Mitral Stenosis

Causes and Pathology

The predominant cause of MS is rheumatic fever,154with rheumatic changes present in 99% of stenotic mitral valves excised at the time of mitral valve replacement. Approximately 25% of all patients with rheumatic heart disease have isolated MS, and approximately 40% have combined MS and MR. Multivalve involvement is seen in 38% of patients with MS, with the aortic valve affected in approximately 35% and the tricuspid valve in approximately 6%. The pulmonic valve is rarely affected. Two thirds of all patients with rheumatic MS are female. The interval between the initial episode of rheumatic fever (seeChapter 83) and clinical evidence of mitral valve obstruction is variable, ranging from a few years to more than 20 years.155

Rheumatic fever results in characteristic changes of the mitral valve; diagnostic features are thickening at the leaflet edges, fusion of the commissures, and chordal shortening and fusion156(Fig. 63-21). With acute rheumatic fever, the changes include inflammation and edema of the leaflets, with small fibrin-platelet thrombi along the leaflet contact zones. Subsequent scarring leads to the characteristic valve deformity, with obliteration of the normal leaflet architecture by fibrosis, neovascularization and increased collagen and tissue cellularity. Aschoff bodies, the pathologic hallmark of rheumatic disease, are seen most frequently in the myocardium, not the valve tissue, with Aschoff bodies identified in only 2% of autopsied patients with chronic valve disease.

These anatomic changes lead to a typical functional appearance of the rheumatic mitral valve. In earlier stages of the disease, the relatively flexible leaflets snap open in diastole into a curved shape because of restriction of motion at the leaflet tips (seeFig. 63-21; see alsoFig. 14-37). This diastolic doming is most evident in the motion of the anterior leaflet and becomes less prominent as the leaflets become more fibrotic and calcified. The symmetrical fusion of the commissures results in a small central oval orifice in diastole that on pathologic specimens is shaped like a fish mouth or buttonhole because the anterior leaflet is not in the physiologic open position (seeFig. 63-21,right; see alsoFig. 14-38). With end-stage disease, the thickened leaflets may be so adherent and rigid that they cannot open or shut, with consequent reduction in or, rarely, even abolition of the first heart sound, and leading to combined MS and MR. When rheumatic fever results exclusively or predominantly in contraction and fusion of the chordae tendineae, with little fusion of the valvular commissures, dominant MR results.

Debate continues about whether the anatomic changes of severe MS result from recurrent episodes of rheumatic fever or from a chronic autoimmune process caused by cross-reactivity between a streptococcal protein and valve tissue (seeChapter 83), or whether calcific valve disease is superimposed. Evidence supporting recurrent infection as an important factor in disease progression includes the correlation between the geographic variability in the prevalence of rheumatic heart disease and the age at which patients present with severe MS. In North America and Europe, where there is approximately 1 case/100,000 population, patients present with severe valve obstruction in the sixth decade of life. By contrast, in Africa, with a disease prevalence of 35/100,000, severe disease often is seen in teenagers. Conversely, evidence favoring superimposed calcific valve disease is the observation that restenosis after mitral valvuloplasty is caused by leaflet thickening and fibrosis, rather than representing recurrent commissural fusion.157

Congenital MS is uncommon and typically is diagnosed in infancy or early childhood (seeChapter 62). MS is a rare complication of malignant carcinoid disease, systemic lupus erythematosus, rheumatoid arthritis, and mucopolysaccharidoses of the Hunter-Hurler phenotype, Fabry disease, and Whipple disease. Methysergide therapy is an unusual but documented cause of MS. The association of atrial septal defect with rheumatic MS is called Lutembacher syndrome.

Other conditions may result in obstruction to LV inflow, including a left atrial tumor, particularly myxoma (seeChapter 85), ball valve thrombus in the left atrium (usually associated with MS), infective endocarditis with large vegetations (seeChapter 64), or a congenital membrane in the left atrium (i.e., cor triatriatum;seeChapter 62). In older patients, extensive mitral annular calcification may result in restriction of the size and motion of the annulus and may extend onto the base of the mitral leaflets, resulting in functional MS, although obstruction rarely is severe.158159Mitral annular calcification often develops in patients with calcific aortic valve disease.160161

Pathophysiology

The most useful descriptor of the severity of mitral valve obstruction is the degree of valve opening in diastole, or the mitral valve orifice area. In normal adults, the cross-sectional area of the mitral valve orifice is 4 to 6cm2(Table 63-7). When the orifice is reduced to approximately 2cm2, which is considered to represent mild MS, blood can flow from the left atrium to the left ventricle only if propelled by a small, although abnormal, pressure gradient. When the mitral valve opening is reduced to 1cm2, which is considered to represent severe MS,162a left atrioventricular pressure gradient of approximately 20mmHg (and therefore, in the presence of a normal LV diastolic pressure, a mean left atrial pressure >25mmHg) is required to maintain normal cardiac output at rest (Fig. 63-22; see alsoFig. 19-14).

