Our hypotheses is that 1) in patients with idiopathic dilated cardio- myopathy, administration of the cardiac tissue specific ace-inhibitor, quinapril, significantly suppresses angiotensin II formation compared to enalapril The suppression is more pronounced in patients with the ace D/D genotype and 2) the additional suppression of ANG II afforded by quinapril correlates with a reduction in left ventricular (LV) wall stress, transmyocardial norepinephrine, and the net balance of cardiac protein synthesis.