PMID- 15569480
OWN - NLM
STAT- MEDLINE
DCOM- 20041230
LR  - 20131121
IS  - 0366-6999 (Print)
IS  - 0366-6999 (Linking)
VI  - 117
IP  - 11
DP  - 2004 Nov
TI  - Effect of homocysteine on plaque formation and oxidative stress in patients with 
      acute coronary syndromes.
PG  - 1650-4
AB  - 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). CONCLUSION: 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.
FAU - Wang, Guang
AU  - Wang G
AD  - Institute of Vascular Medicine, Peking University Third Hospital, Beijing 100083, 
      China.
FAU - Mao, Jie-Ming
AU  - Mao JM
FAU - Wang, Xian
AU  - Wang X
FAU - Zhang, Fu-Chun
AU  - Zhang FC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - China
TA  - Chin Med J (Engl)
JT  - Chinese medical journal
JID - 7513795
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (oxidized low density lipoprotein)
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
SB  - IM
MH  - Acute Disease
MH  - Adult
MH  - Aged
MH  - Chemokine CCL2/blood
MH  - Coronary Artery Disease/*etiology
MH  - Coronary Disease/*blood/complications/metabolism
MH  - Female
MH  - Homocysteine/*blood
MH  - Humans
MH  - Lipoproteins, LDL/metabolism
MH  - Male
MH  - Malondialdehyde/blood
MH  - Middle Aged
MH  - *Oxidative Stress
MH  - Superoxide Dismutase/blood
EDAT- 2004/12/01 09:00
MHDA- 2004/12/31 09:00
CRDT- 2004/12/01 09:00
PHST- 2004/12/01 09:00 [pubmed]
PHST- 2004/12/31 09:00 [medline]
PHST- 2004/12/01 09:00 [entrez]
PST - ppublish
SO  - Chin Med J (Engl). 2004 Nov;117(11):1650-4.