ABSTRACT
Heart failure is caused by the loss of contractile myocytes and/or the loss of contractile material from individual cells. The causes for this are, in the majority, of vascular origin. It appears logical that repairing the infarcted heart requires also a vascular approach besides the challenging task of restarting the arrested mitotic cycle of cardiac myocytes. The task is a formidable one because, with a moderate to severe myocardial infarct, about 30 grams of tissue have disappeared and have to be replaced, and for a chunk of tissue of that size a new vascular system has to be built. However, factors other than acute myocardial infarction contribute to heart failure, in particular the subtle chronic and cumulating loss of individual myocytes in pressure overload, be it from high blood pressure or from aortic valve stenosis1
and from chronic ischemia as in hibernating myocardium,2 resulting in substitution fibrosis.
