title: Low plasma ascorbic acid independently predicts the presence of an unstable coronary syndrome.
abstract: OBJECTIVE
  This study sought to investigate the relations between plasma antioxidant status, extent of atherosclerosis and activity of coronary artery disease.
  
  
  BACKGROUND
  Previous studies indicate that increased antioxidant intake is associated with decreased coronary disease risk, but the underlying mechanisms remain controversial.
  
  
  METHODS
  Plasma samples were obtained from 149 patients undergoing cardiac catheterization (65 with stable angina, 84 with unstable angina or a myocardial infarction within 2 weeks). Twelve plasma antioxidant/oxidant markers were measured and correlated with the extent of atherosclerosis and the presence of an unstable coronary syndrome.
  
  
  RESULTS
  By multiple linear regression analysis, age (p < 0.001), diabetes mellitus (p < 0.001), male gender (p < 0.001) and hypercholesterolemia (p = 0.02) were independent predictors of the extent of atherosclerosis. No antioxidant/oxidant marker correlated with the extent of atherosclerosis. However, lower plasma ascorbic acid concentration predicted the presence of an unstable coronary syndrome by multiple logistic regression (odds ratio [OR] 0.59, 95% confidence interval [CI] 0.40 to 0.89, p = 0.01). The severity of atherosclerosis also predicted the presence of an unstable coronary syndrome (OR 1.7, 95% CI 1.14 to 2.47, p = 0.008) when all patients were considered. When only patients with significant coronary disease were considered (at least one stenosis >50%), ascorbic acid concentration (OR 0.56, 95% CI 0.37 to 0.85, p = 0.008) and total plasma thiols (OR 0.52, 95% CI 0.34 to 0.80, p = 0.004) predicted the presence of an unstable coronary syndrome, whereas the extent of atherosclerosis did not.
  
  
  CONCLUSIONS
  These data are consistent with the hypothesis that the beneficial effects of antioxidants in coronary artery disease may result, in part, by an influence on lesion activity rather than a reduction in the overall extent of fixed disease.
authors.affiliation: Evans Memorial Department of Medicine and Whitaker Cardiovascular Institute, Boston University Medical Center, Massachusetts 02118, USA. jvita@bu.edu
authors.forename: J A
authors.initials: JA
authors.lastname: Vita
authors.forename: J F
authors.initials: JF
authors.lastname: Keaney
authors.forename: K E
authors.initials: KE
authors.lastname: Raby
authors.forename: J D
authors.initials: JD
authors.lastname: Morrow
authors.forename: J E
authors.initials: JE
authors.lastname: Freedman
authors.forename: S
authors.initials: S
authors.lastname: Lynch
authors.forename: S N
authors.initials: SN
authors.lastname: Koulouris
authors.forename: B R
authors.initials: BR
authors.lastname: Hankin
authors.forename: B
authors.initials: B
authors.lastname: Frei
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000097:blood; D000789:Angina, Unstable / Q000097:blood; D000975:Antioxidants; D001161:Arteriosclerosis / Q000097:blood; D001205:Ascorbic Acid / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D003327:Coronary Disease / Q000097:blood*; D005260:Female; D006801:Humans; D016014:Linear Models; D015227:Lipid Peroxidation; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D001205:Ascorbic Acid