Changing strategies in the management of heart failure

Abstract

Forty years ago therapy for congestive heart failure was limited largely to the mercurial diuretics and a variety of cardiac glycoside preparations; these were often ineffective, and the common practice of "pushing" digitalis caused serious, sometimes lethal side effects. Today, a more complete understanding of the regulation of cardiac work and pathophysiology of heart failure is having a profound impact on therapeutic strategy for this common condition. Despite more powerful means to augment myocardial contractility and much more effective diuretics, therapy that relies only on inotropic stimulation and diuresis is no longer optimal for the majority of patients with heart failure. Thus, strategies for the therapy of heart failure must take into account new understanding of mechanisms that initiate, perpetuate and exacerbate the hemodynamic and myocardial abnormalities in these patients. Recognition of the detrimental effects of excessive afterload and the importance of relaxation (lusitropic) as well as contraction (inotropic) abnormalities has led to widespread acceptance of vasodilator therapy, which has dramatically improved our ability to alleviate the symptoms of heart failure. Changes that result from altered gene expression in the hypertrophied myocardium of patients with congestive heart failure can give rise to a cardiomyopathy of overload that, although initially compensatory, may hasten death. These and other advances in our understanding of the pathophysiology, biochemistry and molecular biology of heart failure provide a basis for new therapeutic strategies that can slow the progressive myocardial damage that causes many of these patients to die, while at the same time improving well-being in patients with congestive heart failure.