Ibuprofen Could Reduce Cardioprotective Effect Of Aspirin

A research letter in this week’s issue of THE LANCET suggests that the pain-killer ibuprofen could diminish the well-known beneficial effects of aspirin on preventing cardiovascular disease.

Aspirin makes platelets (blood-clotting cells) less ’sticky’ which is associated with fewer thromboses (clots). Aspirin therefore reduces the chance of heart attacks caused by coronary thrombosis and stroke (cerebral thrombosis). Previous laboratory research has suggested that ibuprofen interacts with aspirin to reduce this ’good’ effect of aspirin on platelet stickiness.

Tom MacDonald and Li Wei from the Medicines Monitoring Unit (MEMO) at the University of Dundee, Ninewells Hospital& Medical School, UK, studied 7107 patients with cardiovascular disease who were discharged from hospital and who were taking prescribed low-dose aspirin. Within this group they compared the death rate (from any cause and from cardiovascular causes) of those patients taking prescribed aspirin alone with those taking prescribed aspirin and ibuprofen. They also compared mortality data for patients taking another common pain-killer (diclofenac) and those taking any of the other Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) in addition to aspirin.

Individuals prescribed both aspirin and ibuprofen (187 patients) had about a doubling of risk of death from any cause and around a 75% increased risk of death from cardiovascular disease, compared with those prescribed aspirin alone. There was no increase in mortality risk for people prescribed aspirin in combination with diclofenac or other NSAIDs.

Tom MacDonald comments: “Although our findings are not conclusive, they do support the hypothesis that ibuprofen may reduce the benefits of aspirin in people with cardiovascular disease. Perhaps it would be prudent that such patients took an alternative pain-killer at least until this issue is further clarified. Furthermore, we also know that aspirin and ibuprofen taken together increases the risk of bleeding from stomach ulcers. So this combination may not only reduce the benefits of aspirin, but may also increase the risks of side effects.”

In an accompanying Commentary (p 542), Garret FitzGerald from x states: “Whilst the results reported by MacDonald and Wei are congruent with the understanding of the clinical pharmacology of aspirin, ibuprofen, and diclofenac, a constraint on the interpretation of their results, which they recognise, is the possibility of confounding by recognised (eg, smoking) and unrecognised variables. The relatively small sample size also limits conclusions about the interaction of aspirin with NSAIDs other than diclofenac and ibuprofen.” He concludes: “The place of aspirin in the secondary prevention of myocardial infarction and stroke is well established. When patients taking aspirin for cardioprotection require chronic treatment of inflammation with an NSAID, the addition of diclofenac or a conventional selective COX-2 inhibitor would seem preferable to ibuprofen.”