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Patients With Asymptomatic Managing Chronic Mitral Regurgitation* William H. Gaasch, MD; Roy M. John, MBBS, PhD; and Gerard P. Aurigemma, MD (CHEST 1995; 108:842-47) LV=left ventricular; NYHA=New York Heart Association Key words: atrial enlargement; atrial fibrillation; cardioversion; left ventricular function; mitral regurgitation; mitral valve repair; vasodilator therapy /Clinicians are generally reluctant to consider surgi^^ cal correction of mitral regurgitation in an asymp¬ tomatic patient. With nothing to gain in the way of symptomatic improvement, such early surgery exposes the patient to perioperative morbidity and mortality and the long-term complications of a prosthetic valve. waiting for the patient to ex¬ Unfortunately, however, or exercise intolerance may allow perience dyspnea time for the development of irreversible depression of left ventricular (LV) function. If this occurs, the patient may be deprived of the full benefit of corrective sur¬ gery. For this reason, surgery might be considered in an asymptomatic patient who appears to be develop¬ ing LV dysfunction. Recognizing the complications of prosthetic valves, in patients with depressed LV function or especially atrial fibrillation or both, surgical repair of the native valve is gaining wide acceptance. Repair procedures for the maintenance of papillary muscle and provide annular continuity; thus, the functional components of the subvalvular apparatus are preserved and postop¬ erative ventricular function is better than that seen af¬ replacement. Moreover, prosthetic valve-re¬ lated complications are eliminated and long-term an¬ is not necessary. For these reasons, the ticoagulation decision to proceed with surgical correction, especially in an asymptomatic patient, is somewhat easier if a repair procedure can be substituted for a valve re¬ ter valve placement. It could also be argued that corrective surgery should be considered before the development of irre¬ versible changes in atrial size or rhythm, even in a pa- Department of Medicine (Cardiology), the Lahey Hitchcock Medical Center, Burlington, Mass; and the University of Massachusetts Medical School, Worcester. Reprint requests: Dr. Gaasch, Director, Cardiovascular Research, Lahey Hitchcock Medical Center, 41 Mall Road, Burlington, MA *From the 01805 tient with little or no symptoms. The rationale for this of the is based on occurrence of thromboembolism in patients who ex¬ frequent hibit persistent postoperative atrial enlargement and atrial fibrillation. Such complications might be avoided if surgery were performed at an earlier stage. For almost 2 decades, vasodilator therapy has been known to affect favorably the hemodynamics of mitral regurgitation. While widely accepted, this notion is on acute or short-term interventions with largely basedvasodilators. there is only parenteralevidence that Unfortunately, vasodilator therapy long-term meager can be useful in the asymptomatic patient. Obviously such therapy, if it could delay the development of symptoms or LV dysfunction and the need for surgery, would be desirable. Based on knowledge of pathophysiology and natural history, the and importance of LV dysfunction and atrial the therapeutic potential of chronic fibrillation, vasodilator therapy, it is possible to develop a rationale with approach knowledge for the management of asymptomatic chronic mitral regurgitation. patients Pathophysiology of Mitral Regurgitation Mitral regurgitation burdens the left ventricle with excessive volume load that leads to a series of com¬ pensatory myocardial and circulatory adjustments.1-3 These adjustments vary over the prolonged course of the disorder, such that the changes that are operative in acute or subacute mitral regurgitation are eventually by other compensatory mechanisms. With replaced acute regurgitation and volume overload, the ventricle uses its preload reserve and the total stroke volume increases via the Frank-Starling mechanism. In addi¬ tion, the low resistance runoff into the left atrium contributes to an increased ejection fraction and a de¬ crease in systolic volume; according to the law of Laplace, systolic load (ie, afterload) declines. Thus, in acute mitral regurgitation, an increased ejection frac¬ tion and increased total stroke