論文

国際誌
2021年2月

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

Thrombosis and haemostasis
  • Atsushi Yamashita
  • ,
  • Kensaku Nishihira
  • ,
  • Toshihiro Gi
  • ,
  • Kazunari Maekawa
  • ,
  • Kinta Hatakeyama
  • ,
  • Saki Horiuchi
  • ,
  • Kei Wada
  • ,
  • Yoshisato Shibata
  • ,
  • Yujiro Asada

121
2
開始ページ
234
終了ページ
241
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1055/s-0040-1716539

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.

リンク情報
DOI
https://doi.org/10.1055/s-0040-1716539
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/32920806
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7861959
ID情報
  • DOI : 10.1055/s-0040-1716539
  • PubMed ID : 32920806
  • PubMed Central 記事ID : PMC7861959

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