TABLE 63-7

Stages of Mitral Stenosis

STAGE

DEFINITION

VALVE ANATOMY

VALVE HEMODYNAMICS

HEMODYNAMIC CONSEQUENCES

SYMPTOMS

A

At risk for MS

Mild valve doming during diastole

Normal transmitral flow velocity

None

None

B

Progressive MS

Rheumatic valve changes with commissural fusion and diastolic doming of the mitral valve leaflets

Planimetered MVA >1.5cm2

Increased transmitral flow velocities

MVA >1.5cm2

Diastolic pressure half-time 30mmHg

None

D

Symptomatic severe MS

Rheumatic valve changes with commissural fusion and diastolic doming of the mitral valve leaflets

Planimetered MVA 1.5cm2

MVA 1.5cm2

(MVA 1cm2with very severe MS)

Diastolic pressure half-time 150 msec

(Diastolic pressure half-time 220 msec with very severe MS)

Severe LA enlargement

Elevated PASP >30mmHg

Decreased exercise toleranceExertional dyspnea

The transmitral mean pressure gradient should be obtained to determine the full hemodynamic effect of the MS and usually is >5 to 10mmHg in severe MS; however, because of the variability of the mean pressure gradient with heart rate and forward flow, it has not been included in the criteria for severity.

LA = left atrium; MVA = mitral valve area; PASP = pulmonary artery systolic pressure.

From Nishimura RA, Otto CM, Bonow RO, etal: 2014 AHA/ACCF guideline for the management of patients with valvular heart disease: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 63:e57, 2014.

FIGURE 63-22

Schematic representation of LV, aortic, and left atrial (LA) pressures, showing normal (NL) relationships and alterations with mild and severe MS. Corresponding classic auscultatory signs of MS are shown at the bottom of the diagram. The higher left atrialvwave of severe MS causes earlier pressure crossover and earlier mitral valve (MV) opening, leading to a shorter time interval between aortic valve (AV) closure and the opening snap (OS). The higher left atrial end-diastolic pressure with severe MS also results in later closure of the mitral valve. With severe MS, the diastolic rumble becomes longer and there is accentuation of the pulmonic component (P2) of the second heart sound (S2) in relation to the aortic component (A2).

The transvalvular pressure gradient for any given valve area is a function of the square of the transvalvular flow rate.162Thus a doubling of flow rate quadruples the pressure gradient. The elevated left atrial pressure, in turn, raises pulmonary venous and capillary pressures, resulting in exertional dyspnea. The first bouts of dyspnea in patients with MS usually are precipitated by tachycardia resulting from exercise, pregnancy, hyperthyroidism, anemia, infection, or AF. All these (1) increase the rate of blood flow across the mitral orifice, resulting in further elevation of the left atrial pressure, and (2) decrease the diastolic filling time, resulting in a reduction in forward cardiac output. Because diastole shortens proportionately more than systole as heart rate increases, the time available for flow across the mitral valve is reduced at higher heart rates. At any given stroke volume, therefore, tachycardia results in a higher instantaneous volume flow rate and higher transmitral pressure gradient, which elevates left atrial pressures further. This higher transmitral gradient, often in combination with inadequate ventricular filling (because of the shortened diastolic filling time), explains the sudden occurrence of dyspnea and pulmonary edema in previously asymptomatic patients with MS who develop AF with a rapid ventricular rate. It also accounts for the equally rapid clinical improvement in these patients when the ventricular rate is slowed.

Atrial contraction augments the presystolic transmitral valvular gradient by approximately 30% in patients with MS (seeFigs. 63-22and19-14). AF is common in patients with MS, with an increasing prevalence with age. In patients with severe MS younger than 30 years, only approximately 10% are in AF, compared with approximately 50% of those older than 50 years. Withdrawal of atrial transport when AF develops reduces cardiac output by approximately 20%, often resulting in symptom onset.

