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European Heart Journal 1991 12(Supplement F):63-69; doi:10.1093/eurheartj/12.suppl_F.63
Copyright © 1991 by the European Society of Cardiology.
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© 1991 The European Society of Cardiology

New therapeutic strategies in chronic heart failure: challenge of long-term beta-blockade

Å Hjalmarson and F. Waagstein

Division of Cardiology, Department of Medicine I, Sahlgren 's Hospital, University of Göteborg Sweden

Correspondence: Åke Hjalmarson, M.D., Division of Cardiology, Sahlgren's Hospital, S-413 45 Göteborg, Sweden

It is claimed that long-term treatment with beta-blockers improves cardiac function and exercise capacity in patients with various forms of congestive heart failure. This was first reported by Waagstein and coworkers in patients with idiopathic dilated cardiomyopathy in 1975 and was later confirmed in 8 further studies in this type of patient. A total of 211 patients with idiopathic dilated cardiomyopathy were treated for 12–19 months. About two thirds of the patients have improved to some extent. Seven other studies reported favourable long-term effects of beta-blockers in 120 patients with other forms of dilated cardiomyopathy, e.g. caused by coronary artery disease, adriamycin, diabetes, or valvular heart disease. Pooled data from 10 studies on 153 patients with various forms of cardiomyopathy, showed that ejection fraction was improved by 40% from 27 to 38%. Only two studies were inconclusive, both with only one month's treatment. In all studies with favourable effects of long-term beta-blockade, treatment was given for more than 2 months and in most cases for about 6 months.

A number of beta-blockers have been used in the studies, including acebutulol, alprenolol, bucindolol, labetalol, metoprolol, practolol and propranolol. In most cases, a rather low dose was given initially and there was a stepwise increase in the dosages. After 6–8 weeks most patients were given beta-blockers in daily doses comparable to those given in patients with angina pectoris and hypertension. There is at present no indication that one beta-blocker is superior to others. It therefore seems reasonable to believe that the effects are due to beta1-blockade. Two studies have included a phase of withdrawal of beta-blocker therapy. This has resulted in marked patient deterioration. Reinstitution of therapy resulted in improvement. This strongly supports the idea that improvement is related to the beta-blocker treatment and is not a spontaneous improvement over time. A number of possible mechanisms might be involved in the beneficial effects of the beta-lockers. It has not been possible to demonstrate any factor that might predict why some patients respond favourably to treatment while others are nonresponders.

Key Words: Congestive heart failure • cardiomyopathy • beta-blockers • cardiac function • exercise capacity


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