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European Heart Journal 1991 12(Supplement B):48-51; doi:10.1093/eurheartj/12.suppl_B.48
Copyright © 1991 by the European Society of Cardiology.
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© 1991 The European Society of Cardiology

Left ventricular function after surgical correction of chronic mitral regurgitation

W. H. Gaasch and M. R. Zile

Department of Medicine (Cardiology), The Medical Center of Massachusetts, Worcester, Massachusetts, USA, and the medical University of South Carolina South Carolina, U.S.A.

Correspondence: William H. gaasch, MD, Chef of Cardiology, The medcenter/memrial, 119 Belmont St, Worcester, MA 01605, U.S.A.

It is generally believed that mitral regurgitation (MR) creates a systolic ‘unloading’ effect by providing a low-resistance ejection into the left atrium; this is thought to increase the left ventricular ejection fraction (EF), and thus to mask a reduced contractile state. Similarly, rnitral valve replacement (MVR), by removing the low-resistance regurgitant leak, has been thought to increase left ventricular afterload (systolic wall stress) and thereby cause the decrease in EF that is ofren seen postoperatively. These concepts have never been confirmed in patients with chronic MR. Accordingly, we evaluated systolic wall stress before and afier MVR and assessed strmahortening relations in two groups of patients with chronic MR (those with compensated and those with decompensated MR).

Calculated values for circumferential and meridional wall stress were found to be normal or high in patients with chronic MR. This indicates that chronic MR is not associated with an unloading effect. In decompensated MR, systolic wall stress tends to increase after MVR; this can conm'bute to a postoperative decline in myocardial fibre shortening and a lower EF. By contrast, patienrs with compensated MR exhibit a decline in systolic wall stress after MVR; despite this postoperalive decline in afierload, fibre shortening falls. This indicates that the fallin fibre shortening after MVR is not the result of increased systolic loading. In such patients, the valve replacement (with loss of integrity of papillary murcles and chordae, and a tethering of posterobasal wall motion by the prosthesis) is most likely responsible for the postoperative decline in fibre shortening and EF.

Key Words: Left ventricular afterload • left ventricular function • left ventricular wall stress • mitral regurgitation • mitral valve replacement • mitral valve repair


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