4.8 Article

Anticardiolipin antibodies and recurrent coronary events - A prospective study of 1150 patients

Journal

CIRCULATION
Volume 102, Issue 11, Pages 1258-1263

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.CIR.102.11.1258

Keywords

antibodies; thrombosis; coronary disease; myocardial infarction

Funding

  1. NHLBI NIH HHS [HL-30616, HL-48259] Funding Source: Medline

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Background-The association of anticardiolipin (aCL) antibodies with coronary artery disease has been shown in several studies but remains controversial. We evaluated the association of aCL and anti-beta(2)-glycoprotein I (a beta(2)GPI) antibodies with the risk of recurrent cardiac events in postinfarction patients. Methods and Results-The study population consisted of 1150 patients with acute myocardial infarction, Levels of IgG and IgM aCL and a beta(2)GPI antibodies were determined on sera collected before hospital discharge. There were 131 recurrent cardiac events (nonfatal myocardial infarctions or cardiac deaths) over a mean follow-up period of 24.6 months. Patients with elevated IgG aCL antibodies had a higher event rate than patients with low levels (P = 0.05). Multivariate Cox analysis after adjustment for relevant clinical covariates showed that elevated levels of IgG aCL (hazard ratio = 1.63; P = 0.01) and low levels of IgM aCL (hazard ratio of 1.76; P = 0.02) antibodies contribute independent risks for recurrent cardiac events. Patients with elevated Ige aCL and low IgM aCL antibody levels had a 3-fold higher risk of recurrent cardiac events than patients with low IgG aCL and elevated IgM aCL antibody levels (P < 0.001), There was no significant association of the a beta(2)GPI antibodies with recurrent cardiac events. Conclusions-In postinfarction patients, elevated IgG aCL and low IgM aCL antibodies are independent risk factors for recurrent cardiac events. Patients with both elevated IgG aCL and low IgM aCL antibodies have the highest risk. These findings shed additional light on the mechanistic role of aCL antibodies in coronary artery disease in patients without autoimmune diseases.

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