BACKGROUND: Extra-lipid effects of statins, such as anti-inflammatory actions, may contribute to their clinical benefit. These effects, with important implications for the concept of a statin "class effect," may be drug specific or may be related to the extent of lipid lowering. METHODS: We randomized 130 patients to treatment with eitheratorvastatin (80 mg daily, n = 63) or pravastatin (40 mg daily, n = 67), and measured serum lipids, C-reactive protein, and fibrinogen at baseline and after 3 months of therapy. RESULTS:Mean C-reactive protein (CRP) levels were significantly reduced in both groups, with a 36% reduction in the atorvastatin group (0.39 +/- 0.36 to 0.25 +/- 0.27, P =.001) and a 22% reduction observed in the pravastatin group (0.40 +/- 0.33 to 0.31 +/- 0.32, P =.003). A reduced or unchanged CRP level was seen in 67.2% of pravastatin-treated patients (45/67) and 73% of atorvastatin- treated patients (46/63) (P =.47). There was no difference between drugs in either the absolute or relative reductions in CRP levels. However, whereas the reduction of CRP with pravastatin was unrelated to the degree of low-density lipoprotein reduction (r = -.05, P =.69), atorvastatin-induced CRP reductions correlated directly to the change in low-density lipoprotein-C (r =.33, P =.009). CONCLUSIONS: High-dose atorvastatin and pravastatin both reduce CRP levels. However, whereas pravastatin's effect on CRP is independent of lipid-lowering efficacy, these data suggest that lipid-dependent mechanisms are, at least in part, active in atorvastatin-treated patients.
RCT Entities:
BACKGROUND: Extra-lipid effects of statins, such as anti-inflammatory actions, may contribute to their clinical benefit. These effects, with important implications for the concept of a statin "class effect," may be drug specific or may be related to the extent of lipid lowering. METHODS: We randomized 130 patients to treatment with either atorvastatin (80 mg daily, n = 63) or pravastatin (40 mg daily, n = 67), and measured serum lipids, C-reactive protein, and fibrinogen at baseline and after 3 months of therapy. RESULTS: Mean C-reactive protein (CRP) levels were significantly reduced in both groups, with a 36% reduction in the atorvastatin group (0.39 +/- 0.36 to 0.25 +/- 0.27, P =.001) and a 22% reduction observed in the pravastatin group (0.40 +/- 0.33 to 0.31 +/- 0.32, P =.003). A reduced or unchanged CRP level was seen in 67.2% of pravastatin-treated patients (45/67) and 73% of atorvastatin- treated patients (46/63) (P =.47). There was no difference between drugs in either the absolute or relative reductions in CRP levels. However, whereas the reduction of CRP with pravastatin was unrelated to the degree of low-density lipoprotein reduction (r = -.05, P =.69), atorvastatin-induced CRP reductions correlated directly to the change in low-density lipoprotein-C (r =.33, P =.009). CONCLUSIONS: High-dose atorvastatin and pravastatin both reduce CRP levels. However, whereas pravastatin's effect on CRP is independent of lipid-lowering efficacy, these data suggest that lipid-dependent mechanisms are, at least in part, active in atorvastatin-treated patients.
Authors: Elizabeth D Kantor; Johanna W Lampe; Thomas L Vaughan; Ulrike Peters; Colin D Rehm; Emily White Journal: Am J Epidemiol Date: 2012-11-08 Impact factor: 4.897