JACC Vol. 15, No. 3 March 1, 1990:564-5
Preservation of Left Ventricular Function in Patients With Mitral Regurgitation: A Realistic Goal For the Nineties* BLASE Charleston,
Reasons for poor outcome after valve replacement for mitral regurgitation. Currently, correction of mitral regurgitation has a higher operative mortality and a worse outcome than surgery for other valve lesions of the left side of the heart. Recent statistics indicate a survival rate of only 50%at 10 years after mitral valve replacement for mitral regurgitation (1,2). This is in sharp contrast to the results for correction of the other left-sided regurgitant lesion, aortic regurgitation, in which operative mortality has decreased from 11% in the 1960sand early 1970sto 6% in recent years, and 10 year survival rate approaches 80% (3,4). Correction of mitral regurgitation is attended by a poor outcome for several reasons: 1) concealed preoperative left ventricular dysfunction predisposes the patient to poor postoperative ventricular function; 2) creation of unfavorable preoperative geometry aggravates the potential for reduced postoperative ventricular performance; 3) frequent coexistence of coronary artery disease as a cause of mitral regurgitation increases the risk of an intraoperative or subsequent myocardial infarction; and 4) severance of chordae tendineae during mitral valve replacement has an adverse effect on ventricular function. Concealed left ventricular dysfunction. Mitral regurgitation affords an additional low pressure pathway for ejection of blood from the left ventricle. This pathway acts to reduce overall resistance to ejection, thereby reducing left ventricular afterload, while the volume overload resulting from the lesion increases preload. Reduced afterload and increased preload in mitral regurgitation augment ejection performance. Although much has been written about the need for
*Editorials published in Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. From the Cardiology Division and the Gazes Cardiac Research Institute, Medical University of South Carolina, Charleston, South Carolina and the Veterans Affairs Medical Center, Charleston. Address for reorints: Blase A. Carabello, MD, Cardiology Division, Medical University of South Carolina, 171Ashley Avenue, Charleston, South Carolina 29425. 01990 by the American College of Cardiology
a load-independent tool to assess clinical left ventricular function, load-dependent indexes of ejection performance are still by far the most commonly used tools to evaluate contractile function. In mitral regurgitation the favorable loading conditions cause these indexes to overestimate ventricular function. In this regard, ejection fraction in the range of 0.55 to 0.60 or echocardiographic shortening fraction in the range of 0.25 to 0.30 is frequently coexistent with significant muscle dysfunction (5,6). Unfavorablepreoperativegeometry and its effect on postoperative loading conditions. The left ventricle in mitral regurgitation dilates with little increase in wall thickness, resulting in a high left ventricular radius (r) to thickness (h) ration (r/h) (7). Afterload estimated by wall stress is derived from the Laplace relation, where wall stress = (pressure x r) + 2h. Thus, as r/h increases, stress increases, increasing afterload despite the unloading effect of the lesion itself. Wall stress is typically normal (rather than subnormal) in compensated mitral regurgitation and actually higher than normal in decompensated mitral regurgitation (8). In this setting of normal or increased afterload, mitral valve replacement or repair, which closes off the low impedance pathway into the left atrium, results in an immediate further increase in afterload (9). This increase in postoperative afterload together with decreased preload (as the volume overload is removed) invariably causes a decrease in ejection performance (6,lO). If some contractile reserve remains, the ventricle may be able to compensate for the imposition of these unfavorable loading conditions; in this case, the decrease in ejection performance is only mild. If all contractile reserve has been exhausted, the unfavorable loading canditions imposed by mitral valve replacement cause a precipitous, uncompensated decrease in ejection performance, which persists for years after mitral valve replacement (11). Coronary artery disease. Mitral regurgitation is the only left-sided valve lesion that can have coronary artery disease as its primary etiology. An estimated 25% of patients undergoing mitral valve repair or replacement have coronary disease as the primary etiologic factor (12,13). If the mitral regurgitation is coincidentally present with myocardial infarction or if myocardial infarction develops consequent to the coronary disease, ventricular function will be worse than that created by the valve lesion itself. Interactionof the valve apparatus in the ventricle: impact of the current study. Early studies by Rushmer et al. (14) and Lillihei et al. (15) demonstrated that the mitral valve apparatus and its attachments to the papillary muscles do more than prevent systolic mitral regurgitation. These attachments enhance long-axis contraction, “priming” the short axis of the left ventricle for its major role in ventricular ejection by causing a shape change toward spherical in early 0735-1097/90/$3.50
CARABELLO EDITORIAL COMMENT
JACC Vol. 15, No. 3 March 1, 1990:.564-5
systole. Thus, the interaction of the mitral valve with the papillary muscles enhances left ventricular performance. The current study in the Journal by Pitarys et al. (16) demonstrates the results of chordal severance on regional myocardial function. Radial shortening in the region of the insertion of the posteromedial papillary muscle decreased sharply after mitral valve replacement with chordal resection. Although this decrease did not produce a statistically significant decrease in global ventricular ejection performance, there was a correlation between postoperative ejection performance and regional dysfunction. Because considerable data indicate that global ejection fraction usually decreases after mitral valve replacement (6,10,1 l), it is likely that the relatively small sample size of the current study (16) is the source of its inability to detect such a decrease. The importance of the current study is not that it failed to detect this decrease, but rather that the regional dysfunction it demonstrated helps to explain why other studies did find a significant decline in ejection performance after mitral valve replacement. This clinical study (16) adds to previous experimental work (17), demonstrating a reduction in chamber elastance caused by the severance of the chordae tendineae. Conversely, clinical studies (1819) demonstrate that preservation of the chordae tendineae helps maintain ventricular performance. The difference in ventricular performance between operations in which the chordae tendineae were preserved versus severed can probably be explained; whereas unfavorable postoperative loading conditions are imposed in both valve repair and valve replacement, replacement with chordal severance further impairs the ventricle’s ability to overcome these unfavorable loading conditions and this results in reduced ejection performance. It is most likely the preservation of ventricular function combined with the obvious advantage of avoiding implantation of a prosthetic valve that explains valve repair has a substantially better result than does replacement (2,18-21). Conclusions. With knowledge gained about the interaction between the left ventricle in mitral regurgitation and the mitral valve apparatus, it is reasonable to expect that mortality can be reduced and long-term outcome for patients with mitral regurgitation improved in the 1990s. As cardiologists recognize the concealed left ventricular dysfunction in this disease and as surgeons improve the art of valve repair, better candidates for surgery will undergo a better operation. Even for those patients who have neglected their disease until ventricular dysfunction is advanced, repair may offer a reasonable outcome by helping to preserve function without causing further depression.
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