Abstract Number: PB0007
Meeting: ISTH 2020 Congress
Background: Arterial thrombus formation is considered to be initiated by platelet adhesion on subendothelial matrix. However, the ruptured sites of atherosclerotic plaques are characterized by less matrix proteins. We recently reported presence of intraplaque erythrocytes and/or fibrin in coronary high-risk plaques.
Aims: We tried to identify factors providing platelet scaffolds at the ruptured sites of coronary plaques, and also studied intraplaque hemorrhage-related findings in ruptured plaques.
Methods: We histologically examined 73 coronary aspirated thrombi with plaque components obtained within 24 hours of the onset of acute myocardial infarction. In addition, we investigated thrombus formation using tissue factor-coated flow chambers under 1,000/s with perfusion of anti-coagulated rabbit blood.
Results: In the aspirated specimens, necrotic debris (95%), macrophages (95%), and cholesterin clefts (81%) were highly frequently observed at the interface areas of plaque components and thrombi. On the other hand, fibrous matrix (47%) and calcification (23%) were found partly as small foci. Tissue factor localized in the necrotic core and macrophages. Fibrin and von Willebrand factor deposited within the plaques and beneath platelet adhesion/aggregation in the all specimens. Extracellular DNA was observed in 15% of the interface area, and citrullinated histone H3 immunopositive area accounted for only 0.5 % of the plaque area. We also found bilirubin deposition, intracellular iron deposition in about one-fifth of the plaques. Biliverdin reductase and ferritin are predominantly expressed in yellowish or grayish macrophages. Iron deposition was also found in degenerative fibrous matrix. In a flow chamber system, the treatment by thrombin inhibitor and monoclonal antibody for von Willebrand factor suppressed platelet adhesion/aggregation and fibrin deposition on tissue factor coated glass under high shear rate.
Conclusions: Fibrin and/or von Willebrand factor rather than matrix proteins and neutrophils extracellular traps may contribute to platelet adhesion at the ruptured areas of coronary plaques.
To cite this abstract in AMA style:Yamashita A, Nishihira K, Maekawa K, Gi T, Horiuchi S, Hatakeyama K, Shibata Y, Asada Y. Contribution of Fibrin and von Willebrand Factor to Platelet Adhesion on Ruptured Atherosclerotic Plaque in Acute Myocardial Infarction [abstract]. Res Pract Thromb Haemost. 2020; 4 (Suppl 1). https://abstracts.isth.org/abstract/contribution-of-fibrin-and-von-willebrand-factor-to-platelet-adhesion-on-ruptured-atherosclerotic-plaque-in-acute-myocardial-infarction/. Accessed January 28, 2022.
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