Drug therapy of chronic heart failure

Chronic heart failure is an irremediable terminal syndrome. The inability of the heart to pump sufficient blood to meet the demands of metabolically active tissues is aggravated by reflex increases in peripheral vasoconstriction induced by the sympathoadrenal and renin-angiotensin-aldosterone systems. Vasoconstriction is partially attenuated by atrial natriuretic hormone, prostaglandin, and bradykinin. The aim of therapy is to improve the pumping performance of the heart and reduce arterial and venous constriction in the hope that this will reduce symtoms and improve the quality of life. Many drugs achieve such benefits, at least initially. Inotropic drugs increase cardiac pumping activity, and drugs acting directly on arteries and veins improve cardiac function by reducing afterload and preload. ACE inhibitors suppress angiotensin II formation, reducing its vasoconstrictive action, its ability to increase aldosterone secretion and the consequent salt retention and expansion of plasma volume. Since the proportionate role played by various hemodynamic factors in individual patients in unknown, it is likely that most benefit will be achieved by a combined therapeutic approach.