CC BY-NC-ND 4.0 · Thromb Haemost 2021; 121(02): 234-241
DOI: 10.1055/s-0040-1716539
Atherosclerosis and Ischaemic Disease

Pathological Features of Ruptured Coronary Plaque and Thrombus Interfaces: Fibrin and von Willebrand Factor as Platelet Scaffolds on Rupture Sites

Atsushi Yamashita
1   Department of Pathology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan
,
Kensaku Nishihira
1   Department of Pathology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan
2   Department of Cardiology, Miyazaki Medical Association Hospital, Miyazaki, Japan
,
Toshihiro Gi
1   Department of Pathology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan
,
Kazunari Maekawa
1   Department of Pathology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan
,
Kinta Hatakeyama
3   Department of Diagnostic Pathology, Nara Medical University, Kashihara, Japan
4   Department of Pathology, National Cerebral and Cardiovascular Center, Osaka, Japan
,
Saki Horiuchi
1   Department of Pathology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan
,
Kei Wada
5   Department of Medical Sciences, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan
,
Yoshisato Shibata
2   Department of Cardiology, Miyazaki Medical Association Hospital, Miyazaki, Japan
,
Yujiro Asada
1   Department of Pathology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan
› Institutsangaben
Funding This study was supported in part by Grants-in-Aid for Scientific Research in Japan (Numbers 19H03445, 16H05163, 16K08670, 19K07437, and 18K08123) from the Japan Society for the Promotion of Science, and the Cooperative Research Project Program of the Joint Usage/Research Center at the Institute of Development, Aging and Cancer, Tohoku University.

Abstract

Arterial thrombus formation is thought to be initiated by platelet adhesion to the subendothelial matrix, but ruptured atherosclerotic plaques are characterized by substantial reduction of matrix proteins compared with stable plaques. Intraplaque erythrocytes and/or fibrin have been reported in high-risk coronary plaques. The aims of the current study were to identify factors that provide scaffolds for platelets at the sites of ruptured coronary plaques and investigate depositions of iron and bilirubin as hemoglobin catabolites in the ruptured plaques. Histological characteristics of plaque components and the thrombus interface were examined in 73 acute coronary aspirated thrombi. Necrotic debris (95%), macrophages (95%), and cholesterin clefts (81%) were observed frequently at the ruptured plaque and thrombus interface. A fibrous matrix (47%), calcification (32%), and extracellular deoxyribonucleic acid (15%) were identified as small foci. Tissue factor was localized in the necrotic core and macrophages. Fibrin and von Willebrand factor were consistently deposited within the plaques and beneath platelet aggregations. The citrullinated histone H3-immunopositive area accounted for only 0.5% of the plaque area. Bilirubin and iron depositions were detected in approximately 20% of the plaques in addition to biliverdin reductase and ferritin expression in macrophages. Fibrin and von Willebrand factor rather than matrix proteins and neutrophil extracellular traps may be major adhesive molecules at the sites of ruptured plaques. Iron and bilirubin deposits may be markers for rupture-prone plaques.

Supplementary Material



Publikationsverlauf

Eingereicht: 02. Juni 2020

Angenommen: 26. Juli 2020

Artikel online veröffentlicht:
13. September 2020

© 2020. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)

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