C-reactive protein (CRP) levels are associated with cardiovascular risk. We assessed the hypothesis that atorvastatin might have anti-inflammatory effects in acute coronary syndromes (ACS) as shown by CRP reduction.

This study was a prospective, randomized, double-blind, placebo-controlled study of 90 consecutive patients admitted within 48 hours of onset of ACS with CRP levels ≥1.4 mg/dL. Patients were assigned to atorvastatin 40 mg daily or placebo over 30 days. C-reactive protein levels, lipid profiles, serum fibrinogen, white cell count, and erythrocyte sedimentation rate were measured at entry, hospital discharge, and 1 month later.

Baseline clinical characteristics did not differ between atorvastatin and placebo groups (mean age 59.3 ± 13.4 vs 61.1 ± 11.5, P = ns); myocardial infarction 52.3% versus 67.4% (P = ns). In both groups, median baseline CRP levels were comparable (5.97 ± 6.2 vs 4.64 ± 4.2 mg/dL, P = ns). C-reactive protein levels were lower in the atorvastatin group versus control group at discharge (1.68 ± 1.65 vs 4.12 ± 4.18 mg/dL) and at 30 days (0.50 ± 0.71 vs 2.91 ± 2.68 mg/dL, both P < .0001). C-reactive protein levels significantly decreased from baseline to discharge and 1 month later in placebo and atorvastatin groups (both P < .0001); however, the reduction was greater in the atorvastatin group (62% vs 11% at discharge [P < .0001]; 84% vs 30% at 1 month [P < .0001]). In addition, atorvastatin was associated with a reduction in total and low-density lipoprotein cholesterol and erythrocyte sedimentation rate at discharge and at 30 days (P < .0001 for all comparisons). No correlation was found between changes in CRP and cholesterol levels.

C-reactive protein levels in ACS were rapidly reduced with atorvastatin. These data provide evidence that statins have fast and early anti-inflammatory effects in addition to lipid-lowering effects in ACS.