Abstract
Congestive heart failure (CHF) is a complex clinical syndrome affecting 1% of the U.S. population. The basic dysfunction, a lack of sufficient blood flow to the periphery, triggers reflex neurohumoral mechanisms that cause systemic vasoconstriction and sodium and water retention as the body attempts to protect vital organs. This, in turn, results in additional work for the failing heart and further deterioration. Vasodilators, in general, and angiotensin converting enzyme (ACE) inhibitors, in particular, interrupt this pathophysiology and improve hemodynamics. Enalapril, a long-acting ACE inhibitor, has been demonstrated to improve New York Heart Association (NYHA) functional class, pulmonary capillary wedge pressure, cardiac index, maximum oxygen uptake, and exercise tolerance in CHF patients. Data from a recent trial provide evidence that a group of patients with severe CHF who were treated with enalapril showed reduced heart size, reduced need for other heart-failure medication, and reduced mortality.
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