Contractile behaviour and intracellular calcium during afterloaded contraction in mitral valve disease

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.