Pravastatin therapy fails to suppress post-PCI inflammatory response measured by serum neopterin and CRP levels

Abstract

Percutaneous coronary intervention (PCI) is known to induce both local and systemic inflammatory states. In addition to lowering lipid levels, statins exert well-proven anti-inflammatory effects. We investigated the effects of pravastatin on serum C-reactive protein (CRP) and neopterin levels in the short term after elective PCI. In this randomized prospective study, 93 patients undergoing elective PCI were enrolled. Group 1 (n=30) received pravastatin at a dose of 10 mg/day, Group 2 (n=29) was given 40 mg/day, and Group 3 (n=34) served as the control group and received no lipid-lowering drugs. Blood samples were drawn before and after PCI to measure serum CRP and neopterin levels. Differences among the groups for continuous variables were evaluated by the ANOVA and the Kruskal-Wallis test as appropriate. The Chi-square test was used for comparison of categorical variables. Demographic features and the characteristics of the PCI, including the number of vessels and lesions and the duration and number of inflations, did not differ among groups (p>0.05). Serum CRP and neopterin levels were significantly increased after PCI (p<0.001). Mean serum neopterin levels before and after the PCI were as follows: Group 1: 13.3±5.9 vs 22.8±15.4 nmol/L, Group 2: 16.9±10.2 vs 22.0±14.9 nmol/L, controls: 15.2±11.9 and 18.8±11.5 nmol/L. Prior pravastatin therapy had no significant effect on these inflammatory markers (F=0.5, p=0.6). Percutaneous coronary intervention induces a pronounced inflammatory response. The pre-procedural administration of 2 different doses of pravastatin seems not enough to suppress this inflammation at the short-term follow-up. Further trials are needed to clarify this issue.