DOI: 10.1093/europace/euag105.236 ISSN: 1099-5129

The dependency of pulsed-field ablation lesions on the properties of ventricular tissue: preclinical assessment in a relevant animal model

G Caluori, K Vlachos, D El-Hamrani, J Magat, M Constantin, L Germain, O Baris, K Bony, M Popa, A Belykh, A Collin, C Poignard, H Cochet, P Jais

Abstract

Background/Introduction

Pulsed-field ablation (PFA) has been proven safe and effective for the treatment of atrial fibrillation. The application of PFA in the treatment of ventricular tachycardia (VT) remains poorly characterized, especially in the presence of complex arrhythmogenic substrates such as fibrotic or lipomatous scar tissue.

Purpose

The characterization of the features of acute and chronic PFA lesions in relationship with the ablation parameters and the properties of healthy and diseased ventricular myocardium.

Methods

A sheep model of post-ischemic ventricular substrate was created using two embolization coils. One mnth later, cardiac MRI and unipolar PFA with a focal lattice catheter were performed. Imaging was repeated acutely and at one month, followed by picrosirius red histopathology.

Results

PFA in ventricular tissue led to durable low-voltage areas in scar and healthy tissue. Temperature feedback, an estimate for contact force, was markedly affected in a dose-dependent manner by the type of the tissue interfacing with the lattice catheter (ΔT=0.95±0.64 °C and 1.90±0.92 °C for scar and healthy tissue respectively, p<0.0001). Acute PFA lesions in healthy tissue presented dose-dependent depth, with no significant change above 2 applications. We observed a consistent reduction of linear and volumetric features between acute and chronic MRI post late-gadoliunium enhancement, albeit with a loss in transmurality of only 8,75±8,32%. This suggested that the ablated wall itself is shrinking during remodeling. Histological observations confirmed these changes, with the presence of either stacked collagen deposition or cardiomyocytes-free areas, the latter significantly more likely detected in the left vs right ventricle (OR 13.6 [2.58-54.33], p<0.001). In scar tissue, PFA led to a significant increase in sub-endocardial dense scar areas compared to pre-ablation values (+13.25% acutely and +6.69% chronically, p<0.01). This correlated with significant changes in the distribution of the calculated extracellular volume index. Histological analysis exploiting collagen birifringence showed that PFA lesions present in average an equal distribution between collagen I and III, whereas post-ischemic scars show a preponderance of collagen III. This suggests different maturation processes between the two type of lesions, and it allowed us to semiquantitatively segment chronic PFA lesions in scars.

Conclusion(s)

PFA in ventricular tissue shows significant chamber and tissue specificity, most likely due to different pre-existing biothermal and structural features. Temperature feedback should be interpreted according to the presence of scar, while increasing the number of deliveries from 2 to 4 is associated with limited and non-significant gain in depth. Mature PFA lesions can be estimated ex vivo inside scar tissue via collagen distribution, and in vivo by exploiting the increased local MRI contrast and extracellular volume distribution.

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