Impairment of endothelial function after a high-fat meal in patients with coronary artery disease

被引:32
|
作者
Zhao, SP [1 ]
Liu, L
Gao, M
Zhou, QC
Li, YL
Xia, B
机构
[1] Cent S Univ, Affiliated Hosp 2, Dept Cardiol, Changsha 410011, Peoples R China
[2] Cent S Univ, Affiliated Hosp 2, Dept Ultrasound, Changsha, Peoples R China
[3] Cent S Univ, Affiliated Hosp 2, Dept Nutr, Changsha, Peoples R China
关键词
triglyceride; high-fat meal; endothelium-dependent vasodilatation;
D O I
10.1097/00019501-200111000-00006
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective To determine the effect of postprandial lipid changes on endothelial function in patients with coronary artery disease (CAD) after a high-fat meal. Methods We studied 50 CAD patients and 25 control participants, who were all normocholesterolemic. Flow-mediated vasodilatation of the brachial artery was evaluated by the high-resolution ultrasound technique before and after a single high-fat meal (800 calories; 50 g fat). Results Postprandial serum triglyceride level increased significantly at 2-7 h and mean flow-mediated vasodilatation was impaired significantly (from 4.22 +/-0.44 to 2.75 +/-0.33%, P<0.01) for 75 subjects. The increment in 2 h serum triglyceride level correlated positively with the decrement in postprandial flow-mediated vasodilatation (r=0.459, P<0.01). Postprandial triglyceride level was significantly higher in CAD patients than in control participants. Flow-mediated vasodilatation was significantly impaired in CAD patients (from 3.04 +/-0.39 to 1.69 +/-0.23%, P<0.01) and control participants (from 6.58<plus/minus>0.52 to 4.87 +/-0.19%, P<0.05) after a high-fat meal. The impairment of flow-mediated dilatation was more severe in CAD patients (44.41%) than in control participants (25.99%, P<0.01). Conclusion Postprandial endothelium-dependent vasodilatation after a single high-fat meal was severely impaired in normocholesterolemic CAD patients and control participants. The disordered postprandial metabolism of triglyceride-rich lipoproteins may play an atherogenic role by inducing endothelial dysfunction. Coronary Artery Dis 12:561-565 (C) 2001 Lippincott Williams & Wilkins.
引用
收藏
页码:561 / 565
页数:5
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