Treatment of congestive heart failure

Tamargo, J.

Ars Pharm.36;(4);547-568, (1995)



Key words: Congestive heart failure, Digoxin, Phosphodiesterase inhibitors, Positive inotropic agents, Vasodilators, Angiotensin converting enzyme inhibitors

Abstract

Congestive heart failure (CHF) can be defined as the inability of the heart to provide cardiac output sufficient to meet tissue demands at normal ventricular filling pressures. The goals of treatment in CHF include relief of symptoms and activity limitation, prevention of progression of the syndrome and prolongation of survival. There are two basic approaches to treatment, to increase of myocardial contractlity and decrease of preload and/or afterload.

Diuretics are the first line of therapy in most patients with symptomatic CHF. They produce rapid and consistent relief improvement of symptoms, since more of them are associated with fluid retention, as manifested by edema and signs of pulmonary congestions. Digoxin is the only indicated oral agent that increase myocardial contractility in the failing heart. It inhibits the membrane bound Na/k-ATPase. Recent studies, however, have also indicated that digoxin restores abnormal baroreceptor function and inhibits central sympathetic outflow. In contrast, phosphodiesterase inhibitors exacerbated cardiac arrhythmias, accelerated progression of the underlying disease and increased mortality. The rationale for vasodilator therapy in CHF is that agents that alter left ventricular loading conditions can improve the performance of the failing heart. Angiotensin converting enzyme inhibitors interfere with the activated neurohumoral systems that produce vasoconstriction and fluid retention and reduced survival. When added to digoxin and diuretics they produced hemodynamic improvement, reduced symptoms and improved the survival.

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