Author + information
- Received June 21, 1993
- Revision received October 20, 1993
- Accepted October 26, 1993
- Published online March 1, 1994.
- Robert Neil Doughty, MB, MRCP∗,
- Stephen MacMahon, PhD, MPh, FACC1 and
- Norman Sharpe, MD, FRACP, FACC
- ↵∗Address for corrospondence: Dr. Robert Doughty, Department of Medicine, University of Auckland School of Medicine, Private Bag 92019, Auckland, New Zealand.
Despite recent improvements in the management of congestive heart failure, the prognosis of many patients with this condition remains poor. The level of neurohormonal activation appears to be predictive of survival, and clinical studies indicate that inhibition of overactivated neurohormonal systems may be beneficial. Activation of the renin-angiotensin-aldosterone system is well documented in heart failure, and angiotensin-converting ensyme inhibition now has an established role in treatment based on evidence of hemodynamic, symptomatic and mortality benefit. Sympathetic nervous system activation also occurs as a compensatory mechanism in heart failure but with long-term deleterious effects, Increasing evidence suggests that beta-adrenergic blockade can produce hemodynamic and symptomatic improvement in heart failure of idiopathic or ischemic etiology. Trials of beta-adrenergic blocking agents in patients after myocardial infarction suggest a beneficial effect on mortality, even among those with heart failure. However, there remains uncertainty as to how generalizable are the results from the postinfarction trials, particularly in the current therapeutic environment with routine angiotensin-converting enzyme inhibitor therapy. Appropriately powered randomized, controlled trials are required to determine precisely the balance of benefit and risk resulting from long-term beta-blocker therapy in patients with heart failure of ischemic and other etiology.
- Received June 21, 1993.
- Revision received October 20, 1993.
- Accepted October 26, 1993.