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AND THE
ANSWER IS . . .
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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