Left ventricular dysfunction, regardless of its cause, results in characteristic hemodynamic derangements and a process of neurohormonal activation. Among the neuronal and hormonal pathways activated are the sympathetic nervous system, the renin–angiotensin–aldosterone system, and the endothelin pathway. Each of these pathways has hemodynamic effects that maintain tissue perfusion and blood pressure, and the sympathetic nervous system also stimulates the heart rate and myocardial contractility. Although these responses initially compensate for hemodynamic derangements, prolonged elevation of norepinephrine, renin, angiotensin I and II, aldosterone, and endothelin becomes directly toxic to the heart, accelerating processes such as apoptosis, myocyte hypertrophy, and interstitial fibrosis. . . .