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[The double control system of heart relaxation].

The systolic performance of the heart is regulated by two separate mechanisms: the first involves an adaptation to load (Frank-Starling), and the second, variations in contractility. Similarly, recent experimental studies have shown a double mechanism of control of the relaxation phase. Cardiac relaxation, as regards the muscle and muscle-pump system, is governed by the constant interrelation of the sensitivity of the contractile system to conditions of load (load dependence) and by the sensitivity to decreasing activation (inactivation dependence). The load dependence of cardiac muscle requires an important and effective intracellular system of calcium sequestration. For given load conditions, relaxation may be modulated by subtle changes in the dissipation of activation. Such variations of dissipation of activation may result from metabolic (coronary circulation), neuro humoral (sympathetic tone), and pharmacological factors (catecholamine, vasodilator therapy, digitalis) affecting the heart as a whole. Also, for a given load dependence, relaxation will be affected by changes in the conditions of load, which are complex in the whole heart (return force, end systolic deformation, arterial impedence, the law of Laplace, increased intra myocardial pressure due to rapid filling of the coronary reservoir). This double system of control of relaxation, with load dependence predominating is very valuable during the rapid filling phase of the heart. In this phase, relaxation is mainly under load and not in activation dependence. This allows perfect return to the presystolic configuration despite the low filling pressures. The continuous interaction of the cardiac load complex during relaxation and its metabolic and neuro humoral control makes it difficult to assess the relative importance of each factor of this double control. The interaction is even more complex in diseased hearts where regional functional abnormalities are often observed. Similarly, any pharmacological intervention may simultaneously affect load and inactivation dependence.