Lower risk of thromboembolic cardiovascular events with naproxen among patients with rheumatoid arthritis.

Abstract

PLATELET AGGREGATION plays a central role in the pathophysiology of thromboembolic cardiovascular events (TCEs) such as myocardial infarction (MI) and stroke.¹ Platelet activation and aggregation are mediated through the cyclooxygenase (COX) 1 isoform. Aspirin, an irreversible inhibitor of COX-1, profoundly inhibits platelet aggregation, prolongs bleeding time,² and has been shown to reduce the incidence of serious TCEs in patients presenting with an acute coronary syndrome³ and in patients with a history of MI,⁴ angina pectoris,⁵ or stroke.⁴ Theoretically, some nonaspirin nonsteroidal anti-inflammatory drugs (NSAIDs), which are nonselective inhibitors of both COX-1 and COX-2, could also have an antithrombotic effect via inhibition of platelet activity. In particular, naproxen has been shown to confer clinically important levels of platelet inhibition.^6,7 In addition, the product circular for naproxen in the United States and other countries states that naproxen reduces platelet aggregation, prolongs bleeding time, and is associated with a risk of bleeding.⁸