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The ability of statins to lower hsCRP was first described for pravastatin using data from the CARE trial (94,101). Subsequent confirmatory work has shown the effect of statins on hsCRP to be an important class effect. A meta-analysis of the effects of statins on nonlipid serum markers—specifically CRP, fibrinogen, homocysteine, LDL-C oxidation, tissue plasminogen activator, plasminogen activator inhibitor, and platelet aggregation—concluded that, of these, only CRP appears to be influenced by statin use (102). Indeed, studies of pravastatin, lovastatin, cerivastatin, simvastatin, and atorvastatin indicate that, on average, median hsCRP levels decline 15-25% as early as 6 wk following initiation of therapy (102) in persons with no history of CVD (48,103-106) and in patients with stable coronary disease (103,107) or ACS (90,108). Ezetimibe, a novel cholesterol absorption inhibitor that prevents absorption of dietary and biliary cholesterol without affecting that oftriglycerides and fat-soluble vitamins, appears to augment the CRP-lower-ing ability of statins (106,109).

More important, the magnitude ofhsCRP cholesterol reduction owing to statin therapy is minimally correlated with the magnitude of reduction in LDL-C (102). Although statins reduce LDL-C levels in virtually all patients, there is wide variation in hsCRP response. Recent research suggests that this variation is important in predicting clinical cardiovascular outcomes, at least in secondary prevention settings. In the PROVE-IT trial of intensive (atorvastatin, 80 mg/d) vs moderate (pravastatin, 40 mg/d) statin therapy, patients who achieved an LDL-C level lower than the sample median of 70 mg/dL after 30 d oftreatment were less likely to experience a recurrent coronary event than those who did not achieve this level (2.7 vs 4.0 events per 100 person-yr;p = 0.008) (96). A virtually identical rate r

LDL > 70 mg/dL, CRP < 2 mg/L LDL < 70 mg/dL, CRP > 2 mg/L

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