Abstract 4268: Use of Cyclo-Oxygenase-2 Inhibitors is not Associated with Accelerated Progression of Coronary Atherosclerosis
While use of cyclo-oxygenase-2 (COX-2) inhibitors has been reported to result in an adverse cardiovascular outcome, the mechanism is unclear. This study investigated whether use of COX-2 inhibitors compared with traditional NSAIDs is associated with accelerated progression of coronary atherosclerosis. Systematic analysis of trials employing IVUS to study plaque progression in patients with angiographic coronary artery disease (REVERSAL, CAMELOT, ACTIVATE, ASTEROID, ILLUSTRATE) was performed. Patients treated with a COX-2 inhibitor (n=464) or only NSAIDs (n=473) were compared with regard to clinical characteristics, cardiovascular outcome and progression of coronary atherosclerosis determined by serial intravascular ultrasound. Clinical and laboratory characteristics were comparable between groups at baseline and follow up. At baseline examination, use of COX-2 inhibitors was not associated with greater percent atheroma volume (PAV, 38.1±9.6 v 38.1±9.2%, p=0.10) or total atheroma volume (TAV, 189.9±84.6 v 186.5±80.6 mm 3, p=0.11). On serial evaluation, use of COX-2 inhibitors did not result in accelerated progression of either PAV (+0.31±0.43 v +0.38±0.42%, p=0.78) or TAV (−3.9±3.4 v −5.3±3.4 mm3, p=0.20). Similar changes in volumes occupied by the lumen (−8.0±2.1 v −12.9±2.1 mm3, p=0.34) and external elastic membrane (−11.8±4.2 v −16.8±4.2 mm3, p=0.37) suggests that the remodeling pattern associated with plaque progression is not modified by the use of COX-2 inhibitors. The rates of cardiovascular events (death, MI, revascularization) were comparable in both groups (26.5% v 22.7%, p = 0.315). Use of COX-2 inhibitors does not modify the rate of atheroma progression and associated arterial remodeling compared to patients taking NSAIDs in patients with coronary artery disease. This suggests that the mechanism underlying any potential increase in cardiovascular events is likely to result from other factors such as thrombosis.