NO balance: regulation of the cytoskeleton in congestive heart failure by nitric oxide.

Congestive heart failure is a leading cause of cardiovascular mortality in the United States and Europe.1 Clinically, this syndrome is characterized by water retention and often left ventricular dilatation with poor systolic contractility. Etiologically, congestive heart failure can be of genetic or acquired origin. In 1993, 2 groups independently reported mutations in the cytoskeletal protein dystrophin as the cause of X-linked dilated cardiomyopathy, a rare inheritable disease that leads to enlargement of ventricular dimensions and to congestive heart failure.1 Over the last decade, the pathophysiological relevance of the cardiac myocyte cytoskeleton for the development of congestive heart failure is being increasingly recognized.