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<p>This report examines differences in risk of myocardial infarction and stroke (cardiovascular events) between the cyclooxygenase-2 (COX-2) inhibitors Rofecoxib, Celecoxib, and Valdecoxib, and the traditional nonsteroidal anti-inflammatory agents (NSAIDs) Naproxen and Ibuprofen, as well as Meloxicam, a preferential COX-2 inhibitor. The population studied was the DoD TRICARE beneficiary population greater than age 40 during the study period. In September of 2004, Rofecoxib was removed from the market due to an increased risk of cardiovascular events. In February of 2005, the Food and Drug Administration (FDA) examined the entire class of COX-2 inhibitors and recommended that Valdecoxib also be withdrawn from the market. According to Department of Defense TRICARE prescription records, COX-2 inhibitor prescription numbers were increasing rapidly and more than $7 million was spent on these agents alone in July of 2004. Logistic regression was used to analyze TRICARE prescription and diagnosis data from calendar years 2002, 2003, and 2004 for cardiovascular event risk comparisons among various NSAIDs. Rofecoxib was found to have a significantly increased risk of cardiovascular events when compared with all other medications in the study, including Valdecoxib. Odds ratios for comparison with Valdecoxib, Celecoxib, Meloxicam, Ibuprofen, and Naproxen were 1.09, 1.14, 1.15, 1.28, and 1.23. Valdecoxib showed a significant increase compared to Ibuprofen, Naproxen, and Celecoxib (odds ratios 1.21, 1.16, and 1.06). Ibuprofen showed a significantly decreased risk relative to all medications except Naproxen. When considering only cardiovascular risk, this study suggests prescribers should consider Ibuprofen or Naproxen as the primary agent of choice, with Meloxicam, and Celecoxib as reasonable second choices. Ultimately, the decision must also weigh the patient's risk of gastrointestinal side effects and cost of therapy.
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<br>Subjects: Steroids; Myocardial infarction; Medicine; Research; Cardiovascular system; Ibuprofen</div>
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Lefebvre, Kim L.</div>
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