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Original Research: COPD |

Cardiovascular Events Associated With Ipratropium Bromide in COPD

Sarika S. Ogale, PhD; Todd A. Lee, PharmD, PhD; David H. Au, MD, MS; Denise M. Boudreau, PhD; Sean D. Sullivan, PhD
Author and Funding Information

From the Pharmaceutical Outcomes Research and Policy Program, Department of Pharmacy (Drs Ogale, Boudreau, and Sullivan), University of Washington, Seattle, WA; Center for Management of Complex Chronic Care (Dr Lee), Hines VA Hospital, Hines, IL; Center for Pharmacoeconomic Research and Department of Pharmacy Practice (Dr Lee), University of Illinois at Chicago, Chicago, IL; Health Services Research and Development, VA Puget Sound Health Care System and Department of Medicine (Dr Au), University of Washington, Seattle, WA; and The Center for Health Studies (Dr Boudreau), Group Health Cooperative, Seattle, WA.

Correspondence to:Todd A. Lee, PharmD, PhD, Hines VA Hospital, 5000 S. 5th Ave (151-H), Hines, IL 60141; e-mail: todd.lee@va.gov


For editorial comments see page 1

Dr Ogale is currently at Genentech Pharmaceuticals, San Francisco, CA.

Funding/Support: This research was funded by the US Department of Veterans Affairs Health Services Research and Development (IIR 03-307).

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;137(1):13-19. doi:10.1378/chest.08-2367
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Background:  Studies have suggested an increased risk of cardiovascular morbidity and mortality associated with the use of ipratropium bromide. We sought to examine the association between ipratropium bromide use and the risk of cardiovascular events (CVEs).

Methods:  We performed a cohort study of 82,717 US veterans with a new diagnosis of COPD between 1999 and 2002. Subjects were followed until they had their first hospitalization for a CVE (acute coronary syndrome, heart failure, or cardiac dysrhythmia), they died, or the end of the study period (September 30, 2004). Cumulative anticholinergic exposure was calculated as the number of 30-day equivalents (ipratropium bromide) within the past year. We used Cox regression models with time-dependent covariates to estimate the risk of CVE associated with anticholinergic exposure and to adjust for potential confounders, including markers of COPD severity and cardiovascular risk.

Results:  We identified 6,234 CVEs (44% heart failure, 28% acute coronary syndrome, 28% dysrhythmia). Compared with subjects not exposed to anticholinergics within the past year, any exposure to anticholinergics within the past 6 months was associated with an increased risk of CVE (hazard ratio [95% CI] for≤four and>four 30-day equivalents: 1.40 [1.30-1.51] and 1.23 [1.13-1.36], respectively). Among subjects who received anticholinergics more than 6 months prior, there did not appear to be elevated risk of a CVE.

Conclusions:  We found an increased risk of CVEs associated with the use of ipratropium bromide within the past 6 months. These findings are consistent with previous concerns raised about the cardiovascular safety of ipratropium bromide.

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