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

Citation
Sp. Zhao et al., Impairment of endothelial function after a high-fat meal in patients with coronary artery disease, CORON ART D, 12(7), 2001, pp. 561-565
Citations number
25
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
CORONARY ARTERY DISEASE
ISSN journal
09546928 → ACNP
Volume
12
Issue
7
Year of publication
2001
Pages
561 - 565
Database
ISI
SICI code
0954-6928(200111)12:7<561:IOEFAA>2.0.ZU;2-5
Abstract
Objective To determine the effect of postprandial lipid changes on endothel ial function in patients with coronary artery disease (CAD) after a high-fa t meal. Methods We studied 50 CAD patients and 25 control participants, who were al l 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 post prandial flow-mediated vasodilatation (r=0.459, P<0.01). Postprandial trigl yceride level was significantly higher in CAD patients than in control part icipants. Flow-mediated vasodilatation was significantly impaired in CAD pa tients (from 3.04 +/-0.39 to 1.69 +/-0.23%, P<0.01) and control participant s (from 6.58<plus/minus>0.52 to 4.87 +/-0.19%, P<0.05) after a high-fat mea l. The impairment of flow-mediated dilatation was more severe in CAD patien ts (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 a nd control participants. The disordered postprandial metabolism of triglyce ride-rich lipoproteins may play an atherogenic role by inducing endothelial dysfunction. Coronary Artery Dis 12:561-565 (C) 2001 Lippincott Williams & Wilkins.