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Pulse field ablation (PFA) uses short bursts of electric field energy to ablate myocardial tissue. There is sparse data on ventricular PFA, particularly in the setting of chronic myocardial Infarction (MI) where the post-MI ventricular wall is composed of interdigitated healthy myocardium, border zone, and dense fibrotic tissue.
Objective
Compare biophysical and histopathologic characteristics of PFA applied to healthy and heterogeneously scarred swine ventricular myocardium.
Methods
Swine underwent 90-minute occlusion of the left anterior descending or left circumflex coronary artery and were survived 30 days. Electroanatomic mapping was used to define normal, MI border and scar. Acute ablations were performed using an irrigated 3.5 mm contact force (CF)-sensing catheter with the CENTAURI System (Galaxy Medical) at a single energy setting (25 Amp) in post-MI and healthy swine. One control post-MI swine did not undergo ablation. Tissues were assessed by gross pathology with 2,3,5-Triphenyltetrazolium chloride (TTC) staining and histologically with hematoxylin & eosin and trichrome stains.
Results
Eight healthy swine underwent PFA of LV and RV, and 6 MI swine underwent PFA of LV mid-scar and border zone. There was no association between CF (7-23 g) or R-wave amplitude reduction with either lesion volume or depth. Lesions in chronic MI swine were of shallower depth and smaller volume compared with lesions in healthy myocardium (Table 1). In healthy myocardium, histology consistently demonstrated well-demarcated ellipsoid lesions with central hemorrhage, and surrounding contraction band necrosis and myocytolysis. PFA lesions in chronic MI infiltrated into the irregular scar border, resulting in contraction band necrosis and edema of surviving myocytes. No contraction band necrosis was noted in surviving myocytes around scar of the non-ablated, control post-MI ventricle.
Conclusion
PFA in and around heterogeneous chronic MI scar is able to effectively ablate surviving myocytes. Smaller lesions observed in scar compared with healthy myocardium may be due to the interaction between applied PFA fields and the relatively lower electrical impedance of fibrotic tissue. Further investigation is required to optimize strategies for PFA in the treatment of ventricular tachycardia.
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