急性冠脉综合征患者内皮依赖舒张功能血浆ox-LDL的变化及意义

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目的探讨急性冠脉综合征(ACS)患者内皮依赖血管舒张功能的变化及氧化低密度脂蛋白(ox-LDL)在其中的作用。方法以2004-03~2004-10在第三军医大学新桥医院心内科住院确诊的51例急性冠脉综合征患者为观察组,其中急性心肌梗死(AMI)22例,不稳定性心绞痛(UAP)29例;以临床及选择性冠状动脉造影排除冠心病的20例为对照组,高分辨率超声测肱动脉反应性充血引起的流量介导血管扩张(FMD)与硝酸甘油介导的血管扩张(NTG)。测定血浆中的NO、ox-LDL水平。结果(1)与对照组相比,急性心肌梗死(AMI)、不稳定型心绞痛(UAP)肱动脉血流介导内皮依赖血管舒张功能FMD均降低[(7·2±1·42)、(7·6±1·12)对(15·46±1·2),P<0·05],而AMI与UAP相比差异无显著性(P>0·05)。含服硝酸甘油后三组血管内径变化的差异无显著性(P>0·05);(2)ACS患者的NO水平较对照组明显降低,其中急性心肌梗死组的NO降低更明显[(48·46±12·24)、(60·42±10·32)对(94·72±12·34)μmol/L,P<0·05];(3)ACS组的ox-LDL水平较对照组明显升高,其中急性心肌梗死组的升高更明显[(586·4±168·5)、(447·4±186·7)对(348·6±172·3)μg/L,P<0·05]。经logisitic回归分析,ox-LDL的风险比值(OR)值大于1,为ACS的危险因素;FMD的OR值小于1,为ACS的保护因素。观察ox-LDL与FMD在急性冠脉综合征中的作用相互独立。结论ACS发病过程与血浆ox-LDL水平、内皮功能受损有关,二者可作为独立危险因素。 Objective To investigate the changes of endothelium-dependent vasodilation and the role of ox-LDL in patients with acute coronary syndrome (ACS). Methods Totally 51 patients with acute coronary syndrome (ACS) diagnosed as hospitalized in Department of Cardiology, Xinqiao Hospital of the Third Military Medical University from March 2004 to October 2004 were selected as the observation group. Among them, 22 cases were acute myocardial infarction (AMI), 22 cases were unstable angina (UAP) ) In 29 cases. The clinical and selective coronary angiography exclude coronary heart disease in 20 cases as control group, high-resolution ultrasound measured bradyarrhythmia caused by flow-mediated vasodilatation (FMD) and nitroglycerin-mediated vasodilation (NTG). Plasma NO, ox-LDL levels were measured. Results (1) Compared with the control group, the brachial artery blood flow induced by acute myocardial infarction (AMI) and unstable angina pectoris (UAP) decreased the endothelium-dependent vasodilatation FMD both [(7.2 ± 1.42), 7 · 6 ± 1 · 12 vs 15 · 46 ± 1 · 2, P <0 · 05], while there was no significant difference between AMI and UAP (P> 0.05). There was no significant difference in the intravascular diameter between the three groups (P> 0.05). (2) The NO level in patients with ACS was significantly lower than that in the control group (P <0.05) · 46 ± 12 · 24), (60 · 42 ± 10 · 32) vs (94 · 72 ± 12 · 34) μmol / L, P <0 · 05] (586.4 ± 168.5), (447.4 ± 186.7) vs (348.6 ± 172.3) μg / L, P <0 · 05]. Logisitic regression analysis showed that the odds ratio (OR) of ox-LDL was greater than 1, which was the risk factor of ACS. The OR of FMD was less than 1, which was the protective factor of ACS. The role of ox-LDL and FMD in acute coronary syndromes was observed independently. Conclusion The pathogenesis of ACS is related to the level of plasma ox-LDL and endothelial dysfunction, both of which may serve as independent risk factors.
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