title: Impact of postprandial hypertriglyceridemia on vascular responses in patients with coronary artery disease: effects of ACE inhibitors and fibrates.
abstract: We analyzed vascular responses (endothelial function, oxidant stress) to postprandial hypertriglyceridemia (PHTG) in patients with coronary artery disease (CAD) to reveal potential therapeutical effects of angiotensin converting enzyme inhibition (ACE-I) and of lipid lowering (fibrate). The study population (n=39, mean age: 60 years) consisted of four groups, all of which had angiographically documented CAD. A high fat group (n=9) consumed a high fat meal, a low fat group (n=9) a low fat meal, and ACE-I (n=10) or fibrate (n=11) groups consumed a high fat meal plus lisinopril or fenofibrate. Serum triglycerides (TG) increased significantly 2 h after eating a test meal in all groups with the exception of the low fat group. In the high and low fat groups changes of serum TG were positively correlated (r=0.664, P<0.005) with changes of phorbol ester-activated leukocyte superoxide anion radical (O(2-.)) formation and were negatively correlated (r=-0.488, P<0.05) with flow-mediated brachial artery dilation (FMD). There was a negative correlation (r=-0.419, P=0.094) between FMD and changes of O(2-.) formation in the high and low fat groups. In the ACE-I and fibrate groups, O(2-.) formation decreased 2 h after eating a test meal (from 5.34+/-1.01 to 3.81+/-1.15 nmol/10(6)cells per min, P<0.01, and from 4.66+/-0.91 to 4.26+/-0.97 nmol/10(6)cells per min, P=0.374, respectively). However, endothelial function did not show any significant changes 2 h after eating a test meal in all groups. PHTG increases oxidant stress and further deteriorates endothelial function, even in patients with CAD. Both ACE-I and fibrates have an antioxidant effect but no acute beneficial effects in terms of endothelial function under conditions of PHTG in CAD patients.
authors.affiliation: Department of Internal medicine, Division of Cardiology, College of Medicine, Konyang University Hospital, 685, Gasoowon-dong, Seo-gu, Daejeon, South Korea. jhbae@kyuh.co.kr
authors.forename: J H
authors.initials: JH
authors.lastname: Bae
authors.forename: E
authors.initials: E
authors.lastname: Bassenge
authors.forename: H J
authors.initials: HJ
authors.lastname: Lee
authors.forename: K R
authors.initials: KR
authors.lastname: Park
authors.forename: C G
authors.initials: CG
authors.lastname: Park
authors.forename: K Y
authors.initials: KY
authors.lastname: Park
authors.forename: M S
authors.initials: MS
authors.lastname: Lee
authors.forename: M
authors.initials: M
authors.lastname: Schwemmer
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D001783:Blood Flow Velocity; D003324:Coronary Artery Disease / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D004041:Dietary Fats / Q000008:administration & dosage; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D011345:Fenofibrate / Q000627:therapeutic use*; D006801:Humans; D015228:Hypertriglyceridemia / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D007962:Leukocytes / Q000378:metabolism; D017706:Lisinopril / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D019518:Postprandial Period; D013481:Superoxides / Q000378:metabolism; D014664:Vasodilation
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D004041:Dietary Fats; D000960:Hypolipidemic Agents; D013481:Superoxides; D017706:Lisinopril; D011345:Fenofibrate