volume occurs as a re¬ sult of an increase in LV preload and a decrease in af¬ terload. The major change that occurs during the evolution from acute to chronic mitral regurgitation is an en¬ new steady state largement of the ventricle. As thischamber of acute the small hyperkinetic develops, an 842 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21720/ on 05/14/2017 Reviews mitral regurgitation is converted into a large compliant chamber that is well suited to deliver a large stroke volume. This comes about through a rearrangement of myocardial fibers in association with the addition of new sarcomeres and the development of eccentric LV As a result, preload at the sarcomere level hypertrophy. returns toward normal. Moreover, the systolic un¬ loadingis that is characteristic of acute mitral regurgita¬ tion gradually replaced by normal systolic wall stresses. Thus, the enhanced total stroke volume, seen in chronic compensated mitral regurgitation, is "me¬ diated through a normal performance of each unit of an enlarged circumference."6 At this time, LV con¬ tractility, loading conditions, and ejection fraction re¬ main in the range of normal; stroke volume is high as a result of the large end-diastolic volume. An enlarged atrium is also seen, but rhythm disturbances compliant are uncommon. During this compensated phase of the disease, most patients remain asymptomatic and sur¬ gery should be postponed. A most elusive and poorly understood aspect of the of mitral regurgitation is the nature of pathophysiology the transition from the compensated to a decompensated state. Such a change may occur as a consequence of progressive increments in the regurgitant volume or chamber size or both. This decompensated state is characterized by substantial and progressive ventricu¬ lar enlargement with high LV diastolic pressure, increased systolic wall stress, and a decline in the ejection fraction; the fall in ejection fraction occurs as a consequence of a depressed contractile state and af¬ terload excess. Progressive atrial enlargement and atrial arrhythmias are seen, pulmonary hypertension and the patient becomes symptomatic. At develops, late this (ie, decompensated) stage, there may be irre¬ versible depression of ventricular and atrial function; thus, it may be too late to expect an optimal result from corrective surgery. Ventricular Enlargement and Dysfunction In the transition from the compensated to decom¬ state, the ventricle progressively enlarges and pensatedfunction In spite of this, the ejection systolic tends todeclines. remain within the broad range of fraction "normal." Some patients experience fatigue, a limited exercise tolerance, or even dyspnea during this transi¬ tion; in such patients, the decision to proceed with surgery is relatively easy and the results are generally good. On occasion, a patient may proceed through the transition and show evidence of LV dysfunction with minimal or no symptoms. If an optimal response to surgery is the goal, it is important to identify such a patient before the development ofirreversible changes in ventricular function. This can be achieved by con¬ ventricle and sidering the markers of afordecompensated of the the identification developing guidelines transitional stage of chronic mitral regurgitation. Schuler et al7 studied the temporal changes in left ventricular size and function before and after mitral valve replacement in 16 patients with chronic mitral corrective surgery was regurgitation. In 12 of the 16,LV associated with a decrease in chamber size and a regression of myocardial hypertrophy; the significantfraction fell but remained within the normal ejection range. In four patients, LV function progressively de¬ teriorated after surgery. These two groups exhibited different preoperative echocardiographic in¬ distinctly dices of ventricular size and function; the four patients with a poor response to valve replacement could be identified (preoperative data) by an end-diastolic di¬ mension exceeding 70 mm, an end-systolic dimension exceeding 50 mm, and a low-normal or depressed ejection fraction. Zile et al8 made similar observations in 20 patients. After surgery, LV end-diastolic dimension fell to nor¬ mal in 16 of the 20 patients; these patients exhibited a dramatic reduction in LV mass and gratifying improve¬ ment