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Machelle Wilchesky, PhD; Pierre Ernst, MD; James M. Brophy, MD, PhD; Robert W. Platt, PhD; Samy Suissa, PhD
Author and Funding Information

From the Donald Berman Maimonides Geriatric Centre (Dr Wilchesky); the Department of Medicine (Drs Ernst, Brophy, and Suissa); the Department of Epidemiology, Biostatistics and Occupational Health (Drs Brophy, Platt, and Suissa); and the Department of Pediatrics (Dr Platt), McGill University; and the Centre for Clinical Epidemiology (Drs Wilchesky, Ernst, and Suissa), Lady Davis Research Institute, Jewish General Hospital.

Correspondence to: Samy Suissa, PhD, Centre for Clinical Epidemiology, Jewish General Hospital, 3755 Côte Ste-Catherine, Montreal, QC H3T 1E2, Canada; e-mail: samy.suissa@mcgill.ca


Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr Ernst has received speaker fees and has served on advisory boards for AstraZeneca; Boehringer Ingelheim GmbH;GlaxoSmithKline; Merck & Co, Inc; Novartis AG; Nycomed GmbH; and Takeda Pharmaceuticals International GmbH. Dr Suissa has received research grants from AstraZeneca, Boehringer Ingelheim GmbH, and GlaxoSmithKline and has participated in advisory board meetings and as a speaker for AstraZeneca; Boehringer Ingelheim GmbH; Forest Laboratories, Inc; GlaxoSmithKline plc; Merck & Co, Inc; Novartis AG; Nycomed GmbH; Takeda Pharmaceuticals International GmbH; and Pfizer, Inc. Drs Wilchesky, Platt, and Brophy have reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;143(2):580. doi:10.1378/chest.12-2495
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To the Editor:

We thank Dr Medford for his interest in and insightful comments on our recent studies in CHEST.1,2 Indeed, we did include congestive heart failure as an adjustment factor in both studies, and, to the extent that congestive heart failure will have accompanying secondary pulmonary hypertension due to left-sided failure, this will have been controlled for. Both studies were, however, performed using administrative, and not clinical, databases and, as such, clinical information pertaining to P-wave dispersion was not available.

Although it is possible that P-wave dispersion could be associated with arrhythmia, it would also need to be associated either positively or negatively with bronchodilator exposure to induce bias in our estimates of risk. That is, confounding bias would only be present in this study if physicians decided to prescribe a bronchodilator on the basis of P-wave dispersion. We believe that this is implausible. As for pulmonary hypertension secondary to COPD, this is related to severity of COPD, for which we have attempted to adjust. The absence of measures of lung function raises the possibility of residual confounding by severity of COPD, which might explain part of the association between bronchodilator use and cardiac arrhythmia.

References

Wilchesky M, Ernst P, Brophy JM, Platt RW, Suissa S. Bronchodilator use and the risk of arrhythmia in COPD: part 1: Saskatchewan cohort study. Chest. 2012;142(2):298-304. [CrossRef] [PubMed]
 
Wilchesky M, Ernst P, Brophy JM, Platt RW, Suissa S. Bronchodilator use and the risk of arrhythmia in COPD: part 2: reassessment in the larger Quebec cohort. Chest. 2012;142(2):305-311. [CrossRef] [PubMed]
 

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References

Wilchesky M, Ernst P, Brophy JM, Platt RW, Suissa S. Bronchodilator use and the risk of arrhythmia in COPD: part 1: Saskatchewan cohort study. Chest. 2012;142(2):298-304. [CrossRef] [PubMed]
 
Wilchesky M, Ernst P, Brophy JM, Platt RW, Suissa S. Bronchodilator use and the risk of arrhythmia in COPD: part 2: reassessment in the larger Quebec cohort. Chest. 2012;142(2):305-311. [CrossRef] [PubMed]
 
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