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Mitral valve is a heart valve, which is composed of two leaflets (anterior and posterior) demarcated by two commissures along an annular ring, separating the left atrium from the left ventricle, and serving as a door and guard for the entrance of blood either from the left atrium or abnormally from the left ventricle due to regurgitation. It opens and closes to allow oxygenated blood to flow from the left atrium into the left ventricle (see figures 104a, 104b, 105a, 105b, 106a, 106b). Its leaflets are attached distally by fibrous strands called chordae tendineae to papillary heart muscles in the cavity of the left ventricle.

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This valve's orifice or door may become too narrow (stenosis, see figure 20a, 20b, 20c, 44a, 44b, 44c, 44d, 44e) due to rheumatic fever sequelae or congenital heart disease including the rare deformity of the "parachute" mitral valve (figure 44 g-1 and figure 44g-2) or too wide to close properly (regurgitation, see figure 45, 69, 109, 118) due to various diseases, such as myocardial infarction (heart attack, see definition of myocardial infarction), infection (48b, 48h), degeneration, myxomatous changes (see figure 115), congenital or genetic causes (see definition congenital heart disease in adults).

Figure 45
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Figure 48b
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Figure 49
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Figure 69
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Figure 107
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Figure 114
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Figure 109
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Figure 115
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Figure 118
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The mitral stenosis and/or regurgitation may be treated with percutaneous balloon valvotomy (valvuloplasty) or open heart surgery (see figure 109), or valve replacement (see figure 49, 69, 107, 114).


There about 500,000 discharge diagnoses of mitral valve disease annually in the United States. However, the estimates of the prevalence of mitral regurgitation are confounded by the presence of benign flow murmurs in many adults and by the small amount of physiologic regurgitation detected on echocardiography in 80% of adults. Only about 18,000 patients undergo mitral valve surgery annually, suggesting that most patients with the diagnosis of mitral regurgitation never need surgical intervention. Thus, the challenge for the clinician is first to determine which patients have the pathologic mitral regurgitation and then to provide them with appropriate care.



Normal mitral valve function depends on the complex interactions of all the components of the valve apparatus ( Fig. 1 ). In surgical series, the most common causes of mitral regurgitation are mitral-valve prolapse ( 20 to 70% of cases), ischemia steamy and ( 13 to 30 %) rheumatic heart disease (3 to 40 percent), and endocarditis (10 t0 12%). Although mitral- valve prolapse , is common in surgical series, most patients with mitral- valve have only mild disease and never need surgery. Mitral-valve prolapse and ischemic disease are also common in patients with milder regurgitation , but the most common causes are ventricular dilatation and systolic dysfunction. In the elderly, mitral regurgitation may be due to annular calcification; typically regurgitation in older people is mild to moderate and intervention is rarely necessary. Accurate identification of the mechanism of mitral regurgitation is essential because the clinical outcome, the medical therapy prescribed and the potential need of surgical intervention depends as much on the cause as on the severity of the disease.

Pathophysiologic Process

Chronic left ventricular volume overload as a result of mitral regurgitation lead compensatory dilatation of the left ventricle. Although this response initially maintains cardiac output, myocardial decompensation eventually results in symptoms of heart failure and increased risk of sudden death. In some patients, left ventricular contractility is an irreversibly impaired in the absence of symptoms. In addition, backflow into the left atrium results in the enlargement of the left atrium,atrial fibrillation and elevated pulmonary pressures.


Mitral regurgitation may be diagnosed on the basis of the presence of a systolic murmur in asymptomatic adults or incidentally when echocardiography is performed for other indications. Some patients with primary disease of the valve leaflets present with symptoms of heart failure, atrial fibrillation, or endocarditis. The symptoms may be precipitated by a superimposed hemodynamic stress, such as that induced by a pregnancy, anemia,or an infection. In patients with secondary regurgitation, valve dysfunction is most often identified during an evaluation of the underlying disease process.

On physical examination, the murmur of mitral regurgitation is classically apical holosystolic murmur that radiates to the axilla. However, physical examination is not always reliable in distinguishing mitral regurgitation from other types of systolic murmurs and does not provide an accurate measure of the severity of regurgitation. On electrocardiography and chest radiography, evidence of enlargement of the left atrium, left ventricle, or both is seen only late in the course of disease and is not sensitive or specific for the diagnosis of mitral regurgitation .


