© 2001 by European Society of Cardiology
Copyright © 2001, European Society of Cardiology
Pronounced postprandial lipemia impairs endothelium-dependent dilation of the brachial artery in men
Department of Internal Medicine, University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria
hannes.gaenzer{at}uibk.ac.at
* Corresponding author. Tel.: +43-512-504-3260; fax: +43-512-504-3263,
Objective: Pronounced postprandial lipemia has been established as a risk factor for cardiovascular disease, but reports regarding its effect on endothelial function have been controversial. In the present study the influence of a standardized fatty meal with its ensuing postprandial lipemia of highly varying magnitude on endothelium-dependent dilation (EDD) was investigated. Methods: In 17 healthy, normolipidemic men EDD of the brachial artery was quantified in two series of three measurements each. In both series initial measurements were performed at 08:00 h after an overnight fast followed by measurements at 12:00 and 16:00 h, in the first series with continued fasting and in the second following the ingestion of a standardized fatty test meal 4 and 8 h postprandially. Results: Measurements of EDD in the fasting state revealed the recently appreciated diurnal variation with higher values in noon and afternoon hours compared with morning values (2.5±1.6% at 08:00, 7.5±2.7% at 12:00, and 7.0±2.1% at 16:00 h, P<0.001 by analysis of variance). Postprandial EDD values measured at 12:00 h were, at the average, lower than fasting EDD values measured at 12:00 h and correlated inversely with the magnitude of postprandial triglyceridemia (r=–0.81, P<0.001). In multivariate analysis, higher postprandial lipemia was associated with impaired postprandial EDD (P<0.001) independent of fasting triglycerides, low density lipoprotein (LDL) and high density lipoprotein (HDL) cholesterol, insulin, age and body mass index. Conclusion: We conclude that pronounced postprandial lipemia is associated with transient impairment of endothelial function. Our findings support the notion that impaired triglyceride metabolic capacity plays an important role in atherogenesis.
KEYWORDS Arteries; Endothelial function; Lipid metabolism; Ultrasound; Vasoconstriction/dilation
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