Calcium responsiveness in canine pacing-induced heart failure.

The specific lesion(s) and potential compensatory alterations of excitation-contraction coupling in heart failure are not clear in detail. We therefore subjected five dogs to 2-5 weeks of rapid ventricular pacing until heart failure developed. Data obtained from these five dogs with pacing-induced heart failure were compared to data from six healthy controls. Under anesthesia, in situ steady state responses of regional contractile function to intracoronary calcium infusion were established. Maximal calcium-activated regional contractile function in dogs with heart failure was 46% less than in controls; calcium sensitivity was unchanged [pCa50 2.55+/-0.31 v 2.82+/-0.17 (+/-s.d.)]. Our data point to a decrease in maximal calcium-activated force and an unchanged calcium sensitivity if an unchanged calcium transient is assumed, or a compensatory increase in calcium sensitivity of failing myocardium if a decreased calcium transient is assumed.