A. Bonz et al., CONTRACTILE BEHAVIOR AND INTRACELLULAR CALCIUM DURING AFTERLOADED CONTRACTION IN MITRAL-VALVE DISEASE, The thoracic and cardiovascular surgeon, 45(6), 1997, pp. 280-286
It was the aim of the present study to analyze left-ventricular contra
ctile behaviour (force development, shortening) and intracellular calc
ium handling using afterloaded contractions of papillary muscle fibres
from patients operated upon for mitral valve stenosis (MVS, n = 12) o
r 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) com
pared to MVS. The peak intracellular calcium transient (ICT) preceeded
the maximum force-and shortening amplitude in MVI and MVS. The amplit
ude of the ICT rose with decreasing afterload, became broader during s
hortening and presented a prolongation of the diastolic decay. Those d
ifferences were much more pronounced in MVI. The calcium-time integral
(CTI) at minimal load (isotonic contraction) was 119 +/- 5% in MVS an
d 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 protei
ns during shortening, a depressed calcium re-uptake into the sarcoplas
mic reticulum during shortening, or altered mechanosensitive ion chann
els in MVI may be involved.