in symptoms. In four patients, LV end-diastolic dimension and mass were unchanged after surgery; all four remained symptomatic despite continued medical of Schuler et al,7 the patients therapy. As in the studies with a poor surgical result exhibited larger preopera¬ tive end-diastolic and end-systolic chamber dimen¬ sions than those with a good response. An end-systolic dimension exceeding 45 to 50 mm had a high predic¬ tive value for identifying patients that were destined to have a poor surgical result. Wisenbaugh et al9 later confirmed a poor outcome in patients with an enddimension exceeding this range. These dimen¬ systolic sions translate into an end-systolic volume of 55 to 65 mL/m2, which is in close agreement with the data re¬ byal.12Borow et al,10 Carabello et al,11 and Craw¬ ported et ford Patients who exhibit one or more of these markers of a decompensated ventricle are at high risk of persistent postoperative LV enlargement, depressed postoperative ventricular function, and a poor or sub- result. While these considerations do optimal clinical not identify the optimal time for mitral valve replace¬ ment 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. Thus, asymptomatic patients with only modest LV enlargement and normal systolic function (ie, compensated mitral regurgitation) can be treated. By contrast, those with evi¬ conservatively dence of a decompensated ventricle would have little to gain by postponing surgery, even though such patients may not expect an optimal surgical result. In therefore, corrective surgery should be per¬ principle, formed during the transition from a compensated to decompensated state. CHEST /108 / 3 / SEPTEMBER, 1995 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21720/ on 05/14/2017 843 Guidelines for the identification of patients who are entering the transitional stage are shown in Table 1. The compensated, transitional, and decompensated stages are defined on the basis of published (preoper¬ ative) data, which distinguish patients who are most those who will likely to havea a suboptimal result from result. Thus, defini¬ experience satisfactory surgical tion of these stages relies on measurements of LV chamber size at end-diastole and end-systole and the ejection fraction; the stages are not based on semiquantitative assessments of the severity of regurgita¬ tion that are obtained from cineangiography or Dop¬ echocardiography. Recognizing that these stages pler and their prognostic implications have not been sta¬ tistically validated in a prospective fashion, they should be used only as general guidelines in a decision anal¬ ysis that includes other clinical data including patient preferences. Atrial Enlargement and Fibrillation Chronic mitral regurgitation often is complicated by the development of atrial fibrillation. If the ventricle is the rate is not excessive, such compensated and notice patients merely palpitations. Except for the in¬ creased risk of stroke and on occasion an increase in the regurgitant volume, there is generally little or no clin¬ ical disability. Certainly, there is a role for direct cur¬ rent cardioversion and antiarrhythmic therapy in such patients. It can be argued, however, that surgery should be performed before atrial fibrillation is per¬ sistent or resistant to cardioversion. This notion is based on the observation that persistent atrial fibrilla¬ tion after corrective surgery places the patient at especially high risk for atrial thrombus and arterial embolism. For this reason, it becomes important to identify factors that influence the maintenance of sinus after corrective surgery. rhythm Betriu et al13 reported their experience with atrial fibrillation after valve replacement surgery in 685 pa¬ tients. Atrial fibrillation was present before surgery in 148 of the 589 survivors. Of the 148, most (n=94) un¬ derwent mitral valve replacement; aortic valve replace¬ ment was performed in 12 and multiple valves were replaced in 42. Within 6 months of surgery, 52 patients converted to sinus rhythm; 38 converted spontane¬ ously, and 14 required cardioversion. The remaining 96 patients remained in or reverted to atrial fibrillation after an initially successful cardioversion. The preop¬ erative variables that were associated with persistence of atrial fibrillation after surgery were a