Background Previous studies suggest that MRI with late gadolinium enhancement (LGE) may identify slowly conducting tissues in scar-related ventricular tachycardia (VT). Objective We tested the feasibility of image-based simulation based on LGE to estimate ablation targets in VT. Methods We conducted a retrospective study in 13 patients who had pre-ablation MRI for scar-related VT ablation. We used image-based simulation to induce VT and estimate target regions according to the simulated VT circuit. The estimated target regions were co-registered with the LGE scar map and the ablation sites from the electroanatomical map in the standard ablation approach. Results In image-based simulation, VT was inducible in 12 patients (92.3%). All VTs showed macro-reentrant propagation patterns, and the narrowest width of estimated target region that an ablation line should span to prevent VT recurrence was 5.0 ± 3.4 mm. Out of 11 patients who underwent ablation, the results of image-based simulation and the standard approach were consistent in 9 patients (82%), where ablation within the estimated target region was associated with acute success (n=8) and ablation outside the estimated target region was associated with failure (n=1). In one case (9%), the results of image-based simulation and the standard approach were inconsistent, where ablation outside the estimated target region was associated with acute success. Conclusions The image-based simulation can be used to estimate potential ablation targets of scar-related VT. The image-based simulation may be a powerful noninvasive tool for pre-procedural planning of ablation procedures to potentially reduce the procedure time and complication rates.

Free-breathing accurate 3D T2 mapping is feasible and may be applicable in myocardial assessment in lieu of current clinical black blood, T2 -weighted techniques.

FA pretreatment blunts myocardial dysfunction during ischemia and ameliorates postreperfusion injury. This is coupled to preservation of high-energy phosphates, reducing subsequent reactive oxygen species generation, eNOS-uncoupling, and postreperfusion cell death.