Echocardiography allows accurate evaluation of the presence or absence, severity and cause of mitral regurgitation. Echocardiography is indicated in patients who have a systolic murmur and any cardiac symptoms, a loud murmur (approximately grade 3/6) alone, or other cardiac findings on physical examination. In most cases, the cause of mitral regurgitation can be deduced from the two dimensional images ( Fig. 202 B). Although Doppler echocardiography provides several methods of quantifying the severity of regurgitation, none have been shown to predict the clinical outcome. Most centers grade regurgitation as mild, moderate or severe using a combination of color flow,continuous, and pulse-wave Doppler imaging.

The most important aspect of the echocardiographic examination is the quantitation of left ventricular systolic performance. Although calculation of the ejection fraction is an imperfect means of assessing contractility, from a practical point of view the ejection fraction in conjunction with the end systolic dimension provides a clinically useful measure of ventricular performance. Transesophageal echocardiography allows accurate assessment of the feasibility of valve repair and should be performed before surgical intervention.


Patients with mitral regurgitation may remain asymptomatic for many years; the average interval from diagnosis to the onset of symptoms is 16 years. There are few data on the rate of hemodynamic progression of disease in patients with mild to moderate regurgitation, since most series are restricted to patients with severe regurgitation. In addition, the available data are difficult to interpret, since the criteria for evaluating the severity of regurgitation vary and are not always clearly defined. Furthermore, even though the clinical outcome is strongly dependent on the cause of the disease, patients with diverse mechanisms of regurgitation are often included in the same study.

In patients with severe symptomatic mitral regurgitation, the clinical outcome is poor: survival rates are as low as 33% at eight years in the absence of surgical intervention.The average mortality rate is approximately 5percent per year; most deaths are related to heart failure, but there is a substantial incidence of sudden death, suggesting that ventricular arrhythmias may be an important feature of the disease process. Other complications include atrial fibrillation,cerebral ischemic events, and endocarditis.

In patients with mitral-valve prolapse the clinical outcome depends on the extent of the leaflet disease and the severity of mitral regurgitation. The progression of disease may be slow and insidious or maybe abrupt, as a result of a chordial rupture leading to the flail leaflet in one study of patients with initially asymptomatic severe mitral regurgitation caused by mitral-valve prolapse, only 28% required surgery within five years because of the onset of symptoms. In contrast, 90 percent of patients with flail mitral-valve leaflet died or underwent surgery within 10 years, whether or not they initially had symptoms.

Mitral regurgitation as a sequelae of rheumatic fever is uncommon in the United States and is typically associated with some degree of mitral stenosis. Ischemic mitral regurgitation encompasses several mechanisms, including papillary muscle dysfunction, regional ventricular dysfunction, and left ventricular dilatation. The outcome is related to the severity of symptoms at presentation and the extent of underlying coronary disease. In patients with dilated cardiomyopathy, mitral regurgitation has diverse causes, including annular dilatation, changes in the shape and size of the left ventricle and systolic dysfunction.


Most patients in whom chronic mitral regurgitation is diagnosed have mild to moderate disease and are unlikely to ever need surgical intervention. Management is directed toward identifying the cause and severity of the regurgitation, treating underlying disease processes, preventing complications, educating the patient ,and evaluating risk factors for coronary disease. In patients with primary mitral-valve disease periodic echocardiography allows early detection of impaired left ventricular systolic function on the basis of measurement of the end systolic dimension and ejection fraction ( table 1 ). Other echocardiographicm measures that are useful in clinical decision making include assessment of the size of the left atrium and pulmonary systolic pressure .

