Beta blockers and the failing heart: is it time for a U-turn?

Since the introduction of 3 adrenoceptor antagonists into clinical practice approximately 30 years ago, these drugs have been regarded as being contraindicated in patients with severely depressed ventricular function because of the risk of precipitating haemodynamic deterioration. It may therefore seem both surprising and paradoxical that the idea of using 0 blockers as a primary therapy for congestive heart failure to improve symptoms and prognosis has gained considerable ground recently. This fundamental shift in opinion has come about for several reasons. (a) There is increasing evidence that the deleterious long-term effects of excessive sympathetic stimulation on cardiac mechanical performance and electrical stability may outweigh any immediate benefits of inotropic support to the failing myocardium, thus providing a clearer rationale for the use of P adrenoceptor antagonists. (b) Subgroup analysis of postinfarction [ blocker trials has shown that the greatest reductions in mortality were seen in patients with mild or moderate heart failure. (c) Most studies of low dose I blockade in patients with congestive heart failure showed sustained improvements in functional capacity, haemodynamic indices, and control of ventricular arrhythmias. (d) By contrast, longterm treatment with 0 adrenoceptor agonists and other inotropes has failed to produce such beneficial responses and there is now clear evidence that these drugs increase mortality. (e) The success of angiotensin converting enzyme inhibitors has lent powerful support to the general principle that blockade of "compensatory" neurohormonal mechanisms may be a beneficial in the treatment of heart failure.