Celecoxib-Induced Change in Atrial Electrophysiologic Substrate in Arthritis Patients

Authors

  • Katerina Pizzuto B.H.Sc.,

    Corresponding author
    1. Queen's University, Kingston, Ontario, Canada
    • Address for correspondence: Dr Damian P. Redfearn, M.B., C.hB., M.D., M.R.C.P.I., F.R.C.P.C., Director of Heart Rhythm Service, FAPC 3, Kingston General Hospital, 76 Stuart Street, Kingston, ON, K7L 2V7, Canada. Fax: 613 548 1387; E-mail: redfeard@kgh.kari.net; Katerina Pizzuto, B.H.S.c., Queen's University, 99 University Avenue, Kingston, ON K7L 3N6, Canada. Fax: 613 548 1387; E-mail: kpizzuto@qmed.ca

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  • Henry L Averns M.B., C.h.B.,

    1. Queen's University, Kingston, Ontario, Canada
    2. Department of Rheumatology, Kingston General Hospital, Kingston, Ontario, Canada
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  • Adrian Baranchuk M.D.,

    1. Queen's University, Kingston, Ontario, Canada
    2. Heart Rhythm Service, Kingston General Hospital, Kingston, Ontario, Canada
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  • Hoshiar Abdollah M.B., Ch.B.,

    1. Queen's University, Kingston, Ontario, Canada
    2. Heart Rhythm Service, Kingston General Hospital, Kingston, Ontario, Canada
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  • Kevin A. Michael M.B., Ch.B.,

    1. Queen's University, Kingston, Ontario, Canada
    2. Heart Rhythm Service, Kingston General Hospital, Kingston, Ontario, Canada
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  • Christopher Simpson M.D.,

    1. Queen's University, Kingston, Ontario, Canada
    2. Heart Rhythm Service, Kingston General Hospital, Kingston, Ontario, Canada
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  • Damian P. Redfearn M.D.

    Corresponding author
    1. Queen's University, Kingston, Ontario, Canada
    2. Heart Rhythm Service, Kingston General Hospital, Kingston, Ontario, Canada
    • Address for correspondence: Dr Damian P. Redfearn, M.B., C.hB., M.D., M.R.C.P.I., F.R.C.P.C., Director of Heart Rhythm Service, FAPC 3, Kingston General Hospital, 76 Stuart Street, Kingston, ON, K7L 2V7, Canada. Fax: 613 548 1387; E-mail: redfeard@kgh.kari.net; Katerina Pizzuto, B.H.S.c., Queen's University, 99 University Avenue, Kingston, ON K7L 3N6, Canada. Fax: 613 548 1387; E-mail: kpizzuto@qmed.ca

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  • Funding: This work was supported by the John F. Sparks Memorial Scholarship, which was awarded to K. Pizzuto by the Queen's University Undergraduate Medical Education Office. Conflict of Interest: The authors declare no conflict of interest.

Abstract

Background

Cyclooxygenase-2 inhibitors, the newest class of nonsteroidal antiinflammatories, pose an increased risk of adverse cardiovascular events, in particular atrial fibrillation (AF). We hypothesized that the COX-2 inhibitor celecoxib alters atrial electrophysiology, and thus promotes the development of AF.

Methods

Three prospective patient cohorts were created: Healthy patients (n = 35), inflammatory arthritis patients with no celecoxib use (n = 22), and inflammatory arthritis patients treated with celecoxib (n = 20). Patients were included in the arthritis cohorts if they were over the age of 18 and had a diagnosis of inflammatory arthritis. Patients in the celecoxib group must be actively treated with celecoxib for more than 2 months. Patients were excluded if they were taking antiarrhythmic mediation, had a diagnosis of AF, refractory hypertension, or congestive heart failure. High-resolution signal-averaged electrocardiogram was recorded and P-wave duration (PWD) was derived.

Results

PWD was significantly longer in inflammatory arthritis patients treated with celecoxib, compared to both healthy and inflammatory arthritis patients (P = 0.049, P = 0.036). There was no difference in the PWD of healthy patients as compared to inflammatory arthritis patients (P = 0.916). Mean PWD (standard error of the mean) of the inflammatory arthritis patients treated with celecoxib was 133.1 (2.7) ms as compared to 125.3 (1.6) ms in the healthy patients and 124.0 (2.9) ms in the inflammatory arthritis patients.

Conclusions

Given that PWD is a well-accepted noninvasive marker of atrial electrophysiology, our results suggest that these patients demonstrate adverse atrial remodeling predisposing to atrial arrhythmia.

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