阿托伐他汀减少稳定型心绞痛患者经皮冠状动脉介入术后心肌和血管内皮损伤的机制研究

The mechanism of atorvastatin protection against myocardium and vessel injury in patients with stable angina pectoris undergoing percutancous coronary intervention

目的 探讨他汀类药物减少对稳定型心绞痛患者经皮冠状动脉介入（PCI）,术后心肌和血管内皮损伤的可能机制.方法 134例既往未服用他汀类药物的稳定型心绞痛患者,其中60例PCI术前12 h内顿服阿托伐他汀40～80 mg者为他汀治疗组,未服用他汀类药物患者74例为非他汀治疗组.记录所有患者临床特征和介入术中情况,并分别于PCI术前及术后6、24h抽取静脉血,测定外周血中循环内皮细胞、肌酸磷酸激酶同工酶（CK-MB）和血脂水平.结果 2组患者在性别、年龄、糖尿病和高血压病患病率、吸烟史、既往血运重建史、超声心动图左心室射血分数、血肌酐、多支血管病变支数、治疗药物、造影下病变特征、介入治疗情况等方面均无明显差异（均P＞0.05）;PCI术后阿托伐他汀和非他汀治疗组静脉血总胆固醇含量分别是（2.74±0.47）和（2.66±0.44）mmol/L,低密度脂蛋白含量分别是（1.81±0.37）和（1.72±0.13）mmol/L,2组间差异无统计学意义（P＞0.05）;阿托伐他汀治疗组PCI术后心肌损伤（CK-MB高于正常值上限）发生率和外周血循环内皮细胞数量明显低于非他汀预处理组[10.0%比23.0%,（3.4±2.7）个/ml比（5.3±2.9）个/ml,均P＜0.05].结论 阿托伐他汀减轻稳定型心绞痛患者PCI术后心肌损伤,可能与保护血管内皮结构完整性有关.

Objective To compare the effects of pre-treatment with or without atorvastatin on plasm creatine kinase-MB and circulating endothelial cells in patients with stable angina pectoris undergoing percutaneous coronary intervention. Methods One hundred and thirty-four patients with stable angina pectoris were divided into 2 groups.Statin group contained 60 patients who were received 40-80 mg atorvastatin within 12 hours before elective procedure. Non-statin pretreatment group contained 74 patients who had never received any statin therapy before procedure. We measured plasm creatine kinase-MB and lipid before and 24 hours after percutaneous coronary intervention. Circulating endothelial cells were also recorded before and 6 hours after procedure. Results Detection of markers of myocardial injury above the one fold of upper normal limit was significantly lower in the statin group than that in the non-statin group（10.0% vs 23.0%, P 〈 0.05）. Vessel injury by circulating endothelial cells difference determination was detected before and after coronary intervention in the statin group（3.4 ± 2.7）piece/ml and the non-statin group（5.3 ± 2.9）piece/ml ,P 〈 0.05. There were no significant differences in plasm cholesterol and low desity lipoprotein after procedure between statin [（2.74 ± 0. 47）, （1.81 ± 0. 37）mmol/L and non-statin （2.66 ±0.44） ,（1.72±0.13）mmol/L]groups（P 〉0.05）. Conclusion Reductin in myocardial injury undergoing coronary intervention in patients with atorvastatin pre-treatment with stable angina pectoris may be related to statin＇s protective effect on vessel endothelial cells, which is not related to lipid-lowing effect.