Abstract
Circulating procoagulant microparticles (MP) are pathogenic markers of enhanced coagulability associated to a variety of disorders and released from stimulated vascular cells. When derived from endothelial cells, MP were found characteristic of thrombotic propensity in primary antiphospholipid syndrome (APS). The prothrombotic status of a patient with antiphospholipid antibodies (APL), a past history of mesenteric vein thrombosis and presenting myocardial infarction and extensive intracardiac thrombosis was examined by measurement of circulating procoagulant MP. MP of platelet and endothelial origins were highly elevated with respect to values detectable in patients with myocardial infarction and no history of APS (6- and 3-fold elevation, respectively) or in healthy volunteers (13- and 25-fold elevation, respectively). In this particular patient, with moderate APL titer, a drastic release of procoagulant MP could have contributed to thrombus growth and the development of extensive intracardiac thrombosis.
Highlights
In primary anti-phospholipid syndrome (APS), arterial or venous thrombosis and recurrent pregnancy loss are common thrombotic manifestations associated with anti-phophospholipid antibodies (APL) [1]
In a particular patient with a past history of mesenteric vein thrombosis and moderate titers of anti-phospholipid antibodies referring for acute myocardial infarction, we hypothesized that APL could have prompted chronic cell stimulation and persisting MP shedding, leading to enhanced thrombin generation possibly accounting for unusual extensive intracardiac thrombi
Testifying to major vascular damage, levels of circulating MP measured in the patient are in accordance with the important platelet and endothelial activation reported in APS [6,15]
Summary
In primary anti-phospholipid syndrome (APS), arterial or venous thrombosis and recurrent pregnancy loss are common thrombotic manifestations associated with anti-phophospholipid antibodies (APL) [1]. In a particular patient with a past history of mesenteric vein thrombosis and moderate titers of anti-phospholipid antibodies referring for acute myocardial infarction, we hypothesized that APL could have prompted chronic cell stimulation and persisting MP shedding, leading to enhanced thrombin generation possibly accounting for unusual extensive intracardiac thrombi. The patient was a 42-year-old man presenting acute myocardial infarction (STEMI) The year before, he had developed mesenteric ischemia due to mesenteric vein thrombosis and anticoagulant anti-phospholipid antibodies were evidenced. Procoagulant MP were captured onto insolubilized annexin V and their PhtdSer content was measured by functional prothrombinase assay using a microplate reader equipped with kinetics software In this assay, blood clotting factor (FXa, FVa, FII) and calcium concentrations were determined to ensure that PhtdSer is the rate-limiting parameter in the generation of soluble thrombin from prothrombin. The presence of APL was verified on two separate occasions one year apart
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