prolonged duration of the arrhythmia (ie, exceeding 1 year) and left atrial enlargement. When preoperative left atrial dimension (echocardiography) was normal, 85% of patients returned to sinus rhythm after surgery; by contrast, when the left atrial size exceeded 50 mm, less than half of the patients returned to sinus rhythm. Table 1.Left Ventricular Size and Function in the Three Stages of Chronic Mitral Regurgitation Compensated Cardiac catheterization End-diastolic Transitional <110 >160 120-150 End-systolic <45 >60 50-55 Ejection >60 <50 53-57 <63 >70 65-68 <42 44-45 >47 >34 <30 31-32 Decompensated volume, mL/m2 volume, mL/m2 fraction, % Echocardiography End-diastolic dimension, mm End-systolic dimension, mm Fractional shortening, % et al14 came to similar conclusions in a Flugelman with mitral stenosis and atrial fi¬ of 40 patients group brillation. After corrective surgery and cardioversion, sinus rhythm was maintained in 24 patients while atrial fibrillation returned in 16. Those that maintained a normal sinus rhythm were younger, had a shorter du¬ ration of symptoms, and had a smaller left atrium when with that of the group with persistent atrial compared fibrillation. These authors also suggested that the functional state of the left ventricle influenced the with which sinus rhythm could be restored frequency and maintained. Reed et al15 assessed preoperative clinical, echocar¬ and hemodynamic data in 176 symptom¬ diographic, atic patients who underwent mitral valve replacement for chronic mitral regurgitation. Their goal was to de¬ termine preoperative predictors of postoperative car¬ diac mortality. The atrial size was significantly smaller in those that survived compared with that in nonsur¬ vivors (47±6 vs 52±5 cm). Although this study does not address the issue of restoration of sinus rhythm after surgery, these and other data support the concept of a malefic effect of atrial fibrillation after corrective surgery. These studies and anecdotal clinical experience support the concept that if postoperative atrial fibril¬ lation and its complications are to be minimized or avoided, corrective surgery shouldbe consideredwithin months of the development of persistent atrial fibril¬ lation or before substantial atrial enlargement is present. This issue assumes its greatest importance in the patient with borderline indications for surgery. Atrial fibrillation is not necessarily an indication for surgery in an asymptomatic patient with compensated ventricular function, but the burden of this arrhythmia in a patient with borderline ventricular function might be used as an indication for surgery, especially if the risk of surgery is low and the valve appears to be ame¬ nable to repair. 844 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21720/ on 05/14/2017 Reviews Mitral Valve Replacement Vs Repair Mitral valve replacement with a mechanical or tissue prosthesis can provide remarkable clinical benefits in selected patients with mitral valve disease. Unfortu¬ nately, the early benefits of tissue valves tend to be neutralized by a gradual increase in the need for reoperation after 7 to 10 years; mechanical valves are more durable and they function satisfactorily for the lifetime of most patients. However, thromboembolic complications occur at the rate of 1 to 2% per year; when atrial fibrillation is present in a patient with a valve, this complication is approximately prosthetic twice as frequent. In patients receiving anticoagulants, occurs at the rate of 1 to clinically significant bleeding The such 2% per year. risk of thromboembolic and bleeding complications form the basis for the decision to proceed with surgery before atrial fibrillation is es¬ tablished. Other complications of mitral valve replace¬ ment include mechanical dysfunction, paravalvular leaks, and endocarditis; while rare, prosthetic valve endocarditis carries a 50% mortality. Prosthetic valves, therefore, are associated with major clinical complica¬ at of at least 3% occur the rate per year.16 Consideration of these issues, not to mention periop¬ erative morbidity and mortality, tempers any enthusi¬ asm for mitral valve replacement in asymptomatic pa¬ tions that tients. Mitral repair procedures are increasinglybeing used the treatment of mitral regurgitation. This trend developed in part to avoid the