The most compelling evidence to support the neurohor-monal approach to the treatment of CHF is the large body of evidence supporting the use of ACE inhibitors in the prevention and management of heart failure . ACE inhibitors, when given to patients with mild, moderate or severe heart failure, have been shown to reduce both morbidity and mortality significantly . Furthermore, when administered to postmyocardial infarction patients who are at high risk of developing heart failure, ACE inhibitors have been shown to delay the development of heart failure as well as to reduce CHF morbidity and mortality.
Therefore, from a pathophysiological perspective, the use of beta-blockers may also be beneficial and, paradoxically, should result in improved ventricular function. Early, small trials of beta-blockers (metoprolol, bucindolol, carvedilol) administered to patients with CHF demonstrated improvements in hemodynamics (cardiac output, ejection fraction [EF], PCWP) and functional ability (NYHA class), in addition to up-regulation of beta-receptors . In general, there were less consistent benefits in exercise tolerance, reflecting the fact that beta-blockers attenuate exercise-induced rises in cardiac output.