Key result
Atorvastatin 20 mg/day for one week significantly reduced COX-2 mRNA expression in peripheral blood monocytes by 66% compared to 24% with routine therapy alone in patients with AMI (P<0.05).
Why the study?
Does atorvastatin reduce COX-2 mRNA expression and CRP levels in patients with early stage acute myocardial infarction?
RCT (n=58)
randomly separated
Does atorvastatin reduce COX-2 mRNA expression and CRP levels in patients with early stage acute myocardial infarction?
Absolute Event Rate: 66% vs 24%
p-value: p=<0.05
Atorvastatin 20 mg/day significantly reduces COX-2 mRNA expression and CRP levels in the early stage of acute myocardial infarction, highlighting its rapid anti-inflammatory effects.
Encourages early atorvastatin in AMI to curb inflammation; confirms rapid pleiotropic effects in RCT.
BACKGROUND: We examined the effect of atorvastatin on the expression of COX-2 in peripheral blood monocytes from patients with early stage of acute myocardial infarction (AMI), and the plasma C-reactive protein (CRP) concentrations were also examined. METHODS: Patients with AMI (n = 40) and with stable coronary heart disease (CHD; n = 18) were registered, and patients with AMI were randomly separated to a group that received routine therapy (group A, n = 20) or to a group that received routine therapy plus atorvastatin at 20 mg/day (group B, n = 20) for a week. Peripheral blood monocytes from patients with AMI both before and after treatment and from patients with stable CHD were isolated and cultured for 24 h. COX-2 mRNA expression was analyzed by reverse transcription-PCR. We measured concentrations of CRP in plasma by ELISA. RESULTS: COX-2 expression was activated in peripheral blood monocytes from patients with AMI [0.92 (0.13)] compared with patients with stable CHD [0.19 (0.08)]; after a week of treatment, COX-2 expression in group B (reduced by 66%) was obviously lower than in group A (reduced by 24%; P <0.05). Plasma concentrations of CRP from patients with AMI [43.3 (14.9) mg/L] were increased compared with those from patients with stable CHD [1.65 (0.78) mg/L; P <0.05]; after a week of treatment, CRP concentrations in group B (reduced by 62%) were lower than in group A (reduced by 35%; P <0.05). COX-2 expression in peripheral blood monocytes from patients with AMI was positively correlated with plasma CRP concentration (r = 0.662; P <0.05). CONCLUSIONS: COX-2 may promote acute inflammatory process after AMI. Atorvastatin may improve the antiinflammatory effects through the COX-2 pathway.
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Deng et al. (2006) conducted an RCT in Acute myocardial infarction (n=58). Atorvastatin vs. Routine therapy was evaluated on Reduction in COX-2 mRNA expression in peripheral blood monocytes (p=<0.05). Atorvastatin 20 mg/day for one week significantly reduced COX-2 mRNA expression in peripheral blood monocytes by 66% compared to 24% with routine therapy alone in patients with AMI (P<0.05).
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