Document Type : Original Article(s)
Authors
1 Associate Professor of Cardiology, Isfahan Cardiovascular Research Center, Isfahan University of Medical Sciences, Isfahan.
2 Resident of cardiology, Isfahan University of Medical Sciences, Isfahan.
3 Professor of Cardiology, Isfahan Cardiovascular Research Center, Isfahan University of Medical Sciences, Isfahan.
4 Isfahan University of Medical Sciences, Isfahan.
5 Researcher Methodology and statistic consultant, Isfahan Cardiovascular Research Center, Isfahan University of Medical Sciences, Isfahan.
Abstract
Abstract INTRODUCTION: Inflammation is now recognized to play an important role at all stages of the atherogenic process that are precursors of myocardial infarction (MI). hs-CRP is one of this markers of inflammation and Statins have both lipid lowering and anti inflammatory effects and it is proposed that aggressive statins treatment can cause lower serum CRP levels. In this study, we compared intensive and moderate atorvastatin treatment effects on mean serum CRP reduction. METHODS: This study is a double-blind clinical trial. Some patients who were up 21 years old and recently suffered non-ST elevation MI during 24 hours and went to the emergency department of Feiz hospital and/or Chamran hospital and were confined to bed in the CCU were entered in study. A total number of 50 patients were divided to two groups of equal number: A-25 patients under treatment with 80 mg Atorvastatin B-25 patients under treatment with 20 mg Atorvastatin. The examinations hs-CRP and lipid profile were done at admission to CCU, discharge from hospital and two months after treatments and results compared in two groups. RESULTS: It was specified that in group treated with 80 mg atorvastatin 12 patients (48%) were males and 9 patients (52%) were females and mean age was 60.1 ± 13.4 years. In group treated with 20mg atorvastatin, 16 patients (64%) were males and 9 patients (36%) were males and mean age was 59.6 ± 11.2 years. In group treated with 80mg atorvastatin mean CRP at CCU admission (baseline), discharge and two months latter was 7 ± 5.5, 5.3 ± 4.1 and 2.3 ± 4.3 respectively and in group treated with 20mg atorvastatin was 7.1 ± 8.3, 5.7 ± 7.4 and 3.5 ± 5.1 respectively. Mean serum LDL (Low density lipoprotein) in patients before and after treatment in group treated with 80 mg atorvastatin was 134.2 ± 33.2 and 117.5 ± 31.9 and in group treated with 20 mg atorvastatin was 141.07 ± 33.4 and 126.4 ± 32.5. Mean serum CRP decreased in both groups after treatment but mean CRP decreased to lower levels in patients treated with 80mg atorvastatin either at discharge from hospital (P = 0.32) or two months after treatment(P = 0.02) compared patients treated with 20mg atorvastatin and this difference between two groups was more significant two months after treatment than at discharge. Also serum LDL was decrease in both groups after treatment but no significant difference was detected (P = 0.77). With Pearson correlation there was correlation between the percent reductions in LDL cholesterol and in CRP levels only for the total patients (P < 0.001), not for the high dose atorvastatin group alone or the low dose atorvastatin group alone (P > 0.05). CONCLUSION: high dose statins cause lower serum CRP levels and their effect on lowering CRP is separated from their lipid lowering effects and is due to their anti inflammatory effects. Keywords: atorvastatin, CRP, MI, st elevation MI
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