CA-531-01 FAT INFILTRATION CONFERS PROPENSITY FOR VENTRICULAR TACHYCARDIA IN THE POST-INFARCT SUBSTRATE

Abstract

Infiltrating adipose tissue (inFAT) is present in the post-infarct substrate, but its role in ventricular tachycardia (VT) arrhythmogenesis is not well-established. To investigate the role of post-infarct inFAT in VT propensity. 24 post-infarct patients who underwent VT ablation were prospectively enrolled across two centers. For each patient, contrast-enhanced computed tomography (CE-CT), late gadolinium-enhanced magnetic resonance imaging (LGE-MRI), and substrate mapping during sinus rhythm were acquired. Voltage amplitude, deceleration zones (DZ) which represent regions of activation slowing, and substrate-based ablation locations were compared with the inFAT and scar distributions. To glean deeper insights into arrhythmogenic propensity, novel hybrid digital heart twins representing the patient-specific inFAT from CT and scar from MRI were reconstructed. VT circuits were then induced, assessed, and compared to mapping data (Fig.A). Combined inFAT and scar had lower voltage and exhibited stronger correlations with voltage amplitude than that of scar alone (0.76±0.56 vs. 1.19±0.47 mV, p<0.0005; r = -0.54 vs. -0.45). inFAT and scar exhibited greater isochronal crowding than scar alone (3(2) vs. 2(1) isochrones, p<0.0005). Most DZs consisted of combined inFAT and scar (71.1%) rather than scar alone. The amount of ablated inFAT was strongly correlated with ablated scar (r = 0.734, p<0.05). In the digital hearts, 140 VTs were induced. The total amount of inFAT, but not scar, was significantly associated with the number of VTs induced (p<0.05). For most VT circuits, the critical isthmus was comprised of both inFAT and scar (110/140 VTs) (Fig.B). In a multivariate regression adjusting for age, infarct age, and VT circuit tissue volume, inFAT remodeling within the VT circuit, but not scar, was a predictor of the amount of DZs (β = 0.355, p<0.05) and clinical ablations (β = 0.323, p<0.005) (Fig.B). Post-infarct inFAT remodeling creates a critical arrhythmogenic substrate for VT that needs to be prioritized during ablation.