title: n-3 fatty acids prevent whereas trans-fatty acids induce vascular inflammation and sudden cardiac death.
abstract: n-3 PUFA have well-recognised cardio-beneficial effects. In contrast, premature coronary deaths are associated with consumption of high levels of trans-fatty acids (TFA). The present study determined the effects of n-3 PUFA and TFA on sudden cardiac death and vascular inflammation. A rat coronary ligation model was used to study the effect of fatty acids on sudden cardiac death, whereas a mouse femoral artery ligation model was used to study compensatory vascular remodelling. Human aortic endothelial cells (HAEC) were utilised for the in vitro studies to investigate expression of inflammatory molecules. Feeding animals an n-3 PUFA-enriched diet caused a sevenfold increase in plasma n-3 PUFA compared with that of the TFA-fed group, whereas a TFA-enriched diet caused a 2.5-fold increase in plasma TFA compared with the n-3 PUFA group. Animals on a TFA diet had a lower survival rate due to sudden cardiac death and exhibited variable degrees of aortic atherosclerotic lesions. Animals on a TFA diet had diminished hindlimb collateral growth, whereas animals on the n-3 PUFA diet exhibited extensive collateral growth about ligated regions. HAEC treated with TFA (trans-18 : 2) showed significantly increased expression of intracellular adhesion molecule-1 and nitrosylation of cellular proteins than those treated with DHA (n-3 PUFA, 22 : 6). The in vivo study demonstrates that, in contrast to TFA, n-3 PUFA improve animal survival after myocardial infarction, prevent development of atherosclerotic lesions and stimulate compensatory vascular remodelling. The in vitro study demonstrates that TFA induce, while n-3 PUFA prevent, vascular inflammation.
authors.affiliation: Cellular Biochemistry and Lipid Biology Laboratories, Methodist Research Institute, Indianapolis, IN, USA. rsiddiqu@clarian.org
authors.forename: Rafat A
authors.initials: RA
authors.lastname: Siddiqui
authors.forename: Kevin A
authors.initials: KA
authors.lastname: Harvey
authors.forename: Nargiz
authors.initials: N
authors.lastname: Ruzmetov
authors.forename: Steven J
authors.initials: SJ
authors.lastname: Miller
authors.forename: Gary P
authors.initials: GP
authors.lastname: Zaloga
mesh_terms: D000818:Animals; D001011:Aorta; D050197:Atherosclerosis / Q000139:chemically induced / Q000473:pathology; D002460:Cell Line; D003331:Coronary Vessels; D016757:Death, Sudden, Cardiac / Q000209:etiology* / Q000517:prevention & control*; D004032:Diet; D004195:Disease Models, Animal; D042783:Endothelial Cells / Q000737:chemistry / Q000187:drug effects; D005227:Fatty Acids / Q000097:blood; D015525:Fatty Acids, Omega-3 / Q000008:administration & dosage*; D005263:Femoral Artery; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D008026:Ligation; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009203:Myocardial Infarction / Q000188:drug therapy; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D044242:Trans Fatty Acids / Q000008:administration & dosage*; D014657:Vasculitis / Q000209:etiology* / Q000517:prevention & control*
chemical_list: D005227:Fatty Acids; D015525:Fatty Acids, Omega-3; D044242:Trans Fatty Acids; D018799:Intercellular Adhesion Molecule-1