Obstruction at the mitral valve level has other hemodynamic consequences, which account for many of the adverse clinical outcomes associated with this disease. Elevated left atrial pressure results in pulmonary artery hypertension, with secondary effects on the pulmonary vasculature and right side of the heart. In addition, left atrial enlargement and stasis of blood flow is associated with an increased risk of thrombus formation and systemic embolism. Typically, the left ventricle is relatively normal, unless there is coexisting MR, with the primary abnormalities of the left ventricle being a small underfilled chamber and paradoxical septal motion caused by RV enlargement and dysfunction.

Hemodynamic Consequences of Mitral Stenosis

Pulmonary Hypertension.

In patients with MS and sinus rhythm, mean left atrial pressure is elevated (seeFig. 63-22), and the left atrial pressure curve shows a prominent atrial contraction (awave), with a gradual pressure decline after mitral valve opening (ydescent). In patients with mild to moderate MS without elevated pulmonary vascular resistance, pulmonary arterial pressure may be normal or only minimally elevated at rest but rises during exercise. However, in patients with severe MS and those in whom the pulmonary vascular resistance is significantly increased, pulmonary arterial pressure is elevated when the patient is at rest. Rarely, in patients with extremely elevated pulmonary vascular resistance, pulmonary arterial pressure may exceed systemic arterial pressure. Further elevations of left atrial and pulmonary vascular pressures occur during exercise and/or tachycardia.

Pulmonary hypertension in patients with MS results from the following: (1) passive backward transmission of the elevated left atrial pressure; (2) pulmonary arteriolar constriction, which presumably is triggered by left atrial and pulmonary venous hypertension (reactive pulmonary hypertension); and (3) organic obliterative changes in the pulmonary vascular bed, which may be considered to be a complication of longstanding and severe MS (seeChapter 74). With moderately elevated pulmonary arterial pressure (systolic pressure 30 to 60mmHg), RV performance is usually maintained. In time, severe pulmonary hypertension results in right-sided heart failure, with dilation of the right ventricle and its annulus, secondary tricuspid regurgitation (TR), and sometimes pulmonic regurgitation. These changes in the pulmonary vascular bed may also exert a protective effect; the elevated precapillary resistance makes the development of symptoms of pulmonary congestion less likely to occur by tending to prevent blood from surging into the pulmonary capillary bed and damming up behind the stenotic mitral valve. This protection, however, occurs at the expense of a reduced cardiac output. In patients with severe MS, pulmonary veinbronchial vein shunts occur. Their rupture may cause hemoptysis. Patients with severe MS exhibit a reduction in pulmonary compliance, increase in the work of breathing, and redistribution of pulmonary blood flow from the base to the apex.

Left Ventricular Function.

The LV chamber typically is normal or small, with normal systolic function and normal LV end-diastolic pressure. However, coexisting MR, aortic valve lesions, systemic hypertension, ischemic heart disease, and cardiomyopathy all may be responsible for elevations of LV diastolic pressure.

Exercise Hemodynamics.

At any given severity of stenosis, the clinical picture is dictated largely by the levels of cardiac output and pulmonary vascular resistance with exertion. The response to a given degree of mitral obstruction may be characterized at one end of the hemodynamic spectrum by a normal cardiac output and high left atrioventricular pressure gradient or, at the opposite end of the spectrum, by a markedly reduced cardiac output and low transvalvular pressure gradient. Thus, in some patients with moderate MS (with a mitral valve area of 1.0 to 1.5cm2), cardiac output may be normal at rest and rises normally during exertion. However, the high transvalvular pressure gradient with exertion elevates left atrial and pulmonary capillary pressures, leading to pulmonary congestion during exertion. By contrast, in other patients with moderate MS, there is an inadequate rise in cardiac output during exertion, resulting in a smaller rise in pulmonary venous pressure. In these patients, symptoms are caused by a low cardiac output rather than by pulmonary congestion. In patients with severe MS (mitral valve area 0.12 second and/or a P wave axis between +45 and 30 degrees) is a principal electrocardiographic feature of MS and is found in 90% of patients with significant MS and sinus rhythm. The electrocardiographic signs of left atrial enlargement correlate more closely with left atrial volume than with left atrial pressure and often regress after successful valvotomy. AF is common with longstanding MS, as noted.

