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Clinical Investigations: COPD |

Detrimental Effects of β-Blockers in COPD*: A Concern for Nonselective β-Blockers

Hanneke J. van der Woude, MD, PhD; Johan Zaagsma, PhD; Dirkje S. Postma, MD, PhD; Trea H. Winter; Marinus van Hulst, MSc, PharmD; René Aalbers, MD, PhD
Author and Funding Information

*From the Departments of Pulmonary Diseases (Drs. van der Woude and Aalbers, and Ms. Winter) and Clinical Pharmacy and Toxicology (Dr. van Hulst), Martini Hospital, Groningen; Department of Molecular Pharmacology (Dr. Zaagsma), University Centre for Pharmacy, Groningen; and Department of Pulmonary Diseases (Dr. Postma), University Hospital Groningen, Groningen, the Netherlands.

Correspondence to: Hanneke J. van der Woude, MD, PhD, Department of Pulmonary Diseases, Martini Hospital, Van Ketwich Verschuurlaan 82, 9721 SW Groningen, the Netherlands; e-mail: jvbhw@home.nl



Chest. 2005;127(3):818-824. doi:10.1378/chest.127.3.818
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Introduction: β-Blockers are known to worsen FEV1 and airway hyperresponsiveness (AHR) in patients with asthma. Both characteristics determine the outcome of COPD, a disease with frequent cardiac comorbidity requiring β-blocker treatment.

Objective: To determine the effects of β-blockers on AHR (provocative concentration of methacholine causing a 20% fall in FEV1 [PC20]), FEV1, and response to formoterol in patients with COPD.

Design: A double-blind, placebo-controlled, randomized, cross-over study.

Setting: An ambulatory, hospital outpatient clinic of pulmonary diseases.

Patients: Patients with mild-to-moderate irreversible COPD and AHR.

Intervention: Fifteen patients received propranolol (80 mg), metoprolol (100 mg), celiprolol (200 mg), or placebo for 4 days, followed by a washout period ≥ 3 days. On day 4 of treatment, FEV1 and PC20 were assessed. Immediately hereafter, formoterol (12 μg) was administered and FEV1 was measured for up to 30 min.

Results: PC20 was significantly lower (p < 0.01) with propranolol and metoprolol treatment (geometric means, 2.06 mg/mL and 2.02 mg/mL, respectively) than with placebo (3.16 mg/mL) or celiprolol (3.41 mg/mL). FEV1 deteriorated only after propranolol treatment (2.08 ± 0.31 L) [mean ± SD] compared with placebo (2.24 ± 0.37 L). The fast bronchodilating effect of formoterol was hampered by propranolol (mean increase in FEV1 at 3 min, 6.7 ± 8.9%) but was unaffected by the other β-blockers (16.9 ± 9.8%, 22 ± 11.6%, and 16.9 ± 9.0% for placebo, metoprolol, and celiprolol, respectively).

Conclusions: Pulmonary effects did not occur by celiprolol. Only propranolol reduced FEV1 and the bronchodilating effect of formoterol. Both metoprolol and propranolol increased AHR. Thus, different classes of β-blockers have different pulmonary effects. The anticipated beneficial cardiovascular effects of a β-blocker must be weighted against the putative detrimental pulmonary effects, ie, effect on FEV1, AHR, and response to additional β2-agonists.

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