Interruption of the Progression of Heart Failure: Are ACE Inhibitors the Solution?

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Abstract
Our options for the medical management of heart failure are aimed at preventing the development of the condition, relieving symptoms, modifying the underlying pathophysiology, and delaying or preventing disease progression. The principal symptoms of heart failure are edema, dyspnea and fatigue. Diuretics are effective in relieving edema, and dyspnea resulting from pulmonary edema. Once pulmonary edema has been treated relatively few agents are effective against residual exercise-induced dyspnea, possibly because of the numerous possible causes of this symptom. Angiotensin-converting enzyme (ACE) inhibitors have, however, been shown to improve dyspnoea by mechanisms that are not related to hemodynamic actions. These agents also improve skeletal muscle blood flow and function, thereby relieving fatigue in heart failure patients. Treatment strategies aimed at modifying the underlying pathophysiology or preventing disease progression have, with the exception of the ACE inhibitors, met with limited success. Large-scale trials have shown, however, that ACE inhibitors improve survival in patients with moderate or severe heart failure, and prevent the development of heart failure in asymptomatic patients. These agents, therefore, represent an important advance in the management of heart failure, and it is anticipated that new insights into their optimal use will follow as the mechanisms by which they exert their beneficial effects become clear.

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