Is contractility depressed in the failing human heart?

Is contractility depressed in the failing human heart? The question must be approached in a stringent manner. Myocardium from failing human hearts has been shown to generate normal physiological force under the ideal conditions of low stimulation and an adequate energy supply. Nevertheless, even when subjected to physiologically conducive conditions, failing myocardium experiences a slowed relaxation, adversely affecting the diastolic properties of the heart. In addition, experiments have shown that increasing the contraction rates of failing hearts clearly results in lowered force and pressure evolution. This information indicates a decrease in contractile reserve in both a systolic and diastolic sense. Not surprisingly, the term end-stage heart failure becomes questionable when applied to myocardium obtained from patients undergoing cardiac transplantation. A number of studies involve such myocardium from feasible regions of the heart perfused within ideal physiological conditions yielding, at times, nonfailing performance. Therefore, it becomes imperative to bear in mind the role of such myocardium within the framework of the entire diseased heart.