title: Autoantibodies to cardiolipin and beta-2-glycoprotein-I in coronary artery disease patients with and without hypertension.
abstract: BACKGROUND
  Autoantibodies to cardiolipin (aCL) and beta2-glycoprotein-I (beta2GPI) are considered proatherogenic. Elevated levels of both antibodies have been reported in hypertension. Nonetheless, there are no data regarding an association between these autoantibodies and hypertension in coronary artery disease.
  
  
  METHODS
  The levels of aCL and anti-beta2GPI antibodies were measured in patients having coronary artery disease with (n = 82) or without (n = 36) hypertension, in association with other major risk factors for coronary artery disease.
  
  
  RESULTS
  The levels of aCL and anti-beta2GPI antibodies were (OD at 405 nm) 0.23 +/- 0.14 and 0.22 +/- 0.12 in the normal blood pressure group, as opposed to 0.24 +/- 0.12 and 0.20 +/- 0.12 in the hypertensive group, respectively (p = 0.67; 0.42). No significant difference in either antibody levels was found between hypertensive patients with normal and abnormal blood pressure measurements. The presence of additional risk factors did not affect antibody levels in normotensive patients. However, in the hypertensive group, the presence of smoking was associated with significantly decreased anti-beta2GPI antibody levels, whereas no change was found in aCL. Further, patients who had hypertension, smoking and hypercholesterolemia, had significantly decreased anti-beta2GPI antibody levels compared with patients without any of these risk factors (0.13 +/- 0.04 versus 0.23 +/- 0.13, respectively; p = 0.02).
  
  
  CONCLUSIONS
  Hypertension is not associated with modification of aCL and anti-beta2GPI antibody levels in coronary artery disease patients. However, there are elevated anti-beta2GPI antibody levels in patients without conventional risk factors compared with patients with these risk factors.
authors.affiliation: Department of Medicine B and Center of Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, and Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
authors.forename: Yaniv
authors.initials: Y
authors.lastname: Sherer
authors.forename: Alexander
authors.initials: A
authors.lastname: Tenenbaum
authors.forename: Sonja
authors.initials: S
authors.lastname: Praprotnik
authors.forename: Joseph
authors.initials: J
authors.lastname: Shemesh
authors.forename: Miri
authors.initials: M
authors.lastname: Blank
authors.forename: Enrique Z
authors.initials: EZ
authors.lastname: Fisman
authors.forename: Micheal
authors.initials: M
authors.lastname: Motro
authors.forename: Yehuda
authors.initials: Y
authors.lastname: Shoenfeld
mesh_terms: D000925:Anticoagulants / Q000097:blood*; D001323:Autoantibodies / Q000097:blood*; D001794:Blood Pressure / Q000502:physiology; D002308:Cardiolipins / Q000097:blood*; D003324:Coronary Artery Disease / Q000097:blood* / Q000209:etiology* / Q000503:physiopathology; D006023:Glycoproteins / Q000097:blood*; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000150:complications* / Q000503:physiopathology; D012307:Risk Factors; D053482:beta 2-Glycoprotein I
chemical_list: D000925:Anticoagulants; D001323:Autoantibodies; D002308:Cardiolipins; D006023:Glycoproteins; D053482:beta 2-Glycoprotein I