Vasodilators are useful in acute mitral regurgitation to decrease aortic pressure and impedance, favoring forward over regurgitant flow during systole. This decreases left ventricular size and left ventricular and atrial pressures, improves forward cardiac output, and decreases the amount of regurgitation. Studies of acute regurgitation with vasodilators, such as hydralazine, nifedipine, and nitroprusside, have demonstrated this effect in the hemodynamics laboratory and, thus, their usefulness for managing acute mitral regurgitation. Studies on the pharmacologic treatment of patients with chronic mitral regurgitation are scant, and the available data are not particularly encouraging. Because afterload is not increased in patients with well-compensated chronic mitral regurgitation, lowering it further may not improve forward flow and would more likely reduce it. Many patients experience vasodilator side effects, and if forward cardiac output is not improved, the patient's overall hemodynamic status is actually worsened. Thus, until further data are obtained, there is no evidence to support vasodilator therapy for asymptomatic patients with chronic mitral regurgitation. In mildly symptomatic patients who presumably have left ventricular dilation and dysfunction, but who want to avoid surgery, vasodilators could be tried. Markedly symptomatic patients, however, are better treated surgically. Patients with systemic hypertension and those with functional mitral regurgitation due to systolic dysfunction should be treated with vasodilators.
Digoxin is useful in atrial fibrillation for controlling the heart rate. Whether it is of any value for improving forward output with mitral regurgitation in patients with normal sinus rhythm is unknown. If there are other indications for using the drug, however, it is not known to be harmful to the overall hemodynamic status of patients with mitral regurgitation.
Oral anticoagulation is indicated for patients in atrial fibrillation and those with concomitant mitral stenosis. Whether patients with moderate-to-severe mitral regurgitation, with large left ventricles and large left atria, who are in normal sinus rhythm and have normal left ventricular function would benefit from anticoagulants is controversial. Eccentric regurgitant jets may produce areas of stasis in the left atrium, according to color-flow Doppler studies. Furthermore, patients with moderate-to-severe mitral regurgitation are always at risk for developing atrial fibrillation. Although an argument can be made for long-term anticoagulation in such patients, no clinical trials support this approach.
Only patients with prosthetic heart valves now require antibiotics to prevent the development of bacterial endocarditis. Patients in whom rheumatic heart disease is the likely cause of mitral regurgitation should also have rheumatic fever antibiotic prophylaxis.
Patients with acute, severe, or decompensated chronic severe mitral regurgitation will need urgent surgical therapy—if it is appropriate to their general medical condition. Such patients can usually be stabilized with intravenous vasodilators, such as hydralazine or nitroprusside, and other therapies for heart failure, such as diuretics. If there is no response to pharmacologic therapy, an intra-aortic balloon pump is indicated. This mechanical approach will reduce arterial and left ventricular pressure in systole, favoring forward flow rather than regurgitant and increased diastolic aortic pressure, and may improve left ventricular contractility. Most patients will stabilize on this therapy, allowing for an appropriate evaluation (eg, coronary angiography), thereby maximizing the benefits of surgery.
Patients with either acute or chronic moderately severe mitral regurgitation will eventually need surgical therapy. The issue is the appropriate timing of surgery. If the physician waits until the symptoms are marked because of left heart failure with depressed left ventricular systolic function and severe pulmonary hypertension, not much symptomatic improvement is achieved after surgery, and left ventricular function remains depressed. On the other hand, if surgery is performed earlier, the patient may become relatively asymptomatic, with normal left ventricular function. Considerable effort has been directed at determining prognostic indicators for avoiding a poor response to surgical therapy. Prospective studies have shown that the following are all markers of a poor prognosis following surgery: an ejection fraction of 60% or less, an end-systolic volume index of 50 mL/m2 or more, an end-systolic dimension on echocardiography of 40 mm or more, significant pulmonary hypertension (PASP > 50 mm Hg or peak exercise PASP > 60 mm Hg), and atrial fibrillation. Although it seems logical that surgery should therefore be performed before these indicators are obtained in a patient, even one who is asymptomatic, this decision analysis has never been tested in clinical trials (Table 20–4).
Table 20–4. General Indications for Considering Mitral Valve Surgery in Patients with Chronic Severe Organic Mitral Regurgitation ||Download (.pdf)
Table 20–4. General Indications for Considering Mitral Valve Surgery in Patients with Chronic Severe Organic Mitral Regurgitation
Symptoms such as dyspnea
Left ventricular ejection fraction ≤ 60%
Left ventricular end-systolic dimension ≥ 40 mm
Left ventricular end-systolic volume index ≥ 50 mL/m2
Pulmonary artery systolic pressure > 50 mm Hg at rest or > 60 mm Hg with exercise
In patients with aortic and mitral regurgitation, if the mitral valve is not obviously diseased and the mitral regurgitation is mild to moderate (1–2+), replacing the aortic valve will often diminish left ventricular size enough to reduce or eliminate the mitral regurgitation. Sometimes a mitral annular ring will be required to reduce mitral annular size. In cases where the mitral valve leaflets and chordae are diseased or the regurgitation is severe, valve repair or replacement will be necessary—at the cost of a higher likelihood of operative mortality or postoperative morbidity. Severe aortic stenosis is often accompanied by mild-to-moderate mitral regurgitation. In this situation, the reduction in left ventricular pressure produced by aortic valve replacement usually reduces the mitral regurgitation, and further mitral surgery can be avoided.
