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The presence of antiphospholipid antibodies in acute myocardial infarction

Tel Aviv University, Department of Medicine B and Research Unit of Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, 52621 Israel

Y. Finkelstein

Tel Aviv University, Department of Medicine B and Research Unit of Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, 52621 Israel

G. Zandeman-Goddard

Tel Aviv University, Department of Medicine B and Research Unit of Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, 52621 Israel

M. Blank

Tel Aviv University, Department of Medicine B and Research Unit of Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, 52621 Israel

M. Lorber

Institute of Clinical Immunology, Department of Medicine B and Research Unit of Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, 52621 Israel

A. Lorber

Institute of Rambam Medical Center, Haifa, Israel, Department of Medicine B and Research Unit of Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, 52621 Israel

D. Faden

Department of Gynecology, Bercia, Italy, Department of Medicine B and Research Unit of Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, 52621 Israel

Y. Shoenfeld

Tel Aviv University, Department of Medicine B and Research Unit of Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, 52621 Israel

This study was undertaken to determine if there is an association between increased titers of five different antiphospholipid antibodies (aPLA) in young patients' sera and the occurrence of acute myocardial infarction (AMI). Antibodies to anticardiolipin (aCL), anti-phosphatidylserine (aPS), antiphosphatidylinositol (aPI), anti-phosphatidylcholine (aPC), and anti-phosphatidylethanol amine (aPEA) were measured in 214 patients (102 patients, 102 healthy controls and 10 patients with antiphospholipid syndrome). These antibodies were measured twice (within 4 h of onset of acute myocardial ischemic chest pain and 3 months after the myocardial infarction) by enzyme linked immunosorbent assay (ELISA).

Elevated titers of four different aPLA were detected in 6.9% of all patients with AMI on hospitalization. Titers of aPLA in AMI were elevated in the younger age group <50 years old (P < 0.001) and in men only (not statistically significant). No correlation was found between the presence of aPLA and cardiovascular risk factors (smoking, hypertension, diabetes mellitus and hypercholesterolemia). Three of the seven patients with increased titers of aPLA did not have any other cardiovascular risk factors. The titers of aPLA were within normal range 3 months after AMI.

Evidence of significantly elevated titers of different aPLA at the early stage of AMI suggests that these autoantibodies are present before the AMI and are not secondary to them. The disappearance of the elevated aPLA 3 months after AMI may be due to an absorption effect or possibly a cyclic phenomenon similarly found in other autoimmune diseases. aPLA may be an additional risk factor for AMI, and should especially be considered in a patient of the younger age group without apparent cardiovascular risk factors.

Key Words: antiphospholipid antibodies • myocardial infarction

Lupus, Vol. 4, No. 4, 309-313 (1995)
DOI: 10.1177/096120339500400413


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