Abstract

Objective To observe the effect of Rosuvastatin on the function of vascular endothelial and inflammatory response in patients with acute myocardial infarction ( AMI) after intervention. Methods Seventy-eight patients with AMI patients underwent coronary angiography and PCI treatment The patients were divided into the control group (38 patients) and the Rosuvastatin group (40 patients) after PCI treatment All patients were routinely used nitrates, low molecular weight heparin,aspirin,clopidogrel,the Rosuvastatin group were treated on the basis of conventional medication plus service Rosuvastatin 10 mg/time, once a day. Both groups were continuous medicated for 6 months. Cardiovascular events of all patients, the serum lipids, inflammation-related biomarkers and indicators of vascular endothelial function were followed up for 6 months after discharge. Results The cardiovascular events in the Rosuvastatin group (5. 0% ) was significantly lower than that of the control group (18.4%) after discharge within 6 months (χ2 = 4. 52, P < 0. 05). After 6 months of discharge, the serum lipids, the serum IL-6, hs-CRP,plasma ET-1 and ox-LDL of Rosuvastatin group ((2. 16 ±0. 54)mmol/L,(4. 16 ±0. 28)mmol/L,(6. 80 ± 2. 65) ng/L, (4. 02 ± 1. 58) mg/L, ( 62. 45 ± 9. 38) ng/L and 381. 65 ± 39. 73, respectively) was significantly lower than those of the control group ((2.47 ±0. 59) mmol/L, (5. 29 ±0. 31 )mmol/L, (9. 39 ±4. 17) ng/L, (5. 76 ± 1. 52)ng/L, (81. 75 ± 10. 23) ng/L and 485. 91 ±42. 68,respectively) (t =2. 423,16. 910,3. 291,4. 952,8. 691 and 11. 173 , respectively , P <0. 01 ). The serum NO of Rosuvastatin group ( ( 62. 17 ± 17. 69 ) μmol/L) was significantly higher than than that of the control group ( (48. 27 ±18. 35 ) μmol/L) (t = 3.406, P < 0.01 ) . The serious adverse events were not observed in the Rosuvastatin group. Conclusions Rosuvastatin reduces inflammatory reaction after PCI in patients with AMI, improves endothelial function, and reduces adverse reactions. Key words: Myocardial infarction; Rosuvastatin; Percutaneous coronary intervention; Inflammatory factor; Endothelial function

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