Function of the cardiac myocyte in the conundrum of end-stage, dilated human heart failure.

Chronic heart failure is a phenotype that marks the final common pathway in a diversity of specific cardiovascular disease states, eg, severe coronary ischemia and myocardial infarction, and chronic hypertension, or it can be idiopathic in nature. A trilogy of clinical signs that includes reduced systolic myocardial function, increased diastolic filling pressure, and an increased likelihood for the occurrence of cardiac arrhythmias is eventually accompanied by a markedly dilated heart. The specific role of cardiac myocyte dysfunction in progressive cardiac dilatation that heralds the end stage of chronic heart failure is 1 facet of the conundrum of the end-stage dilated heart. In this issue of Circulation, Hasenfuss et al1 have studied cardiac muscle isolated from the left ventricle of end-stage, dilated cardiomyopathic hearts removed from patients and cardiac muscle from control, non–heart-failure organ donors in an attempt to discover mechanisms that may underlie cardiomyocyte dysfunction in chronic end-stage heart failure.