European Heart Journal (1991) 12 {Supplement B), 48-51

Left ventricular function after surgical correction of chronic mitral regurgitation W.

H.

GAASCH AND M.

R.

ZILE

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

KEY WORDS: Left ventricular afterload, left ventricular function, left ventricular wall stress, mitral regurgitation, mitral valve replacement, mitral valve repair.

Introduction It is generally believed that the presence of chronic mitral regurgitation (MR) creates a systolic 'unloading' effect by providing a low-resistance ejection into the left atrium. This unloading is thought to increase the left ventricular (LV) ejection fraction (EF) and in this fashion to mask a reduced LV contractile state. Similarly, mitral valve replacement (MVR), by removing the low-resistance leak into the left atrium, has been thought to increase the systolic load and thereby cause a reduced EF. While this may be true in the early postoperative period, several studies indicate that these concepts do not always apply in the late postoperative period. Thus, the purpose of this article is to review the changes in LV afterload (i.e. systolic wall stress) before and after surgical correction of chronic MR and to address two questions. First, is systolic wall stress reduced in chronic MR? Second, is an increase in systolic wall stress responsible for the decreased EF that is seen after MVR? Finally, stress-shortening relations will be assessed and a unified hypothesis regarding pre and postoperative LV function in chronic MR will be developed. Surgical correction of chronic MR usually results in a substantial reduction in LV volume. Patients with compensated LV function may achieve a normal Correspondence: William H. Gaasch, MD, Chief of Cardiology, The Med Center/Memorial, 119 Belmont St, Worcester, MA 01605, U.S.A.

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chamber volume, while those with decompensated ventricles frequently exhibit a persistent LV enlargement, despite successful correction of the regurgitant lesion1'1. These distinctly different responses to surgery dictate that any assessment of postoperative changes in LV function must consider the baseline functional state of the ventricle; compensated and decompensated ventricles must be assessed separately. In addition, LV function should be assessed and evaluated with normalized indices that allow comparisons among hearts of different size1"1. LV systolic stress in chronic MR Using non-invasive (echocardiographic) measurements of LV volume, mass, and function Zile et al.[t] found that meridional wall stresses were not reduced in patients with chronic MR (Table 1). Indeed, they found a tendency for peak systolic stress to be increased; end-systolic stress was normal in compensated MR, but it was increased substantially in decompensated MR. Corin et a/."1 confirmed these observations with haemodynamic and angiographic (cardiac catheterization) measurements. These investigators calculated circumferential wall stresses and found a modest increase in peak systolic stress in compensated and decompensated hearts; end-systolic wall stress was especially high in decompensated MR. Wisenbaugh et a/.'6' similarly noted normal values for © 1991 The European Society of Cardiology

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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, mitral 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 often seen postoperatively. These concepts have never been confirmed in patients with chronic MR. Accordingly, we evaluated systolic wall stress before and after MVR and assessed stress-shortening 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 contribute to a postoperative decline in myocardial fibre shortening and a lower EF. By contrast, patients with compensated MR exhibit a decline in systolic wall stress after MVR; despite this postoperative decline in afterload, fibre shortening falls. This indicates that the fall in fibre shortening after MVR is not the result of increased systolic loading. In such patients, the valve replacement (with loss of integrity of papillary muscles 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.

Left ventricular EF after surgical correction of chronic MR

49

Table 1 Left ventricular systolic wall stress in chronic mitral regurgitation

Meridional stress (4) (dynes . 103 . cm"2)

Normal MR (group A) Before MVR After MVR MR (group B) Before MVR After MVR

Circumferential stress (5) (dynes . 103 . cm"2)

Peak-systolic

End-systolic

Peak-systolic

' End-systolic

209 ±39

65 ±11

348±44

162 ± 19

244 ± 52' 187 ±28

64 ±16 63 ±24

391 ±41*

194 ± 27*

232 ±48 236±44

114 ±40* 150 ± 32*

401± 33*

265 ± 37'

Abbreviations: MR (group A) = mitral regurgitation with compensated LV function. MR (group B) = mitral regurgitation with decompensated LV function. All values are mean ±SD. * =p

Left ventricular function after surgical correction of chronic mitral regurgitation.

It is generally believed that mitral regurgitation (MR) creates a systolic 'unloading' effect by providing a low-resistance ejection into the left atr...
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