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Clinical Investigations: CARDIOLOGY |

Rofecoxib, a COX-2 Inhibitor, Lowers C-Reactive Protein and Interleukin-6 Levels in Patients With Acute Coronary Syndromes*

Daniel Monakier, MD; Michal Mates, MD; Marc W. Klutstein, MD; Jonathan A. Balkin, MBBS; Bernard Rudensky, MD; David Meerkin, MBBS; Dan Tzivoni, MD
Author and Funding Information

*From the Departments of Cardiology (Drs. Monakier, Klutstein, Balkin, Meerkin, and Tzivoni) and Internal Medicine (Dr. Mates), and Laboratory of Clinical Immunology (Dr. Rudensky), Shaare Zedek Medical Center, Jerusalem, Israel.

Correspondence to: Dan Tzivoni, MD, Director, Department of Cardiology, Jesselson Heart Center, Shaare Zedek Medical Center, 12 Hans Beyth St, PO Box 3235, 91031 Jerusalem, Israel; e-mail: cardio@szmc.org.il



Chest. 2004;125(5):1610-1615. doi:10.1378/chest.125.5.1610
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Background: Patients with acute coronary syndromes (ACS) have high levels of inflammatory mediators such as C-reactive protein (CRP) and interleukin (IL)-6.

Aim: To evaluate whether patients with ACS treated with rofecoxib, a COX-2 inhibitor, will have reduced CRP, IL-6, and soluble tumor necrotic factor receptor-1 (sTNF-R1) levels and improved endothelial function.

Methods and results: Thirty-four patients hospitalized with ACS were randomized to receive rofecoxib, 25 mg/d plus aspirin 100 mg/d, or placebo plus aspirin, 100 mg/d, for a period of 3 months. Blood samples for CRP, IL-6, and sTNF-R1 levels were drawn prior to randomization, and after 1 month and 3 months. CRP levels in the rofecoxib group (n = 18) were significantly lower both at 1 month and 3 months compared to the baseline levels (p < 0.02). IL-6 levels were significantly lower at 1 month (p < 0.02) in the rofecoxib group, but not at 3 months. There was no change in endothelial function or sTNF-R1 levels.

Conclusion: Patients recovering from ACS had lower levels of CRP and IL-6 at 1 month and lower CRP levels at 3 months when treated with rofecoxib plus aspirin. Suppression of inflammatory processes may lead to retardation of coronary atherosclerosis and coronary events.

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