(Circulation. 2007;115:288-291.)
© 2007 American Heart Association, Inc.
Editorial |
From the Division of Cardiology, Department of Medicine and Cardiovascular Research Group, Faculty of Medicine, University of Alberta, Edmonton, Canada.
Reprint requests to B.I. Jugdutt, MBChB, MSc, MD, 2C2 Walter MacKenzie Health Sciences Centre, Division of Cardiology, University of Alberta, Edmonton, Alberta, T6G 2R7, Canada. E-mail bjugdutt@ualberta.ca
Key Words: Editorials myocardial infarction pharmacology prostaglandins remodeling
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
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Article p 326
Moreover, randomized clinical trials led to the withdrawal of rofecoxib because of CV concerns. In a trial for the prevention of colorectal adenoma, celecoxib was associated with a dose-related increase in the combined end point of CV death, myocardial infarction (MI), stroke, or heart failure.1 A subsequent publication showed a 2-fold increase in CV risk with celecoxib and a trend to increased blood pressure.2 The Food and Drug Administration reported in April, 2005 that all 3 approved COXIBs (ie, celecoxib, rofecoxib, and valdecoxib) were associated with increased risk of serious adverse CV events compared with placebo, but CV risk was not clearly different when COX-2selective and nonselective NSAIDs were compared.3 A large case-control study reported an increased relative risk of MI in the elderly treated with rofecoxib.4 A Danish study concluded that COXIBS in all doses
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