complications of pros¬ thetic valves. Another advantage of the repair proce¬ dure is that LV function is better maintained than af¬ ter valve replacement.2,5 The decline in LV ejection fraction that is almost always seen after mitral valve is primarily related to disruption of the replacement functional components of the subvalvular apparatus; chordal transection abolishes the continuity between muscles and annulus, and the ejection frac¬ papillary tion declines by an average often percentage units.117 To be sure, the postoperative ejection fraction is not after valve repair.18 Most studies, always preserved indicate that the ejection fraction remains however, after valve repair. Finally, perioperative unchanged mortality appears to be lower with repair than replace¬ in ment.17"20 Patients are selected for repair procedure on the basis of echocardiographic descriptions of valve dis¬ ease. Calcification and scarring of the leaflets and chordae or, on occasion, infection of the valve or an¬ nulus can preclude repair. When mitral prolapse is present and there is little or no calcification, experi¬ enced surgeons can repair the valve with an 80 to 90% success rate. Rheumatic mitral regurgitation can be less amenable to repair. Thus, factors determining the success of the procedure include a careful selection of patients and an experienced surgeon. Ifvalve repair is not possible, valve replacement with chordal preservation has distinct advantages over valve part of the replacement alone. Retention aof at leasteffect on LV subvalvular apparatus provides salutary seen when that is not and fraction geometry ejection the chordae are severed. Thus, postoperative ventric¬ ular function is similar to that seen with valve repair. Chordal preservation can be especially important in patients with decompensated mitral regurgitation in which case attempts should be made to avoid or min¬ imize a postoperative decline in ventricular function.21 Vasodilator Therapy provide a dra¬ Intravenous vasodilator therapy can matic hemodynamic improvement in patients with se¬ mitral regurgitation, especially those with con¬ re¬ gestive heart failure. Thus, sodium nitroprusside duces the regurgitant volume and pulmonary venous pressure while augmenting forward blood flow.22 Based on such observations, it would seem reasonable to use oral vasodilators in patients with mild to mod¬ erate mitral regurgitation who are not yet candidates for surgery. If a beneficial hemodynamic effect could be sustained over months or years, it might be possi¬ ble to delay the development of LV dysfunction or symptoms or both; surgery could also be postponed. Unfortunately, the efficacy of long-term oral vasodila¬ tor therapy in patients with mitral regurgitation, espe¬ those without symptoms, is not well-defined. cially Before reviewing the potential use of oral vasodila¬ tor therapy in patients with chronic mitral regurgita¬ tion, it is important to emphasize that the volume of regurgitant flow is determined hydraulically by the size of the regurgitant orifice and the magnitude and duration of the systolic pressure gradient across the valve. Recognizing that the pressure gradient across the valve is variable and that the regurgitant orifice area may change, it is possible to explain the effects of he¬ modynamic interventions and therapies on regurgitant volume.23"25 For example, venodilators and peptidyl dipeptidase A (angiotensin-converging enzyme) inhib¬ itors can be ofvalue in reducing mitral regurgitant flow in patients with ventricular enlargement and papillary muscle dysfunction; the beneficial effect is brought about by reducing ventricular size and the functional regurgitant orifice area. In some patients with mitral valve prolapse or hypertrophic cardiomyopathy, how¬ ever, venodilators may augment mitral regurgitant flow through an influence on ventricular size and mitral leaflet coaptation; a beta-blocker, by contrast, might have an opposite and beneficial effect. In patients with fixed-orifice mitral regurgitation (ie, those with rheu¬ matic or calcific disease), venodilation could produce a fall in pulmonary venous pressure in association with vere CHEST / 108 / 3 / SEPTEMBER, 1995 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21720/ on 05/14/2017 845 an increase in the regurgitant volume; this can