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Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:744-750

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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:744.)
© 2000 American Heart Association, Inc.


Atherosclerosis and Lipoproteins

Not Acute but Chronic Hypertriglyceridemia Is Associated With Impaired Endothelium-Dependent Vasodilation

Reversal After Lipid-Lowering Therapy by Atorvastatin

Frits H. de Man; Annelies W. E. Weverling-Rijnsburger; Arnoud van der Laarse; Augustinus H. M. Smelt; J. Wouter Jukema; Gerard J. Blauw

From the Departments of Cardiology (F.H.d.M., A.v.d.L., J.W.J.) and General Internal Medicine (A.W.E.W.-R., A.H.M.S., G.J.B.), Leiden University Medical Center; Leiden, the Netherlands.

Correspondence to F.H. de Man, MD, Department of Cardiology, C5-P, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, Netherlands. E-mail deman{at}cardio.azl.nl

Abstract—There is controversy regarding the relation between hypertriglyceridemia (HTG) and endothelial function. This study was designed to investigate endothelial function in a patient group with chronic HTG, before and during lipid-lowering therapy by atorvastatin. In addition, the effects of acute HTG on endothelial function were studied in normolipidemic individuals. Eight male patients with chronic HTG were studied before and after 6 weeks of lipid-lowering treatment with 80 mg atorvastatin once daily. Ten age-matched control subjects were studied at baseline and immediately after a high-dose infusion of artificial triglycerides. The endothelium-dependent response to serotonin was attenuated in the HTG group, whereas the response to acetylcholine was comparable to the response in the control group. The response to the endothelium-independent vasodilator nitroprusside was comparable in both groups. In response to atorvastatin therapy, serum triglyceride and cholesterol levels decreased significantly by 43% (paired t test, P=0.017) and 38% (paired t test, P=0.012), respectively. After 6 weeks of treatment, the forearm blood flow response to serotonin improved from 63% to 106% (ANOVA, P<0.001). Induction of acute HTG in the control subjects did not affect the forearm blood flow responses to serotonin and nitroprusside; however, the response to acetylcholine was paradoxically increased. In conclusion, patients with chronic HTG have an impaired endothelium-dependent vasodilation to serotonin that is normalized after 6 weeks of lipid-lowering therapy by atorvastatin.


Key Words: endothelium • hyperlipoproteinemia • triglycerides




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