Expression of the von Willebrand factor in atrial endocardium is increased in atrial fibrillation depending on the extent of structural remodeling.
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.
Kumagai
Koji
K
Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
Fukuchi
Mitsumasa
M
Ohta
Jun
J
Baba
Shigeo
S
Oda
Katsuhiko
K
Akimoto
Hiroji
H
Kagaya
Yutaka
Y
Watanabe
Jun
J
Tabayashi
Koichi
K
Shirato
Kunio
K
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
D019408:Platelet Endothelial Cell Adhesion Molecule-1; D012333:RNA, Messenger; D014841:von Willebrand Factor; D005337:Fibrin; D005340:Fibrinogen