Endocardial overexpression of von Willebrand factor was significantly correlated with increased myocyte diameter (p<0.01), suggesting it contributes to the thrombotic predilection of atrial fibrillation.
Observational (n=43)
No
Endocardial overexpression of von Willebrand factor occurs during atrial structural remodeling in AF with underlying heart disease, potentially contributing to increased thrombotic risk.
p-value: p=<0.01
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.
Kumagai et al. (Thu,) conducted a observational in Atrial Fibrillation (n=43). Atrial fibrillation with structural remodeling vs. Non-AF controls or AF without structural remodeling was evaluated on Correlation between endocardial von Willebrand factor expression and mean myocyte diameter (p=<0.01). Endocardial overexpression of von Willebrand factor was significantly correlated with increased myocyte diameter (p<0.01), suggesting it contributes to the thrombotic predilection of atrial fibrillation.