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Heart failure therapy in evolution.

During the past 25 years, considerable progress has been made in our understanding of the pathophysiological mechanisms for the development and progression of the heart failure syndrome. On the basis of this growing knowledge, a number of therapeutic approaches have been proposed and tested for the long-term management of chronic heart failure. One of the reasons for the continuing search for newer therapies is to improve prognosis further than achievable with an established therapy. It has been amply documented that clinical heart failure resulting from impaired left ventricular systolic function is associated with a substantial mortality and morbidity and that the more severe the clinical heart failure is, the worse the prognosis. Before the introduction of vasodilator and ACE inhibitor therapy, a 1-year mortality rate of ≈50% was observed with conventional therapy in patients with severe chronic heart failure.1 In the CONSENSUS I trial,2 in which patients with severe heart failure (NYHA functional class IV) were randomized to receive placebo or enalapril (an ACE inhibitor) in addition to contemporary conventional treatment (digitalis and diuretics), the mortality rates with conventional treatment at 6 months and 12 months were 44% and 54%, respectively. The prognosis of patients who initially present with mild to moderate clinical heart failure and are treated conventionally was assessed in the VA Heart Failure Trial I.3 The cumulative mortality rate of these patients over a period of 48 months was 53.6%. The realization that conventional treatment of established clinical heart failure with digitalis and diuretics is associated with very poor prognosis prompted the search for newer therapeutic modalities that might have the potential to correct the hemodynamic abnormalities of heart failure, improve ventricular function, relieve symptoms, and improve survival. Because it was initially postulated that the reduction of left ventricular outflow resistance and wall stress …