Relevant correlation of Galectin-3 with a novel morphological classification system for LAA closure – the end of echocardiographic follow up after occluder implantation?
Authors: Haertel F , Hamadanchi A , Ijuin S , Lustermann P , Gruen K , Schulze C , Franz M , Moebius-Winkler S 
Published: November 2020

Abstract

Introduction
Echocardiographic detection of residual peri-device leakage (PDL) after percutaneous left atrial appendage closure (LAAC) remains crucial. Significance of PDL and cardiac tissue remodeling after LAAC are still poorly understood but might have diagnostic implications. This study aims to characterize and verify if a novel echocardiographic classification system to asses the success of LAAC in combination with quantifiable biomarkers of cardiovascular tissue remodeling can help in the prediction of PDL.

Methods
Patients eligible for LAAC were included. Serum levels of the cardiac remodeling marker Galectin-3 were determined before device implantation (baseline), 45 days (45d) and 6 months (6M) after LAAC using ELISAs. Transesophageal echocardiography (TEE) was carried out to assess success of the LAAC procedure. All echo images were retrospectively evaluated by two independent investigators. Based on the amount of echodensity and luceny inside the devices after LAAC, three types can be distinguished that grade the degree of closure of the LAA. Type A has complete homogenous echodensity in 0, 45, 90 and 135°, indicating completely thrombosed device. Type B shows inhomogeneous echo-lucencies (&lt;50% of device). Type C describes a partially thrombosed device with echo-lucencies &gt;50%. Novel classification according to Hamadanchi, Jena, Germany (Fig. 1).

Results
We included 44 patients (characteristics listed in Table 1). Complete LAAC (without any residual flow) was achieved in 64% (28 patients) after 45 days and in 80% (35 patients) after 6 months. Mean PDL diameter was 3.5±1.5mm. Type A showed the lowest rate of PDL after 45d (Type A: 22% vs. Type B: 33% vs. Type C: 88%; p=0.007) and after 6M (Type A: 12% vs. Type B: 28% vs. Type C: 100%; p=0.002). Galectin-3 levels did not show a relevant difference regarding the type of AF at baseline (paroxysmal AF: 11.7±5.4 ng/ml vs. permanent AF: 12.1±6.3 ng/ml; p=0.45). We observed a significant increase and distribution of serum levels of Galectin-3 [ng/ml] after 45 days among the three types (Baseline: 13.1±5.8; 45d: 16.3±7.2 (Type A) vs. 19.2±8.6 (Type B) vs. 25.8±9.4 (Type C); p=0.031) followed after 6 months by a drop of Galectin-3 for type A and B toward and below baseline levels (6M: 8.9±3.1 (Type A) vs. 12.4±5.5 (Type B)) whereas type C persisted in showing elevated Galectin-3 levels compared to all other types (6M: 17.5±4.5 (Type C); p&lt;0.001), Fig. 2. Correlation analysis shows a significant negative correlation trend between Galectin-3 and mean PDL diameter (−0.51; p=0.016) after 45 days and a relevant positive correlation after 6 months (0.58; p=0.017).

Conclusion
After LAAC, Galectin-3 levels are elevated, as a marker of myocardial fibrosis in the LAA. Depending on the degree of closure of the LAA, Galectin-3 decreases to the baseline level or stays elevated in case of relevant PDL and could therefore be considered as a new biomarker for closure success.

Funding Acknowledgement
Type of funding source: None