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J Am Coll Cardiol, 2001; 37:1436-1442 © 2001 by the American College of Cardiology Foundation |
* Department of Cardiovascular Medicine, Tohoku University, Graduate School of Medicine, Sendai, Japan
Department of Otolaryngology, Tohoku University, Graduate School of Medicine, Sendai, Japan
Department of Thoracic and Cardiovascular Surgery, Tohoku University, Graduate School of Medicine, Sendai, Japan
Department of Cardiovascular Surgery of Tohoku Kosai Hospital, Sendai, Japan
Manuscript received October 25, 1999; revised manuscript received December 6, 2000, accepted December 22, 2000.
Reprint requests and correspondence: Dr. Kunio Shirato, Professor and Chairman, Department of Cardiovascular Medicine, Tohoku University, Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan.
fukuchi{at}int1.med.tohoku.ac.jp
OBJECTIVES
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.
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