occur if the fall in left atrial pressure were greater than the reduction in LV systolic pressure. By contrast, a pure reduction in LV systolic pressure would reduce mitral regurgitation, especially in the hypertensive patient. These considerations of the dynamic determinants of the mitral regurgitant volume are particularly relevant to any discussion of vasodilator therapy for patients with chronic mitral regurgitation. Schon et al26 studied the effect of a peptidyl dipep¬ tidase A inhibitor in 12 patients with chronic mitral regurgitation of mixed causes; nine of the 12 patients were symptomatic (New York Heart Association [NYHA] class 2-3). The LV size and function were evaluated in the baseline state and again after 1 year of (10 to 20 mg/d). Systemic arterial quinapril therapy from fell a mean of 140/84 to 117/75 mm Hg. pressure There was a reduction in regurgitant fraction and re¬ gurgitant volume; LV end-diastolic volume fell from 146 to 109 mL/m2. The ejection fraction and cardiac output did not change, but there was evidence of im¬ proved hemodynamics during exercise. The patients in this study were likely in the stage of transition from compensated to decompensated mitral regurgitation; most were symptomatic. Such patients are generally considered to be candidates for mitral valve replacement or repair, but based on the results of this study, it is possible that surgery could be post¬ poned while attempting a trial of intense medical therapy. Certainly, vasodilator therapy is an appropri¬ ate choice in a symptomatic patient who did not wish to undergo surgery. This study, however, does not ad¬ dress of the management asymptomatic patient with the effects of capto¬ Wisenbaugh et al2' compared in to 32 (25 tid) pril mg placebo patients with chronic chronic mitral regurgitation. mitral regurgitation. The patients were largely asymp¬ (NYHA class I-II) and most had rheumatic disease. After 6 months, there was no difference in systemic arterial pressure, LV end-diastolic volume, end-systolic volume, or ejection fraction between the two groups. The authors concluded that the adminis¬ tration of captopril had "no effect on LV size or per¬ formance in patients with severe mitral regurgitation but mild or no symptoms." Several differences in these two studies may be re¬ sponsible for the disparate results. First, Wisenbaugh tomatic et al27 performed a randomized, double-blind, place¬ bo-controlled study, while Schon et al,26 did not. Sec¬ ond, Schon et al26 treated patients that were more symptomatic and had slightly larger ventricles than those treated by Wisenbaugh et al.27 Third, the patients of Schon et al26 exhibited higher baseline ar¬ terial pressures that fell significantly during the ad¬ ministration of quinapril. By contrast, the patients of Wisenbaugh et al27 had lower arterial pressure that did respond to captopril. Other differences, such as age, gender, concomitant medical therapy, and cause of the not mitral regurgitation, also may have contributed the different results of these two studies. Vasodilator therapy provides the most benefit in patients with the largest hearts, the poorest systolic function, and the most disabling symptoms. For ex¬ ample, hydralazine can produce substantial symptom¬ atic and hemodynamic improvement in patients who are in NYHA functional class 2-4.28 By contrast, there was no significant change in LV size or function in the NYHA class I-II patients reported by Wisenbaugh et al.27 The patients reported by Schon et al26 lie some¬ where between these two extremes. Therefore, al¬ is possible that vasodilator therapy might thoughtheit onset or LV dysfunction, a sal¬ delay effect of of symptoms vasodilator utary long-term therapy in asymp¬ tomatic patients with compensated mitral regurgita¬ tion remains to be proven. to Conclusion with normal LV systolic modest chamber (ie, only enlargement are of chronic mitral compensated stage regurgitation) not candidates for corrective surgery. In the absence of systemic arterial hypertension, there is no evidence that vasodilator therapy has a salutary effect on the course of such patients. However, hypertensive pa¬ tients with mitral valve prolapse can be treated with a beta-blocker or perhaps a calcium channel blocker with the goal of reducing the arterial pressure while avoiding an increase