title: Expression of the von Willebrand factor in atrial endocardium is increased in atrial fibrillation depending on the extent of structural remodeling.
abstract: 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.
  
  
  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.
authors.affiliation: Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
authors.forename: Koji
authors.initials: K
authors.lastname: Kumagai
authors.forename: Mitsumasa
authors.initials: M
authors.lastname: Fukuchi
authors.forename: Jun
authors.initials: J
authors.lastname: Ohta
authors.forename: Shigeo
authors.initials: S
authors.lastname: Baba
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Oda
authors.forename: Hiroji
authors.initials: H
authors.lastname: Akimoto
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Kagaya
authors.forename: Jun
authors.initials: J
authors.lastname: Watanabe
authors.forename: Koichi
authors.initials: K
authors.lastname: Tabayashi
authors.forename: Kunio
authors.initials: K
authors.lastname: Shirato
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D020517:Atrial Appendage / Q000378:metabolism / Q000473:pathology; D001281:Atrial Fibrillation / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D016275:Atrial Function; D004699:Endocardium / Q000378:metabolism*; D005260:Female; D005337:Fibrin / Q000502:physiology; D005340:Fibrinogen / Q000502:physiology; D015870:Gene Expression; D006325:Heart Atria; D006349:Heart Valve Diseases / Q000150:complications / Q000601:surgery; D006801:Humans; D008297:Male; D008875:Middle Aged; D008943:Mitral Valve / Q000601:surgery; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis; D012333:RNA, Messenger / Q000096:biosynthesis; D019851:Thrombophilia / Q000209:etiology; D014841:von Willebrand Factor / Q000096:biosynthesis* / Q000235:genetics / Q000502:physiology
chemical_list: D019408:Platelet Endothelial Cell Adhesion Molecule-1; D012333:RNA, Messenger; D014841:von Willebrand Factor; D005337:Fibrin; D005340:Fibrinogen