Cardiac Arrhythmias in Adult Patients with Asthma

Abstract

Objective. The pathogenesis of cardiac arrhythmias in asthma patients has not been fully elucidated. Adverse drug effects, particularly those of β2-mimetics, may play a role. The aim of this study was to determine whether asthma is associated with the risk of cardiac arrhythmias and electrocardiographic characteristics of arrhythmogenicity (ECG) and to explore the role of β2-mimetics. Methods. A cross-sectional study was conducted among 158 adult patients with a diagnosis of asthma and 6303 participants without asthma from the cohort of the Utrecht Health Project—an ongoing, longitudinal, primary care-based study. All patients underwent extensive examinations, including resting 12-lead electrocardiogram (ECG) and pulmonary function tests. The primary outcome was “any arrhythmia on the ECG” (including tachycardia, bradycardia, premature ventricular contraction (PVC), and atrial fibrillation or flutter). Secondary outcomes were tachycardia, bradycardia, PVC, atrial fibrillation or flutter, mean heart rate, mean corrected QT (QTc) interval length, and prolonged QTc interval. Results. Tachycardia and PVCs were more prevalent in patients with asthma (3% and 4%, respectively) than those without asthma (0.6%, p < .001; 2%, p = .03, respectively). The prevalence of QTc interval prolongation was similar in participants with (2%) and without asthma (3%, odds ratio [OR]: 0.6 and 95% confidence interval [95% CI]: 0.2–2.0). In 74 asthma patients, who received β2-mimetics, tachycardia and PVCs were more common (OR: 12.4 [95% CI: 4.7–32.8] and 3.7 [95% CI: 1.3–10.5], respectively). Conclusions. The adult patients with asthma more commonly show tachycardia and PVCs on the ECG than those without asthma. The patients with asthma received β2-mimetics; the risk of tachycardia and PVCs is even more pronounced.

• β2-mimetic agents
• electrocardiography
• obstructive pulmonary disease
• premature ventricular contractions
• tachycardia

Acknowledgments

We thank Prof. ME Numans, M.D., Ph.D. from the Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands, for providing access to the data of the UHP. We also thank the participating inhabitants of Leidsche Rijn, Utrecht, The Netherlands and the GPs working in this area for providing research data from their routine care.

Declaration of Interest

The authors MJ Warnier, FH Rutten, JA Kors, JWJ Lammers, A de Boer, AW Hoes, and ML De Bruin declare that they have no conflicts of interest in relation to this article.

Funding

This study was supported by Utrecht University. The UHP received grants from the Ministry of Health, Welfare, and Sports (VWS), the Utrecht University, the Province of Utrecht, the Dutch Organisation of Care Research (ZON), the University Medical Center Utrecht (UMC Utrecht), and the Dutch College of Healthcare Insurance Companies (CVZ). The funding source had no involvement in the study design; in the collection, analysis, and interpretation data; in the writing of the report; and in the decision to submit the article for publication.

The Department of Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute for Pharmaceutical Sciences, has received unrestricted research funding from the Netherlands Organisation for Health Research and Development (ZonMW), the Dutch Health Care Insurance Board (CVZ), the Royal Dutch Pharmacists Association (KNMP), the private–public-funded Top Institute Pharma (www.tipharma.nl, includes co-funding from universities, government, and industry), the EU Innovative Medicines Initiative (IMI), EU 7th Framework Program (FP7), the Dutch Medicines Evaluation Board, and the Dutch Ministry of Health and industry (including GlaxoSmithKline, Pfizer, and others).