Not acute but chronic hypertriglyceridemia is associated with impaired endothelium-dependent vasodilation - Reversal after lipid-lowering therapy by atorvastatin
Fh. De Man et al., Not acute but chronic hypertriglyceridemia is associated with impaired endothelium-dependent vasodilation - Reversal after lipid-lowering therapy by atorvastatin, ART THROM V, 20(3), 2000, pp. 744-750
There is controversy regarding the relation between hypertriglyceridemia (H
TG) and endothelial function. This study was designed to investigate endoth
elial 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 mal
e patients with chronic HTG were studied before and after 6 weeks of lipid-
lowering treatment with 80 mg atorvastatin once daily. Ten age-matched cont
rol subjects were studied at baseline and immediately after a high-dose inf
usion of artificial triglycerides. The endothelium-dependent response to se
rotonin was attenuated in the HTG group, whereas the response to acetylchol
ine was comparable to the response in the control group; The response to th
e endothelium-independent vasodilator nitroprusside was comparable in both
groups. In response to atorvastatin therapy, serum triglyceride and cholest
erol 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 fo
rearm blood flow response 6 serotonin improved from 63% to 106% (ANOVA, P<0
.001). Induction of acute HTG in the control subjects did not affect the fo
rearm blood flow responses to serotonin and nitroprusside; however, the res
ponse to acetylcholine was paradoxically increased. In conclusion, patients
with chronic HTG have an impaired endothelium-dependent vasodilation to se
rotonin that is normalized after 6 weeks of lipid-lowering therapy by atorv
astatin.