Left ventricular (LV) extracellular volume fraction (ECV) quantified by cardiac computed tomography (CT) reflects diffuse myocardial fibrosis. In patients with atrial fibrillation (AF) and reduced LV ejection fraction (LVEF), distinguishing tachycardia-induced cardiomyopathy from underlying myocardial disease remains challenging. The prognostic value of ECV for predicting reverse remodeling (RR) after catheter ablation for AF remains uncertain. We retrospectively analyzed 102 patients with LVEF ≤ 50% on echocardiography who underwent cardiac CT before AF ablation between May 2015 and April 2025. RR was defined as a ≥15% reduction in LV end-systolic volume with recovery of LVEF > 50%, or an absolute increase in LVEF of ≥15%. RR occurred in 49 patients (48%). ECV was significantly lower in patients with RR than in those without (31.2 ± 3.5% vs. 37.6 ± 7.8%, p < 0.001). Receiver operating characteristic analysis identified an optimal cutoff of 34.8% (area under the curve 0.77; sensitivity 88%; specificity 62%, p < 0.001). In multivariable logistic regression analysis, lower ECV remained independently associated with RR (odds ratio 0.84; 95% confidence interval 0.75-0.95; p = 0.006). CT-derived ECV was associated with RR after AF ablation in patients with reduced LVEF and may provide additional information for clinical decision-making.

Wide complex tachycardia with right bundle branch block and right axis deviation in young age, fascicular ventricular tachycardia will be the top differential diagnosis to be considered. AV nodal blocking agents like verapamil, diltiazem, and amiodarone are not resolving the WCT with RBBB tachycardia in this case. Not all fascicular VTs are verapamil sensitive unless the verapamil sensitive re-entry pathway is involved.

Excitable biological systems can undergo abrupt transitions from stable rhythmic activity to pathological oscillations through subtle changes in slow-fast dynamical structure. In cardiac ventricular myocytes, such transitions manifest as early afterdepolarizations (EADs), which are closely associated with triggered activity and polymorphic ventricular tachycardia. Although the transient outward K+ current (Ito) shapes early repolarization, its dynamical role in EAD-mediated instability remains incompletely understood. We investigated how Ito suppression modifies excitation dynamics using two-dimensional ventricular tissue simulations combined with bifurcation and slow-fast analyses in a human ventricular myocyte model exhibiting EADs. Reduction of Ito markedly suppressed triggered activity and ventricular tachycardia-like dynamics in a manner dependent on both the magnitude and timing of inhibition. Single-cell bifurcation analysis revealed progressive destabilization of EAD-associated oscillations with decreasing Ito. Slow-fast decomposition further demonstrated that Ito suppression does not eliminate the underlying oscillatory structure of the fast subsystem but instead shifts the plateau potential in a depolarizing direction, thereby displacing system trajectories away from the oscillatory regime responsible for EAD generation. As a result, trajectories bypass the oscillatory attractor and repolarize directly toward the stable resting equilibrium. These findings show that Ito inhibition suppresses pathological oscillations not by structural destruction of the oscillatory bifurcation framework but by modifying trajectory accessibility within it. This work provides a multiscale dynamical systems interpretation of EAD suppression and identifies Ito as a key control parameter governing ventricular electrical stability.

Wide complex tachycardia (WCT) presents a diagnostic challenge, particularly in distinguishing ventricular tachycardia (VT) from supraventricular tachycardia (SVT) with aberrancy. We report an 81-year-old man with recurrent WCT initially suspected to be VT based on clinical and electrocardiographic features. However, inconsistencies across serial electrocardiographic tracings limited diagnostic certainty. Specifically, variations in polarity across all limb leads, except aVR and the precordial leads, raised suspicion for limb lead misplacement, particularly left arm-left leg reversal. This electrocardiographic perplexity further complicated the clinical interpretation. To clarify the underlying arrhythmia mechanism, an electrophysiology (EP) study was performed, which demonstrated inducible tachycardia with simultaneous atrioventricular activation (VA = 0), consistent with typical atrioventricular nodal reentrant tachycardia (AVNRT) with aberrancy. Successful slow pathway ablation rendered the arrhythmia noninducible, and the patient has remained free of recurrent arrhythmia during five months of follow-up. This case highlights the limitations of ECG-based algorithms and the importance of careful ECG interpretation and invasive evaluation.