Aldosterone antagonism and myocardial infarction: from animals to man and back.

Inhibiting the renin-angiotensin system has proven to be one of the most fruitful therapeutic strategies in cardiovascular medicine. Believed to have evolved to maintain blood volume and perfusion pressure in conditions of hemorrhage or hypovolemia, the renin-angiotensin-aldosterone system (RAAS) is upregulated in the setting of left ventricular (LV) dysfunction or heart failure (1). Pharmacologic inhibitors of this system—including renin inhibitors, angiotensinconverting enzyme (ACE) inhibitors, aldosterone antagonists, and angiotensin receptor blockers—were all initially designed for the treatment of hypertension, and, with the exception of renin inhibitors, are currently clinically used for this indication. Nevertheless, the benefits of inhibiting the RAAS have extended well beyond this initial therapeutic target.