title: Blood histamine is associated with coronary artery disease, cardiac events and severity of inflammation and atherosclerosis.
abstract: BACKGROUND
  Mast cells are prevalent in the shoulder of unstable atheromas; cardiac mast cells secrete proteases capable of activating matrix metalloproteinases. Histamine is essential in the inflammatory cascade of the unstable plaque. Ascorbate depletion has been correlated with histaminemia which has been shown to impair endothelial-dependent vasodilation. This study evaluates whether oxidative stress as measured by isoprostanes (PGF(2alpha)) coupled with an inflammatory state characterized by histaminemia predisposes patients to acute coronary syndrome (ACS).
  
  
  METHODS
  Whole blood histamine, serum vitamin C, and serum PGF(2alpha) levels were drawn on 50 patients with ACS as determined by standard diagnostic criteria, 50 patients with stable coronary artery disease (SCAD), and 50 age and sex matched normal controls (C).
  
  
  RESULTS
  Data were analyzed by stepwise discriminant and Spearman's rank correlation coefficient. A significant relationship exists between histamine and PGF(2alpha). As PGF(2alpha) rises above 60 pg/mL, an increase in histamine occurs in both the ACS and SCAD groups. A significant inverse relationship exists between ascorbate and histamine in the ACS versus C groups (P < 0.01) and the SCAD versus C groups (P < 0.01).
  
  
  CONCLUSIONS
  Histamine and isoprostane levels increase in SCAD and ACS patients. Mast cell activation and lipid oxidation generated during atherosclerosis manifest this inflammatory response. Accelerated isoprostane formation and depleted ascorbate paired with histaminemia is active in CAD and predispose patients to acute coronary syndrome. Blood histamine alone may be a better risk factor for coronary events, and a better prognostic indicator than CRP even when combined with lipid indexes.
authors.affiliation: Department of Pathology & Laboratory Medicine, Tulane University Health Science Center, New Orleans, LA 70112-2699, USA. sclejan@tulane.edu
authors.forename: Sanda
authors.initials: S
authors.lastname: Clejan
authors.forename: Shenkar
authors.initials: S
authors.lastname: Japa
authors.forename: C
authors.initials: C
authors.lastname: Clemetson
authors.forename: Sanjeev S
authors.initials: SS
authors.lastname: Hasabnis
authors.forename: Odile
authors.initials: O
authors.lastname: David
authors.forename: J V
authors.initials: JV
authors.lastname: Talano
mesh_terms: D000368:Aged; D001205:Ascorbic Acid / Q000097:blood; D003324:Coronary Artery Disease / Q000097:blood*; D015237:Dinoprost / Q000031:analogs & derivatives*; D028441:F2-Isoprostanes / Q000097:blood; D005260:Female; D006632:Histamine / Q000097:blood*; D006801:Humans; D007249:Inflammation / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D028421:Isoprostanes / Q000097:blood; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D014810:Vitamin E / Q000097:blood
chemical_list: D028441:F2-Isoprostanes; D015850:Interleukin-6; D028421:Isoprostanes; D008055:Lipids; D014810:Vitamin E; C075750:8-epi-prostaglandin F2alpha; D006632:Histamine; D015237:Dinoprost; D001205:Ascorbic Acid