Medical Therapy

No known medical therapies directly affect the disease process in the valve leaflets in patients with mitral-valve prolapse or rheumatic valve disease. There has been sustained interest in the concept of using vasodilator therapy to decrease severity of mitral left ventricular dilatation. The rationale for vasodilator care is that a reduction in the after load may increase aortic flow and decrease mitral backflow. To some extent, this rationale has been validated in small, short term studies that have demonstrated a decrease in systemic vascular resistance and regurgitant fraction and an increase in cardiac output with vasodilator therapy, often with a decrease in ventricular volume and end-diastolic pressure. However, these studies show that vasodilators are most effective in improving symptoms in patients with mitral regurgitation associated with ventricular and impaired systolic function. There are no data that support the use of vasodilator therapy in patients with asymptomatic mitral regurgitation and normal ventricular function. Most important, the use of medical therapy should not delay consideration of surgical intervention in patients with symptoms or evidence of left ventricular systolic dysfunction. Medical therapy is primarily directed toward the treatment of complications of mitral regurgitation and the prevention of endocarditis with antibiotic prophylaxis. If atrial fibrillation occurs, standard approaches to rate control, cardioversion and anticoagulation are indicated. In patients with mitral regurgitation as result of ischemic disease prevention of ischemia with medical therapy, percutaneous transluminal coronary intervention or bypass grafting is appropriate. In patients with mitral regurgitation due to dilated cardiomyopathy, medical therapy for heart failure including afterload reduction,often results in improvement in left ventricular shape, size and systolic function in association with a reduction in the severity of regurgitation .

Mitral-Valve Surgery

The optimal surgical intervention for mitral regurgitation is valve repair. As compared with valve replacement, successful valve repair results in superior hemodynamics and ventricular function, avoidance of a prosthetic valve and the need for long term anticoagulation, and less distortion of ventricular shape. The feasibility of valve repair is highest in patients with mitral- valve prolapse, especially in those whose disease is confined to the posterior leaflet. As surgical techniques improve, an increasing number of patients are becoming candidates for this procedure. When valve repair is not technically possible, every effort is made to maintain the integrity of mitral chordal apparatus. With chordal preservation, there is little change in the ejection fraction after surgery, as compared with an average decline of 10 ejection- fraction units in patients with transected chords. The operative mortality is lower for mitral-valve prolapse than for valve replacement (2 to 4% versus 5 to 10%) In patients with mitral-valve prolapse, long term. clinical outcome is excellent, with survival rates of 80 to 94% at 5 to 10 years with valve repair as compared with 40 to 60% with valve replacement.

In patients with symptoms due to the mitral regurgitation, surgical intervention is indicated, unless they have severe left ventricular dysfunction. In asymptomatic patients with severe mitral regurgitation, the outcome is improved if surgery is performed before the onset of irreversible ventricular dysfunction. No randomized trials have assessed the optimal timing of intervention for asymptomatic severe mitral regurgitation, and the ideal measure of ventricular contractility remains elusive. However, a consensus has been reached that left ventricular end-systolic dimensions and ejection fraction can be used to identify the early systolic dysfunction. The evidence supporting this approach is derived from studies in patients who were undergoing valve surgery for severe mitral regurgitation that assessed the value of preoperative variables as predictors of postoperative ventricular performance. Indicators of early systolic dysfunction are an end systolic dimension of 45mm or more or an ejection fraction of 0.60 or less. Systolic dysfunction is most likely when both valves are abnormal and sequential studies show a progressive deterioration. Other factors that may affect the timing of surgical intervention include the feasibility of valve repair, the onset of atrial fibrillation, and the development of pulmonary hypertension ( Fig. 3 ). There are two noteworthy features of these criteria: the degree of ventricular dilatation seen with isolated volume overload due to mitral regurgitation is much less than that seen in aortic regurgitation ,a condition characterized by combined pressure and volume overload, and these criteria only apply to patients with severe mitral regurgitation.


Assessment of the Severity of Mitral Regurgitation

The current definition of severe mitral regurgitation is based on angiographic and echocardiographic descriptors of the degree of backflow across the valve. An alternative physiological definition would be mitral regurgitation severe enough to result in dilatation of the left ventricle, left atrium or both. However, the best left definition would be regurgitation leading to adverse clinical outcomes. Unfortunately, prospective data based on quantitative measures of severity are not unavailable.Thus, it is not certain that some patients with moderate regurgitation have severe disease that has not yet resulted in the ventricular enlargement. The percentage of patients with mild regurgitation will have a progressive increase in the severity of mitral regurgitation is also unknown.

Medical Therapy for Primary Valve Disease

In patients with severe mitral regurgitation due to primary valve disease, there are no persuasive data that medical therapy decreases the rate of ventricular dilatation or delays valve surgery. Some clinicians argue that medical therapy may even be harmful if it is in creases the severity of the regurgitation in patients with mitral-prolapse, prevents normal adaptive responses of the left ventricle, or delays the recognition of early symptoms or ventricular dysfunction.

