32
Views
25
CrossRef citations to date
0
Altmetric
Original Article

High Prevalence of Anti-β2 Glycoprotein I Antibodies in Patients with Ischemic Heart Disease

, , , , , , , , , & show all
Pages 93-98 | Received 25 Feb 1998, Accepted 17 Dec 1998, Published online: 07 Jul 2009
 

Abstract

Ischemic cardiac manifestations have been reported in a various percentage of patients with anti-phospholipid antibodies. As concerns the relationship between anti-β2 glycoprotein I antibodies (anti-β2-GPI) and ischemic heart disease (IHD), it was investigated in only one coronary primary prevention study. We investigated the prevalence of anti-β2-GPI in a well characterized group of patients with different clinical manifestation of IHD. Sera from 37 patients (mean age 62.7 ± 9.9) with IHD (20 with unstable angina-UA and 17 with effort angina-EA) and from 40 healthy subjects, matched for age and sex, were tested for the presence of IgG and IgM anti-β2-GPI using an ELISA technique. Eleven/37 patients (29.7%) resulted positive for anti-β-GPI. A positivity for IgG anti-β2-GPI was found in 10 patients, 1 patient was positive for IgM and 1 for both isotypes. The prevalence of anti-β2-GPI in the control group resulted significantly lower (2.5%; p < 0.005) than in patients with IHD. Positivity for anti-BZ-GPI was found in 9/20 (45%) patients with UA and only in 2/17 patients (11.8%) with EA (p = 0.0365). IgG anti-β2-GPI levels (median 7.7U/ml, range 2.6–24.1) were significantly higher in patients with UA compared to patients with EA (median 4.6 U/ml, range 2.3–11.5; p = 0.02) and controls (median 3.15 U/ml, range 2.3–9.0; p < 0.0001); also IgM levels resulted higher in patients with unstable angina. A positivity for anti-β2-GPI was observed in 4/13 patients (30.8%) with a previous myocardial infarction (MI) and in 7/24 (29.2%) patients without a previous MI. Our findings suggest that anti-β2-GPI could represent an expression of the T-cell activation detectable in patients with unstable angina. The lack of a significant difference in the prevalence of these antibodies in patients with or without a previous MI suggests that anti-BZ-GPI are not induced by tissue necrosis.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.