C-reactive protein (CRP) is a prototypic marker of inflammation. The effect of tirofiban on CRP levels in patients with non-ST–elevation myocardial infarction (NSTEMI) was investigated.

The present study was prospective and randomized. Patients with NSTEMI received aspirin, clopidogrel, statin, and unfractionated heparin. Patients with NSTEMI were enrolled into either the tirofiban + heparin group (group 1: n = 25) or the heparin group (group 2: n = 32). Levels of CRP were determined at baseline and after 48 and 72 hours. Heparin and tirofiban were discontinued after 48 hours.

Levels CRP of were similar in two groups at baseline; they increased significantly at 48 hours and 72 hours in the control group but not in the tirofiban group. The differences on and after treatment were statistically significant. In group 1, CRP elevation was attenuated after tirofiban infusion compared with group 2.

Products of platelet activation may aid neutrophil accumulation and enhance inflammation. Activated leukocytes and platelets potentate each others' effects. Tirofiban strongly inhibits the platelet aggregation. The decreased platelet aggregation can suppress the inflammatory protein, chemokine, and adhesion molecule expression. After the tirofiban infusion, CRP elevation was atteunated in patients with NSTEMI.