Nonsteroidal antiinflammatory drug use and cardiovascular risks after coronary stent implantation

To determine whether use of nonselective nonsteroidal antiinflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2)-selective inhibitors in patients with coronary stents increased the 3-year rate of major adverse cardiovascular events (MACE).

Population-based cohort study.

The Danish National Patient Registry, the Western Denmark Heart Registry, the Danish Nationwide Prescription Database, the Danish Civil Registration System, and the National Registry of Causes of Deaths.

A total of 13,001 patients who underwent first-ever percutaneous coronary intervention with stent implantation between January 1, 2002, and June 30, 2005.

All patients were followed for 3 years after stent implantation for MACE, defined as the first occurrence of myocardial infarction, stent thrombosis, target-lesion revascularization, or cardiac death. Patients' comorbidities were identified from the hospital registries; time-varying use of NSAIDs and concomitant drugs was determined from the Danish Nationwide Prescription Database. For each clinical outcome (MACE), the 3-year risk was computed. We used Cox proportional-hazards regression analysis to compute hazard ratios (HRs) as a measure of relative risk, controlling for potential confounders. During the follow-up period, 5407 patients (41.6%) redeemed at least one NSAID prescription. There were 686 hospitalizations for myocardial infarction (5.3% of patients), 146 for stent thrombosis (1.1%), and 1091 for target-lesion revascularization (8.4%). A total of 1220 patients (9.4%) died during the follow-up period; 637 (4.9%) died of cardiac causes. Compared with no NSAID use, the adjusted HR for MACE was 1.04 (95% confidence interval [CI] 0.83-1.31) for nonselective NSAID use and 1.00 (95% CI 0.81-1.25) for COX-2 inhibitor use.

Use of nonselective NSAIDs or COX-2 inhibitors was not associated with an increased rate of MACE in patients with coronary stents. However, we cannot rule out small risks associated with individual NSAIDs.