Electrocardiographic evidence of RV hypertrophy correlates with RV systolic pressure. When RV systolic pressure is 70 to 100mmHg, approximately 50% of patients exhibit ECG criteria for RV hypertrophy, including a mean QRS axis greater than 80 degrees in the frontal plane and a R:S ratio greater than 1 in lead V1. Other patients with this degree of pulmonary hypertension have no frank evidence of RV hypertrophy, but the R:S ratio fails to increase from the right to the midprecordial leads. When RV systolic pressure is greater than 100mmHg in patients with isolated or predominant MS, electrocardiographic evidence of RV hypertrophy is consistently found.

Radiography.

Patients with hemodynamically significant MS almost invariably have evidence of left atrial enlargement on the lateral and left anterior oblique views (seeFig. 15-10), although the cardiac silhouette may be normal in the frontal projection. Extreme left atrial enlargement rarely occurs in isolated MS; when present, MR usually is severe (seeFig. 15-8). Enlargement of the pulmonary artery, right ventricle, and right atrium (as well as the left atrium) is commonly seen in patients with severe MS. Occasionally, calcification of the mitral valve is evident on the chest roentgenogram but, more commonly, fluoroscopy is required to detect valvular calcification.

Radiologic changes in the lung fields indirectly reflect the severity of MS (seeChapter 15). Interstitial edema, an indication of severe obstruction, is manifested as Kerley B lines (dense, short, horizontal lines most commonly seen in the costophrenic angles). This finding is present in 30% of patients with resting pulmonary arterial wedge pressures less than 20mmHg and in 70% of patients with pressures greater than 20mmHg. Severe longstanding mitral obstruction often results in Kerley A lines (straight, dense lines up to 4cm in length, running toward the hilum), as well as the findings of pulmonary hemosiderosis and rarely of parenchymal ossification.

Cardiac Catheterization.

Catheter-based measurement of left atrial and LV pressures shows the expected hemodynamics (seeFig. 19-14) and allows measurement of the mean transmitral pressure gradient and, in conjunction with measurement of transmitral volume flow rate, calculation of the valve area using the Gorlin formula (seeChapter 19). Occasionally, diagnostic cardiac catheterization is necessary when echocardiography is nondiagnostic or results are discrepant with clinical findings.171More often, these measurements now are recorded for monitoring before, during, and after percutaneous BMV. Routine diagnostic cardiac catheterization is not recommended for the evaluation of MS.

Hemodynamic Progression

Serial echocardiographic data have described the rate of hemodynamic progression in patients with mild MS.157162The two largest series comprised a combined total of 153 adults, with a mean age of approximately 60 years, with an average follow-up period of slightly more than 3 years. As in most series of patients with MS, 75% to 80% were women. The initial valve area was 1.7 0.6cm2, and the overall rate of progression was a decrease in valve area of 0.09cm2/year. Approximately one third of patients showed rapid progression, defined as a decrease in valve area greater than 0.1cm2/year. These data apply to the older patients with MS seen in developed countries. There are little data on the rate of hemodynamic progression of rheumatic MS in underdeveloped countries, in which the age at symptom onset is much younger.

Clinical Outcomes

Natural history data obtained in the presurgical era indicate that symptomatic patients with MS have a poor outlook, with 5-year survival rates of 62% among patients with MS in NYHA class III but only 15% among those in class IV. Data from unoperated patients in the surgical era still reported a 5-year survival rate of only 44% in patients with symptomatic MS who refused valvotomy (Fig. 63-23).

FIGURE 63-23

Natural history of the respective valvular lesion in 159 patients with isolated MS (solid blue line) or MR (solid purple line) who were not operated on, even though the operation was indicated, compared with patients treated with valve replacement for mitral stenosis (dashed blue line) or mitral regurgitation (dashed purple line). The expected survival rate in the absence of mitral valve disease is indicated by the upper curve (dashed black line).

(From Horstkotte D, Niehues R, Strauer BE: Pathomorphological aspects, aetiology, and natural history of acquired mitral valve stenosis. Eur Heart J 12[Suppl B]:55, 1991.)

