Yes. Treatment with beta-adrenergic receptor blockers decreases the mortality rate in patients with coronary artery disease or heart failure, as well as during the perioperative period in selected patients (eg, those with a history of myocardial infarction, a positive stress test, or current chest pain due to myocardial ischemia). The current evidence supports giving beta-blockers to patients with coronary artery disease and chronic obstructive pulmonary disease (COPD) or asthma, which lowers the 1-year mortality rate to a degree similar to that in patients without COPD or asthma, and without worsening respiratory function.1 However, many clinicians still hesitate to start patients with COPD or asthma on a beta-blocker due to the fear of bronchoconstriction.2
In patients with reversible airway disease, beta-blockers may increase airway reactivity and bronchospasm, as well as decrease the response to inhaled or oral beta-receptor agonists.3 Even topical ophthalmic nonselective beta-blockers for glaucoma can cause a worsening of pulmonary function.4 However, these data are from small trials in the 1970s and 1980s.
On the other hand, not giving beta-blockers can pose a risk of death. In a retrospective study of more than 200,000 patients with myocardial infarction, Gottlieb et al5 found that beta-blockers were associated with a 40% reduction in mortality rates in patients with conditions often considered a contraindication to beta-blocker therapy, such as congestive heart failure, pulmonary disease, and older age.5
Cardioselective beta-blockers with an affinity for the beta-1 receptor theoretically result in fewer adverse effects on the lungs. They competitively block the response to beta-adrenergic stimulation and selectively block beta-1 receptors with little or no effect on beta-2 receptors, except perhaps at high doses. However, this possible high-dose effect requires further study.
The effect of cardioselective beta-blockers on respiratory function was evaluated in two meta-analyses,6,7 one in patients with mild to moderate reactive airway disease, the other in patients with mild to severe COPD. Patients with reactive airway disease who received a single dose of a beta-blocker had a 7.46% reduction in forced expiratory volume in the first second of expiration (FEV1), an effect that was completely reversed by treatment with a beta-agonist inhaler. The FEV1 increased by a statistically significantly greater amount in response to beta-agonists in patients who received beta-blockers (a single dose or continuous therapy) than in those who did not receive beta-blockers. Patients who received continuous cardioselective beta-blockers experienced no significant drop in FEV1, and no new symptoms developed. These results led the authors to conclude that cardioselective beta-blockers do not cause a significant reduction in pulmonary function in patients with mild to moderate reactive airway disease and COPD and are therefore safe to use. A single dose of a cardioselective beta-blocker may produce a small decrease in FEV1, especially in patients with reactive airway disease, but as therapy is continued over days to weeks, there is no significant change in symptoms or FEV1 and no increase in the need for beta-agonist inhalers.
A major limitation of the two meta-analyses was that the patients were younger than most patients who require beta-blockers: the average age was 40 in patients with reactive airway disease, and 54 in patients with COPD. Also important to consider is that only patients with mild to moderate reactive airway disease were included. Patients with severe asthma, especially those with active bronchospasm, may react differently to even cardioselective beta-blockers.