Photon-counting CT characterization of arrhythmogenic substrate in VT ablation

Introduction Catheter ablation is an established treatment for scar-related ventricular tachycardia (VT), but recurrences remain common due to the complexity of arrhythmogenic substrates in structural heart disease (SHD). Cardiac magnetic resonance (CMR) is the reference for myocardial tissue characterization, showing strong concordance with electroanatomical mapping (EAM). Late iodine enhancement cardiac CT may also identify scar, though with lower contrast resolution. Photon-counting CT (PCCT) offers improved spatial resolution and contrast-to-noise ratio, potentially enabling more accurate scar assessment. Preliminary evidence suggests good agreement between PCCT and CMR, but data on its use in VT ablation are currently lacking. Purpose To evaluate whether PCCT can identify myocardial scar in SHD patients and guide VT ablation. Methods We enrolled five consecutive SHD patients undergoing transcatheter VT ablation. They underwent both PCCT and CMR. Images were analyzed using the ADAS-VT segmentation system and integrated in CARTO3 system. Each patient underwent endocardial and/or epicardial EAM to identify abnormal signals (low voltages, fragmented signals, late potentials), followed by targeted radiofrequency ablation. Substrate maps were compared with PCCT and CMR reconstructions. Results In all five consecutive patients (3 ischemic cardiomyopathy, 1 post-myocarditis, 1 dilated cardiomyopathy) PCCT-derived 3D reconstructions allowed clear visualization of the arrhythmogenic substrate. PCCT findings showed excellent topographical concordance with CMR and with low-voltage regions and areas displaying late and fractionated electrograms during EAM. In one patient with prior myocarditis, PCCT accurately delineated an extensive basal inferolateral epicardial scar, guiding epicardial mapping and allowing identification of the critical isthmus during induced VT (Figure 1). In two ischemic patients, PCCT correctly identified inferobasal and apical scar regions, respectively, corresponding to pathological substrate sites subsequently targeted during ablation (Figure 2). In the patient with non-ischemic dilated cardiomyopathy and severe device-related CMR artifact, PCCT enabled substrate characterization and procedural planning when CMR was non-diagnostic. In the patient with an apical aneurysm, PCCT also identified a myocardial channel within the scar, confirmed by the presence of local abnormal ventricular activity on EAM. Radiofrequency ablation was performed in all patients, targeting late/fractionated electrograms and critical isthmus sites identified by combined PCCT–EAM integration. At the end of the procedure, no VT was inducible in any patient. Conclusions PCCT enables accurate identification of myocardial scar areas, demonstrating excellent correspondence with CMR and EAM. It also proved useful in guiding catheter ablation of ventricular tachycardias. Future studies are needed.