Background: Left atrial appendage (LAA) is gaining increasing attention in patients with atrial fibrillation (AF) in the context of cardioembolic stroke. Galectin-3 (Gal-3) is a mediator of profibrotic pathways and is associated with an increased incidence of heart failure. However, the role of Gal-3 in LAA remodelling and thrombus formation in AF has not been evaluated.
Methods: This prospective study included 153 consecutive patients with paroxysmal (n=58), persistent (n=55) or permanent (n=40) nonvalvular AF. The serum level of Gal-3 was measured by enzyme-linked immunosorbent assay. The morphology and function of LAA were determined by transoesophageal echocardiography.
Results: Left atrial appendage thrombus was observed in 22 patients (2 in paroxysmal AF, 11 in persistent AF and 9 in permanent AF). Significant differences among patients with different types of AF were found in terms of LAA morphology (orifice diameter and depth) and function (flow velocity and tissue Doppler contracting velocity) as well as serum levels of Gal-3. Furthermore, patients with persistent or permanent AF had higher levels of Gal-3. High Gal-3 level was closely related to LAA flow velocity and occurrence of LAA thrombus. Multivariate logistic regression analysis revealed that Gal-3 was an independent determinant of LAA thrombus in patients with AF. Receiver operating characteristic (ROC) curves related to LAA thrombus formation established a cut-off point for Gal-3 >18.95ng/ml.
Conclusions: Cardiac rhythm disturbances caused by AF may lead to morphologic and functional remodelling of LAA. The serum level of Gal-3 was significantly correlated with LAA remodelling in patients with AF. High levels of Gal-3 were also a predicator for LAA thrombus formation.
Keywords: Atrial fibrillation; Galectin-3; Left atrial appendage; Transoesophageal echocardiography.
Copyright © 2018 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.