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Impaired brachial artery endothelial function is not predicted by elevated triglycerides
G B Schnell1, A Robertson, D Houston
1Department of Medicine, University of Calgary, Alberta, Canada.
Objectives:
The purpose of this study was to determine if patients with modest hyperlipidemia, and no other risk factors for coronary artery disease (CAD), have impaired endothelium-dependent (ED) vasoactivity.
Background:
Hypercholesterolemia impairs ED vasodilation, but the impact of elevated triglycerides on endothelial function is not as well established.
Methods:
High-resolution ultrasound was used to determine flow-mediated dilation (FMD) in the brachial artery (BA) after a 5-min arterial occlusion (endothelium-dependent stimulus) and nitroglycerin-induced dilation (endothelium-independent stimulus). We studied 40 healthy controls (Group 1), 38 patients with elevated low-density lipoprotein (LDL) cholesterol (Group 2) and 35 patients with elevated triglycerides (Group 3). Patients were excluded if they had known CAD or other risk factors for CAD, or if they were receiving lipid-lowering or vasoactive medications.
Results:
Control patients (Group 1) had normal LDL cholesterol (2.6+/-0.8 mmol/liter) and triglyceride levels (1.0+/-0.5 mmol/liter) compared with Group 2 (5.2+/-1.2 mmol/liter, 1.8+/-0.6 mmol/liter) and Group 3 (3.5+/-0.9 mmol/liter, 4.2+/-2.5 mmol/liter) subjects (p < 0.001). Baseline BA diameters were the same across the three groups. There was no significant attenuation of flow-mediated vasodilation (FMD) in either of the hyperlipidemic groups (Group 1: 10.9+/-5.0% vs. Group 2: 8.6+/-6.1% vs. Group 3: 9.4+/-3.9%; p = 0.14). However, nitroglycerin-induced vasodilation was mildly reduced (Group 1: 21.0+/-5.0% vs. 16.9+/-7.6% vs. 17.3+/-7.7%; p = 0.01). By multivariate analysis, after controlling for baseline diameters, only the ratio of LDL/high-density lipoprotein predicted a minor impairment in FMD.
Conclusions:
In patients free from other cardiac risk factors, modest elevations of triglycerides or LDL cholesterol do not significantly attenuate BA endothelial-dependent vasodilation. Synergism with other cardiac risk factors may be required to significantly impair endothelial function in these patients.