Inhibition of cyclooxygenase-2 improves cardiac function in myocardial infarction.

Induction of cyclooxygenase-2 (COX-2) in ischemic myocardium is thought to increase the production of proinflammatory prostanoids and contribute significantly to the ischemic inflammation. Left ventricular myocardial infarction (MI) was created by ligating the left coronary artery in Lewis rats. Hemodynamic measurements at 4 weeks showed better cardiac function in the group treated with a selective COX-2 inhibitor (DFU; 5 mg/kg/day) for 2 weeks after induction of MI compared to the vehicle treated group. These results suggest that induction of COX-2 contributes to myocardial dysfunction, and that selective inhibition of COX-2 could constitute an important therapeutic target for the treatment of MI.