in the degree of prolapse; those with rheumatic or coronary heart disease also may benefit from these agents or peptidyl dipeptidase A inhibitors. Whether or not vasodilators are used, serial and evaluation of exercise tolerance echocardiography and certainly endocarditis prophylaxis are appropriate. Patients who show progressive LV enlargement and thus appear to be in a stage of transition are generally to be candidates for corrective surgery, even thought if they are not yet symptomatic. A stronger argument for surgery, preferably valve repair, can be made if left atrial enlargement and atrial fibrillation also are present. If, because of patient preference or other consider¬ ation, conservative vasodilator therapy is selected, fre¬ Asymptomatic patients function and quent follow-up examinations are mandatory. Most patients develop exercise intolerance, dysp¬ before serious changes in ventricular fatigue function are present (ie, before the decompensated stage). Occasionally, however, an asymptomatic pa¬ tient presents with marked ventricular enlargement and mildly depressed ejection fraction. Although it may be too late to expect an optimal result, most such patients are candidates for surgery after a short period of intensive medical therapy that includes vasodilator nea, or agents. 846 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21720/ on 05/14/2017 Reviews rhythm after mitral valve surgery for mitral References 1 Gaasch WH, Levine HJ, Zile MR. Chronic aortic and mitral re¬ gurgitation: mechanical consequences ofthe lesion and the results of surgical correction. In: Gaasch WH, Levine HJ, eds. The ven¬ tricle. Boston: Martinus Nijhoff Publishing, 1985; 237 2 Carabello BA. Mitral valve disease. Curr Probl Cardiol 1993; 18:421-80 3 Gaasch WH, O'Rourke RA, Cohn LH, et al. Mitral valve disease. In: Schlant RC, Alexander RW, eds. Hurst's the heart. New York: McGraw-Hill, 1993; 1483 4 Ross J Jr, Sonnenblick EH, Taylor RR, et al. Diastolic geometry and sarcomere lengths in the chronically dilated canine left ven¬ tricle. Circ Res 1971; 28:49-61 5 Gaasch WH, Zile MR. Left ventricular function after surgical correction of chronic mitral regurgitation. Eur Heart J 1991; 12(B):48-51 6 Ross J Jr: Adaptations of the left ventricle to chronic volume overload. Circ Res 1974; 35(II):64-70 7 Schuler G, Peterson KL, Johnson A, et al. Temporal response of left ventricular performance to mitral valve surgery. 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Circu¬ lation 1995; 91:1022-28 Galloway AC, Colvin SB, Baumann FG, et al. Current concepts of mitral valve reconstruction for mitral insufficiency. Circulation 1988; 78:1087-98 Cohn LH. Surgery for mitral regurgitation. JAMA 1988; 260:2883-87 21 Rozich JD, Carabello BA, Usher BW, et al. Mitral valve replace¬ ment with and without chordal preservation in patients with chronic mitral regurgitation. Circulation 1992; 86:1718-26 Chatterjee K, Parmley WW, Swan HJC, et al. Beneficial effects of vasodilator agents in severe mitral regurgitation due to dysfunction of subvalvular apparatus. Circulation 1973; 48:684-90 23 Keren G, Katz S, Strom J, et al. Dynamic mitral regurgitation: an important determinant of the hemodynamic response to load al¬ terations and inotropic therapy in severe heart failure. Circulation 22 1989; 80:306-13 24 25 Jeang MK, Petrovich LJ. Adyanthaya AV, et al. Effects of isosorbide dinitrate on rheumatic and non-rheumatic mitral regurgita¬ tion. Texas Heart Institute J 1986; 13:453-57 Takenaka K, Sakamoto T, Amano W, et al. Effect of amylnitrite on mitral valve prolapse and mitral regurgitation: a transesoph¬ ageal echocardiographic study. Am J Noninvas Cardiol 1991; 5:257-61 26 Schon HR, Schroter G, Barthel P, et al. Quinapril therapy in pa¬ tients with chronic mitral regurgitation. J Heart Valve Dis 1994; 3:303-12 Wisenbaugh T, Sinovich V, Dullabh A, et al. Six month pilot study of captopril for mildly symptomatic severe isolated mitral and isolated aortic regurgitation. J Heart Valve Dis 1994; 3:197-204 28 Greenberg BH, DeMots H, Murphy E, et al. Arterial dilators in mitral regurgitation: effects on rest and exercise hemodynamics and long-term clinical follow up. Circulation 1982; 65:181-87 27 CHEST /108 / 3 / SEPTEMBER, 1995 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21720/ on 05/14/2017 847