The end stage heart failure due to ischemic or dilated cardiomyopathy is characterized by a dilated, relatively thin-walled ventricle. It is proposed that the structural basis of ventricular expansion is due to side-to-side slippage of myocytes within the wall, representing one of the potential mechanisms for chamber dilatation and wall thinning. In this regard, an alternative etiology for the detrimental cardiac architectural rearrangement has been seen in dilated failure that can be used for postulating the occurrence of maladaptive remodelling of cardiac myocyte morphology. Myocytes increase in length by an increase in the number of sarcomeres in series, thus increasing chamber diameter in an attempt to maintain cardiac output. Furthermore, The thinning of the ventricular wall in failure is due to inadequate transverse growth of cardiac myocytes coupled with scattered myocyte cell loss throughout the ventricular wall. The ultimate consequence is that the ratio of myocyte length to myocyte width is increased in heart failure.