Vasodilators. A re-evaluation of their role in heart failure.

Abstract

Over the past 25 years, the concept of circulation in heart failure has evolved from that of a simple circuit with a weak pump and high pressures to a complex integrated system of cellular modification, cardiac compensation and systemic neurohumoral responses. The original model of cardiac afterload as the systemic vascular resistance has been refined to reflect the interdependence of preload and afterload and the central role of atrioventricular valve regurgitation. It is becoming increasingly apparent that the impact of vasodilator therapy far exceeds the direct haemodynamic effects on preload and afterload, and depends on the mechanism by which vasodilation is achieved, with increasing emphasis on those agents which oppose neurohumoral activation. The potential goals of therapy have broadened to include not only haemodynamic stabilisation through tailored therapy for patients referred with advanced heart failure, but also the prevention of disease progression for patients with asymptomatic ventricular dilation. As the different profiles of heart failure have come to be recognised, the purpose and design of vasodilator treatment must now be considered individually for each patient.