NEW YORK, NY. An elevated resting heart rate is an independent risk factor for cardiovascular disease and associated mortality. Beta-blockers (propranolol, atenolol, metoprolol) are effective in lowering heart rate and have been found to reduce mortality among patients with heart failure and angina. There is also evidence that beta-blocker therapy reduces the severity and mortality of heart attacks (myocardial infarctions). This has led to the assumption that the slower the heart rate the better and has resulted in beta-blockers being routinely prescribed for patients with elevated blood pressure (hypertension) even though there is no clinical evidence that reducing heart rate is of benefit in these patients.

Dr. Franz Messerli and colleagues at Columbia University of Physicians and Surgeons now report that prescribing beta-blockers for patients with hypertension is precisely the wrong thing to do. Their meta-analysis encompassed 9 randomized, controlled clinical trials evaluating the effects of beta-blockers among hypertensives. A total of 34,096 patients were treated with beta-blockers, 30,139 were treated with other anti-hypertensive agents (diuretics, ACE inhibitors or calcium channel blockers) and 3,987 were given a placebo.

All patients were followed for an average of 3.5 years (minimum 1 year) by which time their average systolic blood pressure had decreased by about 13% in both the beta-blocker group and the comparison group. In addition, average resting heart rate had decreased by 12% in the beta-blocker group, while a statistically non-significant decrease of 1% was observed in the comparison group (other anti-hypertensive agents). Surprisingly, the New York researchers observed an inverse relationship between the extent of heart rate reduction and cardiovascular mortality during the studies. In other words, the more effective the beta-blockers were at reducing heart rate, the greater the mortality. Similar correlations were observed for nonfatal myocardial infarction (MI), heart failure and stroke. In all cases, the incidence of these conditions increased as the heart rate was lowered using beta-blocker therapy.

The researchers conclude that, "In contrast to patients with MI and heart failure, beta-blocker-associated reduction in heart rate increased the risk of cardiovascular events and death for hypertensive patients." They speculate that the beta-blocker induced heart rate reduction increases central aortic pressure or pulse pressure and that this is responsible for the adverse effects observed in patients with hypertension.

In an accompanying editorial, Dr. Normal Kaplan of the University of Texas points out that beta-blockers have numerous other adverse effects including precipitation of diabetes, weight gain, and a decrease in exercise endurance. Despite this, atenolol was the 4th most prescribed drug in the US in 2005 with 44 million prescriptions a year.

Bangalore, S, et al. Relation of beta-blocker-induced heart rate lowering and cardioprotection in hypertension. Journal of the American College of Cardiology, Vol. 52, October 28, 2008, pp. 1482-89
Kaplan, NM. Beta-blockers in hypertension: Adding insult to injury. Journal of the American College of Cardiology, Vol. 52, October 28, 2008, pp. 1490-91

Editor's comment: It should be kept in mind that 78% of the participants in the clinical trials were prescribed atenolol (Tenormin), so it is not entirely clear whether beta-blockers as such, or atenolol in particular, are responsible for the adverse effects. It is quite possible that one of the newer vasodilating beta-blockers such as nebivolol (Bystolic) would not have the same detrimental effects as atenolol since it does not increase the central aortic pressure. Nevertheless, with the evidence at hand, it would seem that lone afibbers with hypertension would be far better of taking an ACE inhibitor, calcium channel blocker, or potassium-sparing diuretic rather than a beta-blocker for reducing their blood pressure.