LV size or function, pulmonary hypertension, or new onset atrial fibrillation (show figure 1A-1B and show table 9) [1] . Surgery may also be reasonable in asymptomatic patients with preserved left ventricular function if mitral valve repair is performed in experienced centers and it is estimated that the likelihood of successful repair without residual MR is greater than 90 percent.

Asymptomatic patients with severe chronic MR who do not meet criteria for intervention can be safely treated with watchful waiting as long as the patient is carefully monitored [22] . Such patients should be seen every 6 to 12 months or sooner if symptoms occur. Repeat transthoracic echocardiography should be obtained at these visits. The six month interval is preferred if stability has not been documented, there is evidence of progression, or measurements are close to the echocardiographic cutoff values for mitral valve surgery (show table 3). (See "Serial monitoring" above).

Surgery may be offered early in patients with borderline values for LV size or function in whom access to such monitoring is limited. On the other hand, a somewhat higher threshold for surgery is used if valve replacement is required. (See "Indications for and types of corrective surgery in severe chronic mitral regurgitation", section on Outcomes with watchful waiting).

Mitral valve replacement versus repair — Two surgical procedures confined to the mitral valve itself are available for the treatment of chronic MR: valve repair and valve replacement. The choice of procedure depends, at least in part, upon the cause of the MR, the anatomy of the mitral valve, and the degree of left ventricular dysfunction.

In most patients, mitral valve repair at experienced surgical centers is the preferred approach because of both functional and survival benefits compared to valve replacement (show figure 2). (See "Indications for and types of corrective surgery in severe chronic mitral regurgitation", section on Valve repair versus valve replacement).

When required, mitral valve replacement can be performed with a mechanical or bioprosthetic valve. Mechanical valves have the disadvantage of requiring lifelong warfarin therapy, while bioprosthetic valves have the disadvantage of limited durability due to valve degeneration, particularly in patients under age 65. (See "Complications of prosthetic heart valves").

When valve replacement is necessary, the following recommendations for the selection of a bioprosthetic or mechanical mitral valve were made by the 2006 ACC/AHA guidelines when valve replacement (show table 10) [1] :

• Bioprosthetic valves are recommended in patients who cannot or will not take warfarin or have a clear contraindication to warfarin therapy.
• Among patients who can take warfarin, the weight of evidence supports the following approach:

- A mechanical valve in patients under age 65 who have long-standing AF.


- A bioprosthetic valve in patients ≥65 years of age.


Among patients under age 65 who are in sinus rhythm, patient preference plays a central role in the choice of valve. The guidelines suggested that a bioprosthetic valve should only be considered after a detailed discussion with the patient of the risks of warfarin therapy compared to the likelihood of repeat valve replacement in the future.

Concurrent coronary disease — Many patients with nonischemic chronic MR requiring surgery also have significant coronary artery disease. Obstructive coronary lesions are usually revascularized at the time of mitral valve surgery, since concurrent bypass surgery typically adds little morbidity or mortality to the procedure [1] . A separate issue, which is discussed elsewhere, is the management of ischemic mitral regurgitation. (See "Ischemic mitral regurgitation").

Assuming that the patient is not severely hemodynamically unstable, coronary angiography was recommended by the ACC/AHA guidelines in patients who have or are suspected to have coronary disease (and who may have ischemic MR) and in those at risk for coronary disease (show table 11) [1] . At risk was defined as men ≥35 years of age, women ≥35 years of age with coronary risk factors, and postmenopausal women. A higher age threshold of ≥45 years was recommended in patients without ischemic symptoms or coronary risk factors in whom MR is due to mitral valve prolapse because of a very low rate of significant coronary disease in younger patients with mitral valve prolapse. (See "Indications for and types of corrective surgery in severe chronic mitral regurgitation", section on Predicting coronary disease).

Exercise after valve repair — The effect of exercise in patients with repaired mitral valves has not been well studied. The 36th Bethesda conference cited above recommended that such patients should not participate in sports that are associated with a risk of bodily contact or trauma that might disrupt the repair [13] . They can participate in low-intensity competitive sports (class IA) and selected patients can participate in low and moderate static and low and moderate dynamic competitive sports (class IA, IB, and IIA) (show table 7).