An alternative approach to understanding the pathophysiological mechanisms of chronic heart failure.

No single well established hypothesis for the mechanisms of heart failure currently exists. Those definitions that do exist are either not universally applicable or are not exclusive to heart failure. The pathogenesis of heart failure has been considered by some to be too complex to define with multiple pathophysiological processes being implicated. The many clinical and neurohumoral features of heart failure may be more dependent on the severity of the condition and its speed of onset rather than its etiology. This suggests a potential single common pathway or pathogenic mechanism in all forms of heart failure regardless of cause. This viewpoint uses the framework of myocardial mechanics and energetics to propose an alternative, simplified definition and unifying hypothesis for the pathogenesis of chronic heart failure. Chronic heart failure may be understood as follows. Cardiac output and stroke volume are determined by the tissues' requirements; the ejection fraction is determined by both myocardial shortening and degree of end-diastolic wall thickness; the end-diastolic volume is determined by the requirement to normalize stroke volume. We will argue that chronic heart failure can be viewed as a condition where the dominant compensatory mechanism is through regulation of ventricular end-diastolic volume. Consequently, in conditions where there is a fall in tissue perfusion, stroke volume and tissue perfusion are returned toward normal predominantly via this feedback mechanism. It is important for researchers, clinicians and their patients that we strive for a comprehensive, inclusive and unambiguous unifying hypothesis for pathophysiological mechanisms of heart failure.