Increased expression of TF on monocytes, but decreased numbers of TF bearing microparticles in blood from patients with acute myocardial infarction

To the Editor: Occlusive thrombus formation after disruption of an atherosclerotic plaque is thought to be the cause of acute myocardial infarction (AMI). Tissue factor (TF) is regarded as a key regulator of this process (1). We read with great interest the paper by Maly et al. (2), which measured TF activity and microparticle count in platelet free plasma. The authors reported that TF activity and microparticle counts were decreased in platelet free plasma of patients with unstable angina and patients with AMI compared to healthy controls and a group of patients with stable angina pectoris. To the best of our knowledge, this was the first study that reported a decrease of circulating procoagulant microparticles in patients with an arterial thrombosis. Yet, the results of this study are in line with the current concept of cellbased coagulation (1). In this concept, TF bearing microparticles are recruited from circulating blood by binding to a surface of activated cells (platelets, monocytes, endothelial cells), where the delivered TF together with the activated cell surfaces stimulates thrombin generation and further (occlusive) thrombus growth. Maly et al. already very properly observed that their results should be interpreted with caution, because they were the first to measure TF activity in patients with acute coronary syndrome and the numbers of patients and controls were limited. However, recent findings in our laboratory strongly support their results. Using flow cytometry, we measured the concentration of TF bearing microparticles in platelet free-plasma from 12 patients presenting with AMI at our emergency department and 23 healthy controls. Concentration of microparticles with TF on their surface was measured as described previously (3). In addition, we measured also the expression of TF on monocytes by multiparameter flow cytometry. Isolation and labeling was done as described in previous study (4). Monocytes are assumed to be the main source of TF bearing microparticles (1). As depicted in Fig. 1, TF expression on monocytes in AMI patients (91.3 ± 6.7%) was significantly elevated (P = 0.003, Mann–Whitney U) when compared to controls (64.7 ± 24.6%). From this we can conclude that circulating monocytes are strongly activated in a procoagulant way in patients with AMI. Yet, the numbers of circulating microparticles bearing TF on their membrane were significantly decreased in peripheral blood of AMI patients with respect to controls (24496 ± 30369 vs. 50428 ± 16226 microparticles ⁄ ll; P =0.0001). We believe that our findings are in line with the results of Maly et al. (2) suggesting that the depletion of procoagulant microparticles, but not tissue factor exposing monocytes, in the peripheral blood is caused by adhesion to the coronary thrombus. Indeed, Morel et al. demonstrated recently in patients with AMI that microparticle numbers were considerably