Overall clinical outcomes are greatly improved in patients who undergo surgical or percutaneous relief of valve obstruction on the basis of current guidelines.12However, longevity is still shortened compared with that expected for age, largely because of complications of the disease process (AF, systemic embolism, pulmonary hypertension) and side effects of therapy (e.g., prosthetic valves, anticoagulation).

Complications

Atrial Fibrillation.

The most common complication of MS is AF (seeChapter 38).157The prevalence of AF in patients with MS is related to the severity of valve obstruction and patient age. In historical series, AF was present in 17% of patients 21 to 30 years of age, 45% of those 31 to 40 years, 60% of those 41 to 50 years, and 80% of those older than 51 years. Even when MS is severe, the prevalence of AF is related to age. In more recent BMV studies, the prevalence of AF ranged from 4% in a series of 600 patients from India, with a mean age of 27 years, and 27% in a series of 4832 patients from China, with a mean age of 37 years, to 40% in a series of 1024 patients from France, with a mean age of 49 years.

AF may precipitate or worsen symptoms caused by loss of the atrial contribution to filling and to a short diastolic filling period when the ventricular rate is not well controlled. In addition, AF predisposes affected patients to left atrial thrombus formation and systemic embolic events. AF conveys a worse overall prognosis in MS patients than in the general population. In patients with AF and MS, 5-year survival is only 64%, compared with 85% in patients with AF but without MS.

Systemic Embolism.

Systemic embolism in patients with MS is caused by left atrial thrombus formation. Although systemic embolization most often occurs in patients with AF, 20% of patients with MS and a systemic embolic event are in sinus rhythm. When embolization occurs in patients in sinus rhythm, the possibility of transient AF or underlying infective endocarditis should be considered. However, up to 45% of patients with MS who are in normal sinus rhythm demonstrate prominent spontaneous left atrial (Video 63-13) contrast (a marker of embolic risk) on TEE (seeChapter 14). Atrial thrombi have been documented in a few patients with MS in sinus rhythm, and many patients with new-onset AF have left atrial thrombi. It is postulated that the loss of atrial appendage contractile function, despite electrical evidence of sinus rhythm, leads to blood flow stasis and thrombus formation. Additional evidence implicates inflammatory markers, endothelial dysfunction, and platelet activation as inciting mechanisms for thromboembolism.172173

The risk of embolism correlates directly with patient age and left atrial size174and inversely with the cardiac output. Before the advent of surgical treatment, this serious complication of MS developed in at least 20% of patients at some time during the course of their disease. Before the era of anticoagulant therapy and surgical treatment, approximately 25% of all fatalities in patients with mitral valve disease were secondary to systemic embolism.

Approximately half of all clinically apparent emboli are found in the cerebral vessels. Coronary embolism may lead to myocardial infarction and/or angina pectoris, and renal emboli may be responsible for the development of systemic hypertension. Emboli are recurrent and multiple in approximately 25% of patients who develop this complication. Rarely, massive thrombosis develops in the left atrium, resulting in a pedunculated ball valve thrombus, which may suddenly aggravate obstruction to left atrial outflow when a specific body position is assumed or may cause sudden death. Similar consequences occur in patients with free-floating thrombi in the left atrium. These two conditions usually are characterized by variability in the physical findings, often on a positional basis. They are very hazardous and necessitate surgical treatment, often on an emergency basis.

Infective EndOcarditis.

MS is a predisposing factor for endocarditis (seeChapter 64) in less than 1% of cases in clinical series of bacterial endocarditis. The estimated risk of endocarditis in patients with MS is 0.17/1000 patient-years, which is much lower than the risk in patients with MR or aortic valve disease.

Medical Management

Drug Treatment.

The medical management of MS is directed primarily toward the following: (1) prevention of recurrent rheumatic fever; (2) prevention and treatment of complications of MS; and (3) monitoring disease progression to allow intervention at the optimal time point.157Patients with MS caused by rheumatic heart disease should receive penicillin prophylaxis for beta-hemolytic streptococcal infections to prevent recurrent rheumatic fever, per established guidelines (seeChapter 83). Prophylaxis for infective endocarditis is no longer recommended (seeChapter 64). Anemia and infections should be treated promptly and aggressively in patients with valvular heart disease. Of note, however, blood cultures should always be considered before initiation of antibiotic therapy in patients with valve disease, because the presentation of endocarditis often is mistaken for a noncardiac infection.

