title: Increased von Willebrand factor in the endocardium as a local predisposing factor for thrombogenesis in overloaded human atrial appendage.
abstract: OBJECTIVE
  We investigated immunoreactive von Willebrand factor (vWF), a platelet adhesion molecule, in the endocardial endothelium and its relationship to thrombogenesis in the human atrial appendage.
  
  
  BACKGROUND
  Intra-atrial thrombogenesis is generally thought to be induced by blood stasis in the atrial appendage involved with atrial fibrillation (AF). Little attention has been paid to alterations of the endocardial endothelium on which the thrombus develops.
  
  
  METHODS
  Atrial appendage tissue was obtained at heart surgery or at autopsy from AF and non-AF cardiac patients and from noncardiac patients. Immunohistochemistry for endothelial cell markers including vWF, CD31, CD34 and endothelial nitric oxide synthase (eNOS) and platelet glycoprotein Ib/IX or IIb/IIIa was performed and semiquantitatively graded.
  
  
  RESULTS
  In contrast to the apparent immunostaining for CD31, CD34 and eNOS, only focal or little immunoreactive vWF was seen in the endocardium of noncardiac patients. Immunoreactive vWF in the endocardial endothelium was increased in most cardiac patients, particularly in the left, but not in the right, atrial appendage of patients with mitral valvular disease, irrespective of whether AF was present. Platelet adhesion/thrombus formation in the endocardium was found in limited sites in which the overlying endothelium was deficient in eNOS and CD34. When warfarin-treated cases were excluded, there was a significant correlation between the immunohistochemical grade for vWF and the degree of platelet adhesion/thrombus formation in the endocardium.
  
  
  CONCLUSIONS
  Immunoreactive vWF in the endocardial endothelium was increased in overloaded human atrial appendage, which may be a local predisposing factor for intraatrial thrombogenesis.
authors: Department of Cardiovascular Medicine, Tohoku University, Graduate School of Medicine, Sendai, Japan.
authors: M
authors: M
authors: Fukuchi
authors: J
authors: J
authors: Watanabe
authors: K
authors: K
authors: Kumagai
authors: Y
authors: Y
authors: Katori
authors: S
authors: S
authors: Baba
authors: K
authors: K
authors: Fukuda
authors: T
authors: T
authors: Yagi
authors: A
authors: A
authors: Iguchi
authors: H
authors: H
authors: Yokoyama
authors: M
authors: M
authors: Miura
authors: Y
authors: Y
authors: Kagaya
authors: S
authors: S
authors: Sato
authors: K
authors: K
authors: Tabayashi
authors: K
authors: K
authors: Shirato
mesh_terms: D000328:Adult; D000368:Aged; D020517:Atrial Appendage / Q000473:pathology*; D001281:Atrial Fibrillation / Q000473:pathology*; D001794:Blood Pressure / Q000502:physiology; D001810:Blood Volume / Q000502:physiology; D003327:Coronary Disease / Q000473:pathology; D004699:Endocardium / Q000473:pathology*; D004730:Endothelium, Vascular / Q000473:pathology; D005260:Female; D006331:Heart Diseases / Q000473:pathology*; D006333:Heart Failure / Q000473:pathology*; D006344:Heart Septal Defects, Atrial / Q000473:pathology; D006349:Heart Valve Diseases / Q000473:pathology; D006801:Humans; D007124:Immunoenzyme Techniques; D020766:Intracranial Embolism / Q000473:pathology; D008297:Male; D016253:Microscopy, Immunoelectron; D008875:Middle Aged; D013927:Thrombosis / Q000473:pathology*; D014841:von Willebrand Factor / Q000378:metabolism*
chemical_list: D014841:von Willebrand Factor