High prevalence of anti-β2 glycoprotein I antibodies in patients with ischemic heart disease

Alessandro Farsi, Maria Paola Domeneghetti, Sandra Fedi, Monia Capanni, Betti Giusti, Rossella Marcucci, Letizia Giurlani, Domenico Prisco, Angelo Passaleva, Gian Franco Gensini, Rosanna Abbate

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34 Citations (Scopus)

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-β2-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-β2-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 7.7 U/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-β2-GPI are not induced by tissue necrosis.

Original languageEnglish
Pages (from-to)93-98
Number of pages6
JournalAutoimmunity
Volume30
Issue number2
Publication statusPublished - 1999

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Myocardial Ischemia
Glycoproteins
Antibodies
Unstable Angina
Myocardial Infarction
Immunoglobulin M
Primary Prevention
Anti-Idiotypic Antibodies
Phospholipids
Healthy Volunteers
Necrosis
Enzyme-Linked Immunosorbent Assay

Keywords

  • Anti-β2 glycoprotein I antibodies
  • Ischemic heart disease
  • Unstable angina

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Farsi, A., Domeneghetti, M. P., Fedi, S., Capanni, M., Giusti, B., Marcucci, R., ... Abbate, R. (1999). High prevalence of anti-β2 glycoprotein I antibodies in patients with ischemic heart disease. Autoimmunity, 30(2), 93-98.

High prevalence of anti-β2 glycoprotein I antibodies in patients with ischemic heart disease. / Farsi, Alessandro; Domeneghetti, Maria Paola; Fedi, Sandra; Capanni, Monia; Giusti, Betti; Marcucci, Rossella; Giurlani, Letizia; Prisco, Domenico; Passaleva, Angelo; Gensini, Gian Franco; Abbate, Rosanna.

In: Autoimmunity, Vol. 30, No. 2, 1999, p. 93-98.

Research output: Contribution to journalArticle

Farsi, A, Domeneghetti, MP, Fedi, S, Capanni, M, Giusti, B, Marcucci, R, Giurlani, L, Prisco, D, Passaleva, A, Gensini, GF & Abbate, R 1999, 'High prevalence of anti-β2 glycoprotein I antibodies in patients with ischemic heart disease', Autoimmunity, vol. 30, no. 2, pp. 93-98.
Farsi A, Domeneghetti MP, Fedi S, Capanni M, Giusti B, Marcucci R et al. High prevalence of anti-β2 glycoprotein I antibodies in patients with ischemic heart disease. Autoimmunity. 1999;30(2):93-98.
Farsi, Alessandro ; Domeneghetti, Maria Paola ; Fedi, Sandra ; Capanni, Monia ; Giusti, Betti ; Marcucci, Rossella ; Giurlani, Letizia ; Prisco, Domenico ; Passaleva, Angelo ; Gensini, Gian Franco ; Abbate, Rosanna. / High prevalence of anti-β2 glycoprotein I antibodies in patients with ischemic heart disease. In: Autoimmunity. 1999 ; Vol. 30, No. 2. pp. 93-98.
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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-β2-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-β2-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 7.7 U/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-β2-GPI are not induced by tissue necrosis.",
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