European Heart Journal (1991) 12 (Supplement B), 66-69
Left ventricular function in rheumatic mitral stenosis W.
GAASCH AND E.
Department of Medicine (Cardiology), The Medical Center of Central Massachusetts/Memorial, Worcester, Massachusetts, U.S.A.
KEY WORDS: Left ventricular function, left ventricular volume, mitral stenosis, rheumatic heart disease. Haemodynamic factors contributing to clinical disability in patients with rheumatic mitral stenosis have been under discussion and investigation for decades. Prior to the development of left heart catheterization, a low cardiac output in the presence of little or no pulmonary hypertension was taken as evidence for a myocardial "insufficiency'. With the use of left heart catheterization, it was possible to exclude the presence of coronary artery disease and to assess directly the size and function of the left ventricle. Such studies indicate a tendency toward low-normal left ventricular end-diastolic volumes and low-normal ejection fractions. Modest reductions in the ejection fraction may be due to: (1) a restriction or tethering of posterobasal myocardium by the scarred mitral apparatus, or (2) abnormal interventricular septal motion related to right ventricular overload and unequal filling of the two ventricles. These and other factors, such as limited LV distensibility and variable diastolic suction, may affect ventricular function in rheumatic mitral stenosis. Thus, left ventricular dysfunction can generally be explained without implicating a rheumatic myocardial factor. Introduction
Regional wall motion abnormalities With the development of left heart catheterization techniques, it became possible to assess directly the size and function of the left ventricle and to evaluate regional function in a quantitative fashion. Thus, many investigators report a modest reduction in the LV ejection fraction in patients with mitral stenosis'3"7'; some report regional wall motion abnormalities in such patients'31. Most of these observations are relatively non-specific, since coronary or other associated disease could contribute to ventricular dysfunction in patients with mitral stenosis. For this reason it is unlikely that any single explanation or unifying hypothesis would apply in an individual patient. Therefore, the emphasis in this review will be on two relatively well defined abnormalities of LV function: (1) abnormal myocardial function near the base of the LV due to a restriction or tethering effect of the scarred, calcified, and immobile mitral apparatus, and (2) abnormalities of interventricular septal motion due to alterations in the relative size and function of the right and left ventricles. TETHERING EFFECT OF THE MITRAL APPARATUS
Correspondence: William H. Gaasch, MD, Chief of Cardiology, The Med Center/Memorial, 119 Belmont St, Worcester, MA 01605, U.S.A.
0195-668X/91/0B0066 + 04 $03.00/0
Using a quantitative angiographic analysis of LV function Holtzer et al.m described generalized © 1991 The Europeae Society of
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Haemodynamic factors contributing to clinical disability in patients with rheumatic mitral stenosis have been under discussion and investigation for decades, but there is still little agreement as to the frequency and significance of depressed left ventricular (LV) myocardial function in such patients. Other factors being equal, circulatory dysfunction in rheumatic mitral stenosis may be due to the mechanical obstruction imposed by the stenotic valve or to depressed function of the LV myocardium. Prior to 1950, it was perhaps relatively unimportant to attempt a separation of the independent contributions of each of these two factors, but with the development of surgical procedures which relieve the mechanical obstruction, it became necessary to identify those patients whose disability was due to myocardial dysfunction. Such patients would obviously not be candidates for mitral valvotomy. Stimulated in part by the development of surgical procedures that could relieve the mechanical obstruction, Harvey et a/.1", Fleming and Wood'21, and others assessed the relative contributions of mitral obstruction and myocardial 'insufficiency' to circulatory dysfunction and they concluded that myocardial insufficiency was the predominant lesion in some patients with rheumatic mitral stenosis. Harvey et al. emphasized a low-normal cardiac output with little or no pulmonary hypertension and a subnormal response in cardiac output to exercise; almost 20% of their patients were felt to have myocardial insufficiency, presumably due to rheumatic carditis. Fleming and Wood also described a low cardiac output and normal to moderate pulmonary hypertension in patients in whom mechanical obstruction of the valve did not
seem to be of sufficient severity to explain disabling symptoms. They found an incidence of only 3% and suggested that atrial fibrillation might contribute to this syndrome. These early studies were based primarily on clinical grounds and right heart catheterization data, but even with modern methodologies it appears that myocardial dysfunction may contribute to clinical disability in some patients with mitral stenosis.
LVF in rheumatics MS
Figure 1 Left ventricular cineangiogram from a patient with rheumatic mitral stenosis (right anterior oblique projection). The end-diastolic frame is on the left and the end-systolic frame on the right. A distortion and hypokinesis of the posterobasal region is indicated by brackets. (Adapted from Heller SJ and Carleton RA. Abnormal left ventricular contraction in patients with mitral stenosis. Circulation 1970; 42: 1099-110.)
THE RIGHT VENTRICULAR EFFECT
Systolic abnormalities of septal motion may be present in a variety of disorders; in mitral stenosis with pulmonary hypertension and right ventricular
regional dysfunction contrasts to the high-normal shortening observed toward the apex. (Adapted from Heraandez-Lattuf PR, Quinones MA, Gaasch WH. Usefulness and limitations of circumferential fibre shortening velocity in evaluating segmental disorders of left ventricular contraction. Br Heart J 1974; 36: 1167-74.).
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contraction abnormalities in several patients with overload, the septum may be hypertrophied, hypokiisolated mitral stenosis; two showed wall motion netic, or even frankly dyskinetic. Although the exact abnormalities confined to basilar segments. They mechanisms underlying abnormal septal motions are suggested that such regional dysfunction could be due unknown, the combination of right ventricular to the residual effects of rheumatic myocarditis (i.e. a enlargement and paradoxical septal motion are useful myocardial factor). Heller and Carleton181 and Grant"1 diagnostic features of right ventricular volume suggested another possibility; they postulated that overload. immobilization and atrophy of the posterobasilar wall In many patients with mitral stenosis a brief might be related to thickening of the mitral apparatus posterior or leftward motion of the interventricular and a tethering and restriction of the adjacent septum is prominent in early diastole, just after the myocardium; this could cause segmental or regional mitral valve opens (Fig. 3). This exaggerated dysfunction without a rheumatic myocardial factor per displacement of the septum is due to unequal filling of se (Fig. 1). The notion that a tethering effect causes or the two ventricles'121. Mitral stenosis restricts filling of contributes to basilar wall motion abnormalities is supported by the observations of reduced wall motion in the area adjacent to prosthetic mitral valves and annuloplasty rings and that LV function is better in patients with flexible annuloplasty rings than in those with stiff rings"01. LV cineangiographic techniques provide quantitative information on regional myocardial function. An example of such an analysis is shown in Fig. 2. The patient had critical mitral stenosis (valve area = 0-8 cm2) with moderate calcification of the mitral annulus, leaflets, and chordae; the LV ejection fraction was normal'11'. The mean circumferential fibre base apex shortening rate (mean VCF) was reduced at the base A B D (chords A and B adjacent to the immobile mitral annulus) while it was slightly increased at the mid Figure 2 Mean velocity of circumferential fibre shortening ventricular level (chord C) and toward the apex (VCT) in several regions of the left ventricle from base (A) to (chord D). These data indicating a regional apex (D). The data are from eight normal hearts (mean ± SD) 2 dysfunction correspond with the notion that the and one with mitral stenosis. The mitral valve area was 0-8 cm diseased mitral apparatus limits motion of the and the left ventricular ejection fraction 72%. In this example, VCT was abnormal in the basilar segments (