High prevalence of anti-beta2 glycoprotein I antibodies in patients with ischemic heart disease.
Ischemic cardiac manifestations have been reported in a various percentage of patients with anti-phospholipid antibodies. As concerns the relationship between anti-beta2 glycoprotein I antibodies (anti-beta2-GPI) and ischemic heart disease (IHD), it was investigated in only one coronary primary prevention study. We investigated the prevalence of anti-beta2-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-beta2-GPI using an ELISA technique. Eleven/37 patients (29.7%) resulted positive for anti-beta2-GPI. A positivity for IgG anti-beta2-GPI was found in 10 patients, 1 patient was positive for IgM and 1 for both isotypes. The prevalence of anti-beta2-GPI in the control group resulted significantly lower (2.5%; p < 0.005) than in patients with IHD. Positivity for anti-beta2-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-beta2-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-beta2-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-beta2-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-beta2-GPI are not induced by tissue necrosis.
Farsi
A
A
Istituto di Clinica Medica Generale e Cardiologia, University of Florence, Italy.
Domeneghetti
M P
MP
Fedi
S
S
Capanni
M
M
Giusti
B
B
Marcucci
R
R
Giurlani
L
L
Prisco
D
D
Passaleva
A
A
Gensini
G F
GF
Abbate
R
R
D000368:Aged; D000787:Angina Pectoris / Q000097:blood / Q000276:immunology; D000789:Angina, Unstable / Q000097:blood / Q000276:immunology*; D000918:Antibody Specificity; D016736:Antiphospholipid Syndrome / Q000097:blood / Q000276:immunology*; D000990:Antithrombin III / Q000032:analysis; D001323:Autoantibodies / Q000097:blood / Q000276:immunology*; D001327:Autoimmune Diseases / Q000097:blood / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D006023:Glycoproteins / Q000276:immunology*; D006801:Humans; D007075:Immunoglobulin M / Q000276:immunology; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000453:epidemiology / Q000276:immunology; D010446:Peptide Fragments / Q000032:analysis; D010447:Peptide Hydrolases / Q000032:analysis; D011516:Prothrombin / Q000032:analysis; D012307:Risk Factors; D053482:beta 2-Glycoprotein I
D001323:Autoantibodies; D005338:Fibrin Fibrinogen Degradation Products; D006023:Glycoproteins; D007075:Immunoglobulin M; D010446:Peptide Fragments; C046193:antithrombin III-protease complex; D053482:beta 2-Glycoprotein I; C036309:fibrin fragment D; C045879:prothrombin fragment 1.2; D000990:Antithrombin III; D011516:Prothrombin; D010447:Peptide Hydrolases