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Detrimental effects of beta-blockers in COPD: a concern for nonselective beta-blockers

Hanneke J van der Woude1, Johan Zaagsma, Dirkje S Postma

  • 1Department of Pulmonary Diseases, Martini Hospital, Van Ketwich Verschuurlaan 82, 9721 SW Groningen, the Netherlands. jvbhw@home.nl

Chest
|March 15, 2005
PubMed

Insights

Beta-blockers like propranolol and metoprolol can worsen airway hyperresponsiveness (AHR) in COPD patients, while celiprolol does not. Propranolol also reduced FEV(1) and formoterol

Area of Science:

  • Pulmonary Medicine
  • Cardiology
  • Pharmacology

Background:

  • Beta-blockers are known to exacerbate FEV(1) and airway hyperresponsiveness (AHR) in asthma patients.
  • COPD outcomes are influenced by FEV(1) and AHR, and cardiac comorbidities often necessitate beta-blocker use.

Purpose of the Study:

  • To evaluate the impact of different beta-blockers on AHR, FEV(1), and bronchodilator response in COPD patients.
  • To compare the pulmonary effects of propranolol, metoprolol, and celiprolol against a placebo.

Main Methods:

  • A double-blind, placebo-controlled, randomized, cross-over study involving 15 patients with mild-to-moderate COPD and AHR.
  • Patients received propranolol, metoprolol, celiprolol, or placebo for 4 days, with assessments of FEV(1) and AHR (PC(20)) on day 4.
  • The response to formoterol (a beta(2)-agonist) was measured after beta-blocker administration.

Main Results:

  • Propranolol and metoprolol significantly increased AHR (decreased PC(20)) compared to placebo and celiprolol.
  • FEV(1) decreased only with propranolol treatment.
  • Propranolol impaired the bronchodilating effect of formoterol, while metoprolol and celiprolol did not.

Conclusions:

  • Celiprolol demonstrated no adverse pulmonary effects in COPD patients.
  • Propranolol and metoprolol increased AHR, with propranolol also reducing FEV(1) and blunting the response to formoterol.
  • The choice of beta-blocker in COPD patients requires balancing cardiovascular benefits against potential detrimental pulmonary effects on FEV(1), AHR, and bronchodilator response.
Abstract

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