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European Heart Journal 1991 12(Supplement B):19-21; doi:10.1093/eurheartj/12.suppl_B.19
Copyright © 1991 by the European Society of Cardiology.
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© 1991 The European Society of Cardiology

Left ventricular function in acute non-ischaemic mitral regurgitation

R. M. Jeresaty

University of Connecticut School of Medicine, Section of Cardiology, Saint Francis Hospital and Medical Center Hartford Connecticut, U.S.A.

Correspondence: Robert M. Jeresaty, MD, Chief. Seaion of Cardiology. Saint Francis Hospital and Medical Center, 114 Woodland Street, Hartford. Connecticut 06105-1299 U.S.A.

Acute nonischaemic mitral regurgitation (MR) has recently generated considerable interest because of its causal relationship to ruptured chordae tendineae and infective endocarditis, advances in its diagnosis by echo Doppler studies, and its management by afterload reduction and reconstructive surgery. It is fundamentally different from chronic MR because the previously normal, unprepared left ventricle (LV) and lefi atrium (LA) confront a sudden dramatic increase in volume. As the normal-sized left atrium suddently receives a marked regurgitant flow, its pressure rises and is transmitted into the pulmonary capillaries causing pulmonary congestion and oedema. At onset, the LV function is usually well preserved and the pulmonary oederna does not reflect LV failure. In acute MR, the LV empties into the left atrium, thus reducing its radius and its systolic pressure, resulting in a decline in wall tension according to Laplace's law. With a reduction in LV wall tension, there is a marked increme in contractile shortening with marked increase in total LV output. The left ventricle may fail early in acute severe MR because it is forced to clilate rapidly before hypertrophy can occur, whereas in chronic MR both the LV diastolic volume and mass increme proportionately. With chronic persistence of MR, LV dysfunction and failure occur as a manifestation of the ‘cardiomyopathy of overload’[1]. Fortunately because of the low energy cost per unit of work in shortening, m opposed to that used for tension development, there is only a slight increase in myocardial oxygen consumption in acute MR. In patients with LV failure secondary to acute MR, the ejection fraction may be only slightly decremed. The end-systolic dimension is more useful as a predictor of LV function than the ejection fraction. In the management of acute MR, afterload reduction by vasodilators and intra-aortic balloon pump is extremely effective by reducing the impedance to LV ejection, the regurgitant orifice and the regurgitant fraction.

Key Words: Acute mitral regurgitation • ventricular function


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