SELECTED ARTICLES FROM THE RECENT LITERATURE 2003

12/29/03

Beta-blocker use in asthmatics

Summary
Beta blocker (BB) agents have traditionally been considered contraindicated in individuals with reactive airways diseases such as asthma and some cases of COPD. This recommendation has been based on concerns about BB therapy inducing increased bronchoconstriction in such patients. However, as reviewed by Salpeter of Stanford Univ/Santa Clara Valley Medical Center in San Jose, CA, there have been recent major changes in the thinking about the use of BB agents. The Beta-adrenergic system involves Beta-1 and Beta-2 receptors in the heart while Beta-2 receptors predominate in the airways and other non-cardiac tissues. Stimulation of the Beta-1 receptor in the heart leads to increased cardiac rates and contractility. Beta-2 stimulation in the airways causes bronchial relaxation and protection against the release of circulating bronchoconstrictive agents. The earlier BB agents were all non-selective for Beta-1 and Beta-2 receptors so there was an understandable concern about worsening of asthma during use of these agents. However, the chronic use of the more selective beta-1 selective blockers such as atenolol and metaprotenol has been shown in several studies to not significantly increase asthma or worsen pulmonary function. Indeed, there was a mean 9% greater bronchodilator response to inhaled albuterol in individuals after they were treated with Beta-1 -selective blocker drugs. This increased Beta-2 agonist response in likely due to an increased density of Beta-2 receptors on airway tissues in those treated with Beta-1 selective blocker drugs.

Reference
J Respir Dis 2003;24:484-91

Editor's Comments
The impression of the author of this review that Beta-1 selective blockers such as atenolol or metaprolol do not adversely affect reactive airways disease is similar to that expressed by the same author after a meta-analysis of a Cochrane database (Cochrane Database Syst Rev 2001;2:CD002992; see my previous review of that report in this Current Literature section). The finding that Beta agonist (albuterol) induced bronchodilatation is actually enhanced in those treated with Beta-1 selective blockers was also contained in that meta-analysis with a somewhat greater mean increased response (14%). It has been known for some time that the density of Beta-2 receptors in the airways decreases during extensive use of agents such as albuterol. This mechanism has been postulated as the cause of overall increased morbidity in those using inhaled albuterol excessively as monotherapy. Apparently, the opposite occurs (an increased expression of Beta-2 receptors) during Beta-1 selective blockade.

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