Impact of postprandial hypertriglyceridemia on vascular responses in patients with coronary artery disease: effects of ACE inhibitors and fibrates.
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.
Bae
J H
JH
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
Bassenge
E
E
Lee
H J
HJ
Park
K R
KR
Park
C G
CG
Park
K Y
KY
Lee
M S
MS
Schwemmer
M
M
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
D000806:Angiotensin-Converting Enzyme Inhibitors; D004041:Dietary Fats; D000960:Hypolipidemic Agents; D013481:Superoxides; D017706:Lisinopril; D011345:Fenofibrate