Thorac Cardiovasc Surg 1997; 45(6): 280-286
DOI: 10.1055/s-2007-1013750
Original Cardiovascular

© Georg Thieme Verlag Stuttgart · New York

Contractile Behaviour and Intracellular Calcium During After loaded Contraction in Mitral Valve Disease

A. Bonz, C. F. Vahl, S. Hagl
  • Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany
Further Information

Publication History

1997

Publication Date:
19 March 2008 (online)

Abstract

It was the aim of the present study to analyze left-ventricular contractile behaviour (force development, shortening) and intracellular calcium handling using afterloaded contractions of papillary muscle fibres from patients operated upon for mitral valve stenosis (MVS, n = 12) or mitral valve incompetence (MVI,n = 15). Isometric force development and passive resting tension at Lmax were similar in MVI and MVS (n.s.). Isotonic shortening amplitudes were reduced in MVI (p < 0.0001) compared to MVS. The peak intracellular calcium transient (ICT) preceeded the maximum force- and shortening amplitude in MVI and MVS. The amplitude of the ICT rose with decreasing afterload, became broader during shortening and presented a prolongation of the diastolic decay. Those differences were much more pronounced in MVI. The calcium-time integral (CTI) at minimal load (isotonic contraction) was 119 ± 5% in MVS and 165 ± 14% in MVI (p < 0.0001). The data reveal a severe diastolic calcium overload during shortening in left-ventricular MVI myocardium. An increased dissociation rate of calcium from the contractile proteins during shortening, a depressed calcium re-uptake into the sarcoplasmic reticulum during shortening, or altered mechanosensitive ion channels in MVI may be involved.

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