Timing of Surgical Intervention

When severe mitral regurgitation and severely reduced ventricular function are both present, it can be difficult to determine whether ventricular dysfunction is the cause or a consequence of chronic regurgitation. In either case, the surgical outcome is poor when the ejection fraction is less than 0.3, unless chordal continuity is preserved. In some patients, a trial of medical therapy for heart failure and an evaluation of the other causes of left ventricular dysfunction being clarify the situation. Because the optimal approach to these patients is controversial clinical decision making must be individualized on the basis of the evaluation of the ventricular and valve function, the likelihood of valve repair,the presence of other underlying conditions and the patients'preferences.

Valve Repair in Patients with Secondary Mitral Regurgitation

Some studies of patients with ischemic mitral regurgitation suggest that revascularization alone decreases the serverity of regurgitation,whereas other studies suggest that concurrent valve repair or the placement of an annuloplasty ring is necessary. Revascularization might be effective if regurgitation is due to ischemia or if revascularization improves the shape of the mitral valve. However,if there is irreversible myocardial damage or if remodeling does not occur, then mitral regurgitation may persist. In the absence of randomized clinical trials the surgical decision is currently individualized on the basis of mechanism of regurgitation in each patient.In patients with dilated cardiomyopathy ,mitral regurgitation is due to change in the shape of the valve apparatus , so that the severity of regurgitation is often decreased by medical therapy that restores ventricular size and shape .Some centers advocate mitral valve sugery inthese patrients,but this approach is not widely accepted.


The American College of Cardiology and the American Heart Association have developed detailed guidelines for evaluation, follow-up, and optimal timing of surgical intervention in patients with severe mitral regurgitation. Appropriate candidates for mitral-valve surgery include patients with symptoms, except those with severe ventricular dysfunction and in patients with no symptoms who have mild to moderate ventricular dysfunction. Surgery is indicated in asymptomatic patients with preserved ventricular function if there is ahigh likelihood of valve repair or if there is evidence of pulmonary hypertension or recent atrial fibrillation.Guidelines also address the use of echocardiography, the prevention of rheumatic fever and endocarditis, and indications for anticoagulation.


In the case of patients with a cardiac murmur, the threshold for echocardiographic evaluation should be low.When the valve is anatomically abnormal, the periodic clinical an echocardiographic follow-up allows early identification of symptoms, complications, and systolic dysfunction. In patients with secondary mitral regurgitation, echocardiography serves as a first step toward the evaluation and treatment of the underlying disease process. Patient education is vital, both to ensure compliance with follow-up and allow the patient to participate in the decision making process. Surgical intervention in patients with severe mitral regurgitation is indicated at the onset of symptoms or in the presence of convincing evidence of left ventricular dysfunction. Valve repair rather than valve replacement should be performed whenever possible. We should remain cautious in recommending valve surgery for asymptomatic patients who are considered to have severe regurgitation but who have no evidence of consequences of hemodynamic abnormalities. However, the excellent anatomical and clinical outcomes of valve repair make surgical intervention appropriate earlier in the course of disease in many patients with severe mitral regurgitation as a means of preventing chronic volume overload.

Otto,C.M.,Evaluation and Management of Chronic Mitral Regurgitation, N Engl J Med,Vol.345,No 10,9/6/2001,PP.740-746.

Mitral Valve Percutaneous Balloon Valvotomy (PMV)

This is a procedure in which a cardiac catheter containing a balloon expanding device is inserted percutaneously through the right femoral vein and on into the right side of the heart. This device has a cutting mechanism (i.e. needle) which allows the catheter to be passed through the interatrial septum (see figures 35a, 104b) and thus into the left atrium.
From there the balloon mechanism can be advanced through the mitral valve and inflated accordingly to treat the mitral stenosis.

The balloon catheter can also be advanced with the help of a guide wire out the aortic valve into the ascending aorta. In order to pass various larger dilating balloon catheters across the atrial septum and the stenotic mitral valve, the hole in the interatrial septum may need to be dilated as well. The balloons are ultimately positioned to straddle the mitral valve and one or two simultaneous inflations are performed. (see figure 69, 108).