Literature DB >> 11893822

Autoantibodies to cardiolipin and beta-2-glycoprotein-I in coronary artery disease patients with and without hypertension.

Yaniv Sherer1, Alexander Tenenbaum, Sonja Praprotnik, Joseph Shemesh, Miri Blank, Enrique Z Fisman, Micheal Motro, Yehuda Shoenfeld.   

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).
CONCLUSION: 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. Copyright 2002 S. Karger AG, Basel

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Year:  2002        PMID: 11893822     DOI: 10.1159/000047411

Source DB:  PubMed          Journal:  Cardiology        ISSN: 0008-6312            Impact factor:   1.869


  3 in total

1.  Immune dysregulation accelerates atherosclerosis and modulates plaque composition in systemic lupus erythematosus.

Authors:  Aleksandar K Stanic; Charles M Stein; Adam C Morgan; Sergio Fazio; MacRae F Linton; Edward K Wakeland; Nancy J Olsen; Amy S Major
Journal:  Proc Natl Acad Sci U S A       Date:  2006-04-24       Impact factor: 11.205

Review 2.  Natural killer T cells and atherosclerosis: form and function meet pathogenesis.

Authors:  Nicole A Braun; Roman Covarrubias; Amy S Major
Journal:  J Innate Immun       Date:  2010-03-17       Impact factor: 7.349

3.  The lupus susceptibility locus Sle3 is not sufficient to accelerate atherosclerosis in lupus-susceptible low density lipoprotein receptor-deficient mice.

Authors:  N S Wade; B G Stevenson; D S Dunlap; A S Major
Journal:  Lupus       Date:  2009-10-22       Impact factor: 2.911

  3 in total

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