Current Treatment Options for CHF Management: Focus on the Renin-Angiotensin-Aldosterone System

Heart failure (HF) is highly prevalent in our society and its incidence is increasing in concert with the growing aged population. Experimental and clinical studies have consistently shown that HF is ameliorated by inhibition of the renin-angiotensin-aldosterone system (RAAS). Acknowledging that heightened activation of the RAAS contributes significantly to HF progression has led to the development of pharmacologic antagonists of RAAS components that have greatly improved both symptoms and prognosis of patients suffering from this syndrome. Angiotensin-converting enzyme (ACE) inhibitors represent the first developed agents that block the production of angiotensin II, and have been shown to be effective across a broad spectrum of patients with HF, including those with asymptomatic left ventricular dysfunction to overt HF. Initiation of ACE inhibitors prior to the onset of symptoms in those with left ventricular systolic dysfunction, and as early as feasible following a myocardial infarction, has been shown to reduce mortality and the development of overt HF in several clinical trials. Clinical data also support the use of angiotensin II receptor antagonists as an alternative to ACE inhibitors in patients who are allergic to, or intolerant of, ACE inhibitors. Agents that antagonize aldosterone via blockade of mineralocorticoid receptors improve clinical outcomes in patients with advanced HF or those with reduced ejection fraction and HF following an acute myocardial infarction. Maximally inhibiting the RAAS, in conjunction with other neurohormonal systems (eg, the sympathetic nervous system by b-adrenergic blockade), leads to improved clinical outcomes in HF, a highly prevalent and costly disease in our society.