Non-Steroidal Anti-Inflammatory Drugs: An Overview of Cardiovascular Risks

Abstract

While aspirin may offer protection, other non-aspirin non-steroidal anti-inflammatory drugs (NSAIDs) can cause serious cardiovascular side effects and complications. This has led to a general "black box" warning for cardiovascular adverse events for NSAIDs. This review explores the different mechanisms underlying the protective effects of aspirin, the NSAID associated renovascular effects causing hypertension, edema and heart failure, the cardiovascular effects causing myocardial infarction and stroke, and the possible deleterious interaction between NSAIDs and aspirin.

Keywords: NSAIDs; aspirin; cardiovascular events.

Figure 1

Left: schematic representation of the inhibition of COX-1 (large green figure) by a nonselective NSAID (central blue figure). The entrance channel to COX-1 is blocked by the NSAID. Binding and transformation of arachidonic acid (bottom yellow figure) within COX-1 is prevented. Middle: inhibition of COX-2 by a nonselective NSAID (central blue figure). Right: inhibition of COX-2 by COX-2 selective NSAID (central red figure). The COX-2 side pocket allows specific binding of the COX-2 selective NSAID’s rigid side extension. The entrance channel to COX-2 is blocked. The bulkier COX-2-selective NSAID will not fit into the narrower COX-1 entrance channel, allowing uninhibited access of arachidonic acid into COX-1. Adapted from Hawkey CJ [23].