Endocardial Changes in Nonvalvular Atrial Fibrillation Without Atrial Thrombus—Thrombomodulin and Tissue Factor Pathway Inhibitor

Atrial fibrillation (AF) is a well-known cause for thromboembolism. Although blood stasis in the left atrium and hypercoagulable state of the blood have been emphasized as important mechanisms, limited attention has been paid to the endocardial changes in maintaining the balance of local coagulation, which may also contribute to the thrombus formation in AF. In the present study, left atrial appendage samples were obtained at heart surgery from nonvalvular AF and non-AF patients without atrial thrombus. Immunohistochemistry for endocardial markers including thrombomodulin (TM) and tissue factor pathway inhibitor (TFPI) was performed and semiquantitatively graded. In immunohistochemistry analysis, decreased expression of TM was found in patients with nonvalvular AF compared with those without AF (P < .001). There was no difference in TFPI expression between the 2 groups (P = .213). Patients with TM score of 0 or 1 seemed to have larger left atrial diameter (LAD) than those with TM score of 2 or 3 (44.0 (7.9) vs 40.6 (3.9); P = .009), while no relationship between LAD and TFPI expression was found (43.4 (7.0) vs 42.9 (7.8); P = .485). In conclusion, TM expression in the atrial endocardium is decreased in nonvalvular AF without atrial thrombus, while TFPI expression is not. Downregulated TM expression might be associated with enlarged LAD.