[Annexin V levels in survivors of early myocardial infarction].

INTRODUCTION AND OBJECTIVES Annexin V has an anticoagulant effect in vitro that derives from its ability to displace coagulation proteins from phospholipid surfaces, prolonging phospholipid-dependent coagulation reactions. Antiphospholipid antibodies (APL) and annexin V have an affinity for anionic phospholipids, so it has been hypothesized that one of the thrombotic mechanisms of APL may be due to displacement of annexin V from phospholipid surfaces. We studied plasma annexin V levels and analyzed its relationship to risk factors and several blood markers. PATIENTS AND METHOD We studied 62 patients < 45 years old who had suffered myocardial infarction. The control group comprised 23 healthy subjects of similar age and sex. We analyzed the presence of APL, anti-beta2 glycoprotein I (beta2-GPI), anti-beta2-GPI/phospholipid complexes and anti-annexin V antibodies. We determined plasma annexin V levels. Cholesterol, HDL-cholesterol, triglycerides, antigenic tissue plasminogen activator and its inhibitor, von Willebrand factor, and fibrinogen levels were measured. RESULTS We detected only 2 patients with positive anti-beta2-GPI/phospholipid complexes and 2 patients with positive anti-annexin V antibodies. We did not detect any positive APL or anti-beta2-GPI antibodies. In the control group there was only 1 patient with positive APL and anti-beta2-GPI antibodies. The myocardial infarction group showed significantly lower levels of annexin V than the control group: 0.640 ng/ml (0.520-0.818 ng/ml) vs 1.570 ng/ml (1.140-2.390 ng/ml), p < 0.01. There were no statistical associations between annexin V levels and other variables. CONCLUSIONS The low levels of annexin V in young myocardial infarction patients could indicate a procoagulant trend. This hypercoagulable state was unrelated to the presence of APL.