Expression of the von Willebrand Factor in Atrial Endocardium is Increased in Atrial Fibrillation Depending on the Extent of Structural Remodeling

Koji Kumagai, Mitsumasa Fukuchi, Jun Ohta, Shigeo Baba, Katsuhiko Oda, Hiroji Akimoto, Yutaka Kagaya, Jun Watanabe, Koichi Tabayashi, Kunio Shirato

研究成果: Article査読

39 被引用数 (Scopus)

抄録

Background: The incidence of stroke in patients suffering atrial fibrillation (AF) is increased when left atrial enlargement occurs. Recently, the platelet adhesive molecule, von Willebrand factor (vWF), located in the atrial endocardium, has been shown to be increased in patients with a variety of heart diseases compared with patients who have no cardiac problems. Methods and Results: We investigated the expression of vWF mRNA and protein in the endocardium as a possible prothrombotic alteration of AF in association with atrial structural remodeling. Atrial appendage specimens were obtained during either heart surgery or at an autopsy from AF patients with and without underlying heart disease. The immunohistochemical and in situ hybridization signals for vWF in the endocardium were well correlated and varied widely among the individual atrial appendages examined. The increased expression of vWF in the endocardium was associated with enlarged left atrial dimensions in mitral valvular disease or increased myocyte diameters in the underlying myocardium. Platelet adhesion/aggregation on the endocardium was always found under the fresh thrombi and was colocalized with strong vWF staining, but not necessarily with fibrinogen and/or fibrin staining. Conclusions: Endocardial overexpression of vWF may occur during the process of atrial structural remodeling contributing to the thrombotic predilection of AF in association with underlying heart disease.

本文言語English
ページ(範囲)321-327
ページ数7
ジャーナルCirculation Journal
68
4
DOI
出版ステータスPublished - 2004 4

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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