Anticoagulant therapy is indicated for prevention of systemic embolism in patients with MS and AF (persistent or paroxysmal), any previous embolic events (even if in sinus rhythm), and documented left atrial thrombus. Anticoagulation also may be considered for patients with severe MS and sinus rhythm when there is severe left atrial enlargement (diameter >55mm) or spontaneous contrast on echocardiography. Treatment with warfarin is used to maintain the international normalized ratio (INR) between 2 and 3.175

Asymptomatic patients with mild to moderate rheumatic mitral valve disease should have a history and physical examination annually, with echocardiography every 3 to 5 years for mild stenosis, every 1 to 2 years for moderate stenosis, and annually for severe stenosis. More frequent evaluation is appropriate for any change in signs or symptoms. All patients with significant MS should be advised to avoid occupations requiring strenuous exertion.

In patients with severe MS, with persistent symptoms after intervention or when intervention is not possible, medical therapy with oral diuretics and the restriction of sodium intake may improve symptoms. Digitalis glycosides do not alter the hemodynamics and usually do not benefit patients with MS and sinus rhythm, but these drugs are of value in slowing the ventricular rate in patients with AF and in treating patients with right-sided heart failure. Hemoptysis is managed by measures designed to reduce pulmonary venous pressure, including sedation, assumption of the upright position, and aggressive diuresis. Beta-adrenergic blocking agents and rate-slowing calcium antagonists may increase exercise capacity by reducing heart rate in patients with sinus rhythm, especially in patients with AF.

Treatment of Arrhythmias.

AF is a frequent complication of severe MS. Management of AF for patients with MS is similar to management for AF of any cause (seeChapter 38). However, it typically is more difficult to restore and maintain sinus rhythm because of pressure overload of the left atrium in conjunction with effects of the rheumatic process on atrial tissue and the conducting system.

Immediate treatment of AF includes administration of intravenous heparin followed by oral warfarin. The ventricular rate should be slowed, as stated in the American College of Cardiology/American Heart Association (ACC/AHA) guidelines for the management of AF,175initially with an intravenous beta blocker or nondihydropyridine calcium channel antagonist, followed by long-term rate control with oral doses of these agents. When these medications are ineffective or when additional rate control is necessary, digoxin or amiodarone may be considered. Digoxin alone for long-term management of AF may be considered in patients with concurrent LV dysfunction or a sedentary lifestyle. An effort should be made to reestablish sinus rhythm by a combination of pharmacologic treatment and cardioversion. If cardioversion is planned in a patient who has had AF for more than 24 hours before the procedure, anticoagulation with warfarin for more than 3 weeks is indicated. Alternatively, if TEE results show no atrial thrombus, immediate cardioversion can be carried out provided the patient is effectively anticoagulated with intravenous heparin before and during the procedure, and with warfarin chronically thereafter. Paroxysmal AF and repeated conversions, spontaneous or induced, carry the risk of embolization. In patients who cannot be converted or maintained in sinus rhythm, digitalis should be used to maintain the ventricular rate at rest at approximately 60 beats/min. If this is not possible, small doses of a beta-adrenergic blocking agent, such as atenolol (25mg daily) or metoprolol (50 to 100mg daily), may be added. Beta blockers are particularly helpful in preventing rapid ventricular responses that develop during exertion. Multiple repeat cardioversions are not indicated if the patient fails to sustain sinus rhythm while on adequate doses of an antiarrhythmic.

Patients with chronic AF who undergo surgical mitral valve repair or replacement may undergo the maze procedure (atrial compartment operation). More than 80% of patients undergoing this procedure can be maintained in sinus rhythm postoperatively and can regain normal atrial function, including a satisfactory success rate in those with significant left atrial enlargement. Early intervention with percutaneous valvotomy may prevent the development of AF.176

Mitral Valvotomy

Percutaneous Balloon Mitral Valvotomy

Patients with mild to moderate MS who are asymptomatic frequently remain so for years, and clinical outcomes are similar to those in age-matched normal subjects. Severe or symptomatic MS, however, is associated with poor long-term outcomes if the stenosis is not relieved mechanically (seeFig. 63-23). Percutaneous BMV (seeChapter 56) is the procedure of choice for the treatment of MS; surgical intervention is now reserved for patients who require intervention and are not candidates for a percutaneous procedure.157

BMV is recommended for symptomatic patients with moderate to severe MS (i.e., a mitral valve area