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AND THE ANSWER IS . . .

4

In the early days of beta-blocker therapy, it was reported that such treatment could exacerbate reactive airways diseases such as asthma and COPD. However, these articles (mainly case reports) described use of relatively non-selective beta-blockers such as propanolol which inhibited binding of both beta-1 and beta-2 agonists to their receptors. It was recognized that the desirable effect of beta-blocker therapy was at the beta-1 receptor while beta-2 blockade could increase bronchoconstriction. The more recently available beta-blocker agents (e.g., atenolol) are relatively selective for the beta-1 receptor (cardio- selective). Therefore, one would expect little if any beta-2 blockade with use of these drugs. In a recent meta-analysis of 29 studies in this area, it was found that challenge of mild-moderate asthmatics with a single dose of cardio-selective beta-blocker drugs led to a small mean decrease in FEV-1 (7.5%) without any increased symptoms or need for rescue therapy with inhaled albuterol (1). Indeed, in studies where responsiveness to inhaled albuterol was assessed, there was actually a slightly greater bronchodilating effect of albuterol inhaled following the challenge with a cardio-selective beta-blocker agent. Therefore, the authors concluded that cardio-selective beta-blockers can be given safely to individuals with adequately controlled mild to moderate persistent asthma, even if asthma control requires chronic use of inhaled corticosteroids. However, as pointed out in an editorial accompanying the report described above (2), one cannot conclude at this time whether use of these cardio-selective beta-blockers would be safe in those with severe asthma. Also, it is not clear from these findings whether the chronic use of cardio-selective beta-blockers for months to years would be as safe in those with chronic mild to moderate asthma.

References
1. Ann. Intern Med 2002; 137:715-25
2. Ann Intern Med 2002;137:766

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