title: Effect of homocysteine on plaque formation and oxidative stress in patients with acute coronary syndromes.
abstract: BACKGROUND
  Cardiovascular diseases, especially coronary artery disease (CAD), are major causes of death in industrialized countries. Elevated concentrations of plasma homocysteine (Hcy) have been associated with an increased risk of CAD. Increased plasma levels of chemokine, characterized by their ability to induce migration and activation of leukocytes, may contribute to the pathogenesis of CAD. This study was designed to investigate the changes of plasma Hcy, monocyte chemoattractant protein-1 (MCP-1) and oxidative stress markers in acute coronary syndrome patients.
  
  
  METHODS
  A total of 149 subjects were divided into four groups: 50 patients with unstable angina, 30 patients with acute myocardial infarction, 20 coronary restenosis patients after percutaneous coronary intervention and 49 healthy control subjects. Plasma levels of Hcy, MCP-1, malondialdehyde and superoxide dismutase were measured.
  
  
  RESULTS
  Plasma levels of Hcy and MCP-1 showed significant increases in unstable angina, acute myocardial infarction and restenosis patients compared with control subjects (P < 0.05, respectively). Plasma levels of malondialdehyde were significantly increased in unstable angina and acute myocardial infarction patients when compared with control subjects (P < 0.05, respectively). Plasma superoxide dismutase levels were significantly reduced in acute myocardial infarction patients when compared with control group (P < 0.01).
  
  
  CONCLUSIONS
  Hcy might act as an atherogenic factor through promoting chemokine, reactive oxygen species and oxidized low density lipoprotein production and thereby convert a stable plaque into an unstable potentially occlusive lesion.
authors.affiliation: Institute of Vascular Medicine, Peking University Third Hospital, Beijing 100083, China.
authors.forename: Guang
authors.initials: G
authors.lastname: Wang
authors.forename: Jie-Ming
authors.initials: JM
authors.lastname: Mao
authors.forename: Xian
authors.initials: X
authors.lastname: Wang
authors.forename: Fu-Chun
authors.initials: FC
authors.lastname: Zhang
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D018932:Chemokine CCL2 / Q000097:blood; D003324:Coronary Artery Disease / Q000209:etiology*; D003327:Coronary Disease / Q000097:blood* / Q000150:complications / Q000378:metabolism; D005260:Female; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D008077:Lipoproteins, LDL / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D018384:Oxidative Stress; D013482:Superoxide Dismutase / Q000097:blood
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D008077:Lipoproteins, LDL; C099252:oxidized low density lipoprotein; D006710:Homocysteine; D008315:Malondialdehyde; D013482:Superoxide Dismutase