The pulmonary hypertension that often accompanies mitral regurgitation may lead to tricuspid and pulmonic regurgitation. The latter usually resolves when the pulmonary pressure is reduced by mitral valve surgery, and pulmonary valve replacement is rarely necessary. Tricuspid regurgitation, if mild-to-moderate and associated with moderately severe pulmonary hypertension, will usually resolve after successful mitral surgery. If the tricuspid regurgitation is moderately severe, but the leaflets are not diseased, a tricuspid ring may be effective; if tricuspid valve disease is present, repair or replacement will be necessary. One clinical indicator for the need for tricuspid valve repair or replacement is a mean right atrial pressure of more than 15 mm Hg; however, the decision for this is often made during surgery, after the mitral procedure has been completed.
The onset of heart failure symptoms should prompt consideration of surgical treatment. Symptoms such as dyspnea, fatigue, and edema develop in some patients before the echocardiographic signs of severe mitral regurgitation develop. The importance of other symptoms, such as a history of arrhythmias or recurrent systemic emboli, is less certain. If the hemodynamic indicators are absent, other therapies for these conditions should be attempted first, before surgery.
Other factors to be taken into account when deciding when to perform surgery are the type of operation—valve repair or replacement—and the type of prosthetic valve, should one be needed. It is now possible in many patients with mitral regurgitation to repair rather than replace the mitral valve. Patients with mitral valve prolapse, ruptured chordae tendineae, or a ruptured papillary muscle are especially likely to respond to reparative surgery, whereas patients with markedly deformed valves and fused chordae from rheumatic heart disease or patients with infective endocarditis are less likely to be helped by mitral valve repair and often require valve replacement. Repair is preferable, especially for the patient with normal sinus rhythm because there is no need for long-term anticoagulation therapy following surgery. In addition, mitral valve repair is generally associated with better preservation of left ventricular systolic function following surgery and is therefore highly advantageous for patients with a low left ventricular ejection fraction and a repairable mitral valve. Thus, if it is likely that mitral valve repair can be done, there is less reluctance about operating in asymptomatic patients that otherwise meet criteria for surgery.
If valve replacement is necessary, ventricular function can be preserved by leaving the chordae intact; chordal tethering of the papillary muscles is presumed to improve left ventricular performance. With valve replacement, the choice between a mechanical and a bioprosthetic valve may influence the timing of surgery.
In general, mechanical prosthetic valves are preferred because of their better long-term reliability. Bioprosthetic valves can be chosen when valve longevity is not an issue or when patients want to try to avoid anticoagulation therapy. The latter would apply mainly to young women with normal sinus rhythm who want to become pregnant. They will be much easier to treat without anticoagulation therapy—a feasible goal with a bioprosthetic valve. These patients must realize, however, that this valve will need to be replaced in approximately 10–15 years, as a result of deterioration. This should give these patients time for several pregnancies, if they so desire.
Generally, patients with a mechanical valve and no contraindications to anticoagulation therapy should be treated with such agents. The incidence of systemic emboli is higher with mitral than with aortic prosthetic valves. Without anticoagulation, there is a 1–3% per year chance of systemic emboli with a bioprosthetic valve in the mitral position, so aspirin therapy is recommended for patients with bioprosthetic valves. The use of warfarin for 3 months after bioprosthetic mitral valve replacement is sometimes done until the endothelium grows over the sewing ring, reducing the risk of thrombus development. Patients with other risks for thrombus formation, such as atrial fibrillation, should also receive warfarin.
Percutaneous approaches to mitral valve repair and replacement are developing rapidly. One approach is to put a clip at the tip of the mitral leaflets creating a double orifice valve similar to the surgical Alfieri technique. Initial studies suggest that it may be ideal for patients with severe functional mitral regurgitation due to dilated cardiomyopathy, where surgical risk is high. Another is to deliver an annuloplasty ring percutaneously, reducing the annulus size. Finally, stent-mounted tissue valves can be deployed in the mitral area. At this time, these devices have not been released for routine use in the United States, but they hold great promise for the future.
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Feldman T, et al. Percutaneous repair or surgery for mitral regurgitation. N Engl J Med
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Webb JG, et al. Percutaneous transvenous mitral annuloplasty: initial human experience with device implantation in the coronary sinus. Circulation