title: Not acute but chronic hypertriglyceridemia is associated with impaired endothelium-dependent vasodilation: reversal after lipid-lowering therapy by atorvastatin.
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.
authors.affiliation: Department of Cardiology, Leiden University Medical Center, The Netherlands.
authors.forename: F H
authors.initials: FH
authors.lastname: de Man
authors.forename: A W
authors.initials: AW
authors.lastname: Weverling-Rijnsburger
authors.forename: A
authors.initials: A
authors.lastname: van der Laarse
authors.forename: A H
authors.initials: AH
authors.lastname: Smelt
authors.forename: J W
authors.initials: JW
authors.lastname: Jukema
authors.forename: G J
authors.initials: GJ
authors.lastname: Blauw
mesh_terms: D000109:Acetylcholine / Q000008:administration & dosage; D000208:Acute Disease; D000924:Anticholesteremic Agents / Q000008:administration & dosage*; D000069059:Atorvastatin; D001794:Blood Pressure / Q000187:drug effects; D002908:Chronic Disease; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology*; D016166:Free Radical Scavengers / Q000008:administration & dosage; D006538:Heptanoic Acids / Q000008:administration & dosage*; D006801:Humans; D015228:Hypertriglyceridemia / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology*; D007275:Injections, Intravenous; D008297:Male; D008875:Middle Aged; D009599:Nitroprusside / Q000008:administration & dosage; D011758:Pyrroles / Q000008:administration & dosage*; D012701:Serotonin / Q000008:administration & dosage; D014280:Triglycerides / Q000008:administration & dosage; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D014665:Vasodilator Agents / Q000008:administration & dosage
chemical_list: D000924:Anticholesteremic Agents; D016166:Free Radical Scavengers; D006538:Heptanoic Acids; D011758:Pyrroles; D014280:Triglycerides; D014665:Vasodilator Agents; D009599:Nitroprusside; D012701:Serotonin; D000069059:Atorvastatin; D000109:Acetylcholine