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HMG辅酶A还原酶抑制剂与改善冠状动脉疾病患者的全身内皮功能有关。

HMG CoA reductase inhibitors are related to improved systemic endothelial function in coronary artery disease.

作者信息

Järvisalo M J, Toikka J O, Vasankari T, Mikkola J, Viikari J S, Hartiala J J, Raitakari O T

机构信息

Department of Clinical Physiology, Turku University Central Hospital, Turku, Finland.

出版信息

Atherosclerosis. 1999 Dec;147(2):237-42. doi: 10.1016/s0021-9150(99)00189-6.

DOI:10.1016/s0021-9150(99)00189-6
PMID:10559508
Abstract

Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase (statins) may enhance vascular endothelial function independent of their cholesterol lowering effect. To test this hypothesis, we surveyed two groups of patients (age 55+/-7, mean+/-SD) with coronary artery disease that were matched for age, blood pressure and serum lipid levels. Group 1 comprised 23 men without lipid-lowering medication and Group 2 included 22 patients with ongoing HMG CoA reductase inhibitor medication. Flow-mediated (endothelium-dependent) arterial dilatation (FMD) and nitrate-mediated (smooth muscle dependent) dilatation (NMD) were measured in the brachial artery using high resolution ultrasound. FMD was considerably higher in group 2 (4.3+/-2.6 vs. 2.6+/-2.8%; P<0.05). In multivariate regression model, statin use was the only significant (P<0.05) predictor of FMD. In all subjects, FMD correlated with statin dose (P<0.05 for trend). NMD was non-significantly higher in group 2 (11.4+/-5.0 vs. 9.0+/-4.2%, P=0. 08). We conclude that patients with established coronary artery disease on HMG CoA reductase inhibitor therapy have better vascular endothelial function than similar patients without the medication. These data provide further support for the idea that HMG CoA reductase inhibitors enhance endothelial function independent of their lipid-lowering effects. This may suggest that these drugs could be beneficial in secondary prevention of coronary artery disease regardless of the serum cholesterol concentration.

摘要

3-羟基-3-甲基戊二酰辅酶A(HMG CoA)还原酶抑制剂(他汀类药物)可能独立于其降胆固醇作用而增强血管内皮功能。为验证这一假设,我们调查了两组冠状动脉疾病患者(年龄55±7岁,均值±标准差),这两组患者在年龄、血压和血脂水平方面相匹配。第1组由23名未服用降脂药物的男性组成,第2组包括22名正在服用HMG CoA还原酶抑制剂的患者。使用高分辨率超声测量肱动脉的血流介导(内皮依赖性)动脉扩张(FMD)和硝酸盐介导(平滑肌依赖性)扩张(NMD)。第2组的FMD显著更高(4.3±2.6对2.6±2.8%;P<0.05)。在多变量回归模型中,他汀类药物的使用是FMD的唯一显著(P<0.05)预测因素。在所有受试者中,FMD与他汀类药物剂量相关(趋势P<0.05)。第2组的NMD略高但无统计学意义(11.4±5.0对9.0±4.2%,P = 0.08)。我们得出结论,接受HMG CoA还原酶抑制剂治疗的已确诊冠状动脉疾病患者比未服用该药物的类似患者具有更好的血管内皮功能。这些数据为HMG CoA还原酶抑制剂独立于其降脂作用增强内皮功能这一观点提供了进一步支持。这可能表明,无论血清胆固醇浓度如何此类药物在冠状动脉疾病的二级预防中可能有益。

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