Not acute but chronic hypertriglyceridemia is associated with impaired endothelium-dependent vasodilation - Reversal after lipid-lowering therapy by atorvastatin

Citation
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
Citations number
38
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
ISSN journal
10795642 → ACNP
Volume
20
Issue
3
Year of publication
2000
Pages
744 - 750
Database
ISI
SICI code
1079-5642(200003)20:3<744:NABCHI>2.0.ZU;2-3
Abstract
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.