Abstract
Over the past decade, there has been a paradigm shift in the understanding of heart failure pathophysiology. Heart failure is no longer conceptualized as a hemodynamic disorder resulting from changes in renal and hormonal function. Rather, the syndrome of heart failure is more complex and is characterized by abnormal myocyte growth, proliferation of cells in the extracellular matrix, and myocyte cell loss (apoptosis)-all of which culminate in significant structural remodeling of the heart and loss of ventricular function. The loss of ventricle function is preceded by an initiating event such as myocardial infarction, which leads to changes in cell function, activation of specific neurohormones and peptides, which in turn are linked to the remodeling of the ventricle, and progression of heart failure. This article discusses how changes in myocyte and nonmyocyte structure may contribute to the progression of heart failure. Insight into these mechanisms will provide a better understanding of newer pharmacologic approaches in the treatment of heart failure.