title: Plasma homocysteine levels and the left ventricular systolic function in coronary artery disease patients.
abstract: BACKGROUND
  Numerous studies have shown a relationship between hyperhomocysteinemia, atherothrombosis and cardiovascular mortality. However, an association between hyperhomocysteinemia and the extent of coronary artery disease (CAD) remains controversial whereas its relationship with left ventricular systolic function has not been established.
  
  
  METHODS
  One hundred and fifty-seven patients with angiographically defined CAD were included. The relationships between hyperhomocysteinemia, severity of CAD and left ventricular systolic function were studied. Left ventricular systolic function was determined primarily by ventriculography. The severity of CAD was determined through coronary angiography using the Gensini score and the number of vessels with > or = 50% stenosis.
  
  
  RESULTS
  The mean fasting plasma homocysteine level was 13.4 mumol/l+/-0.5 SE. Elevated levels of homocysteine correlated significantly with increased severity of CAD both by the Gensini scores (r-value = 0.344, P < 0.0005) and the total number of diseased vessels (r-value = 0.387, P < 0.0005). The patients with hyperhomocysteinemia were found to have significantly reduced left ventricular ejection fraction (r-value = -0.382, P < 0.0005). A multivariate regression analysis revealed homocysteine level to be an independent predictor of left ventricular systolic function. In addition, adjusted analysis revealed hyperhomocysteinemia to be associated with global left ventricular dysfunction.
  
  
  CONCLUSIONS
  In patients with CAD, homocysteine levels correlate independently with left ventricular systolic function. The mechanism of this association between homocysteine and left ventricular systolic function is unknown but may be due to a direct effect of homocysteine on myocardial function separate from its effects on coronary atherosclerosis.
authors.affiliation: University of Chicago-Pritzker School of Medicine, Illinois 60637, USA. sbokhari@medicine.bsd.uchicago.edu
authors.forename: Syed W
authors.initials: SW
authors.lastname: Bokhari
authors.forename: Zubaria W
authors.initials: ZW
authors.lastname: Bokhari
authors.forename: Jason A
authors.initials: JA
authors.lastname: Zell
authors.forename: Don W
authors.initials: DW
authors.lastname: Lee
authors.forename: David P
authors.initials: DP
authors.lastname: Faxon
mesh_terms: D000368:Aged; D008076:Cholesterol, HDL / Q000097:blood; D003324:Coronary Artery Disease / Q000097:blood* / Q000503:physiopathology; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology; D005260:Female; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000503:physiopathology; D008297:Male; D015999:Multivariate Analysis; D044469:Racial Groups; D012720:Severity of Illness Index; D013318:Stroke Volume / Q000502:physiology; D013599:Systole / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000097:blood* / Q000503:physiopathology
chemical_list: D008076:Cholesterol, HDL; D006710:Homocysteine