Uncoupling between left ventricular contractility and relaxation after direct-current counter shocks

Abstract

Left ventricular (LV) contractility and relaxation are physiologically coupled on the basis of intracellular calcium cycling. The relation has been reported to be unique. However, this may not be always true if relaxation is predominantly impaired. Direct current counter (DC) shocks develop myocardial interstitial edema, inducing diastolic heart failure. Thus, we hypothesized that LV contractility-relaxation coupling would be altered in an experimental model of diastolic dysfunction by DC shocks. The relation between Emax (LV contractility index) and the time constant of LV pressure decay (tau) was evaluated in isovolumic contraction of seven isolated, blood perfused dog hearts. There existed a hyperbolic relation between Emax and tau in control (= pre-DC) hearts. After the application of five consecutive 80 J DC shocks, Emax was unchanged (from 4.6 ± 1.0 to 5.2 ± 0.8 mmHg · ml⁻¹· 100 g) but tau was markedly prolonged (from 36 ± 12 to 74 ± 38 ms, P < 0.01). Thus, DC shocks induced a strikingly upward displacement of the hyperbolic curve compared with the control. The slope of the linear relation between Emax and the reciprocal of tau (= a relaxation velocity index normalized for contractility) significantly decreased after DC shocks. We conclude that the coupling between LV contractility and relaxation is not unique, but can be altered acutely by DC shocks. A dissociation of contractility-relaxation coupling may be of help for distinguishing diastolic heart failure and exploring its pathogenesis.