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  • Polymorphic VT VF storms can occur in patients with


    Polymorphic VT/VF storms can occur in patients with severe TC-E 5006 failure, independent of their underlying causes. Recent experimental studies using a pacing-induced heart failure model showed that heart failure facilitates acute shortening of the APD immediately after VF termination [73]. Persistent elevation of intracellular Ca2+ due to Ca2+ overload following VF activates inward Ca2+-sensitive currents during the late phase 3 of the action potential, which induces triggered activity and spontaneous VF (i.e., late phase 3 EAD). This arrhythmogenic post-shock APD shortening after VF defibrillation occurs in heart failure via upregulation of the apamin-sensitive small-conductance K+ current (IKAS) in failing hearts [74]. In this heart failure model, blocking IKAS prevents recurrent VF, resulting in the termination of VF storms. In fact, IKAS upregulation also occurs in human hearts with severe heart failure [75]. Notably, amiodarone blocks IKAS[76]. In addition, sympathetic stimulation accelerates post-shock APD shortening, late phase 3 EADs, and VF recurrence by non-ischemic activation of IKATP[4]. Myocardial ischemia during VF further enhances IKATP activation. It has been reported that amiodarone also inhibits sarcolemmal IKATP[77]. Taken together, the combined use of intravenous amiodarone and beta-blockers is a reasonable treatment for polymorphic VT/VF storms in patients with heart failure. Amiodarone has been shown to increase the short-term survival of patients with shock-refractory VT/VF when compared with lidocaine [78]. This beneficial effect of amiodarone may be partially attributable to the prevention of immediate VT/VF recurrence (i.e., severe form of electrical storms) mimicking shock-refractory VT/VF. RFCA is also useful in treating polymorphic VT/VF storms resistant to medical therapies in patients with non-ischemic cardiomyopathy. Purkinje-like potentials recorded along the scar border zone can be ablation targets [79].
    Conflict of interest
    Introduction Among the spectrum of arrhythmias that are treatable with catheter ablation, the elimination of reentrant circuits within ventricular scar remains challenging. As long-term success rates for AV nodal reentrant tachycardia, bypass-tract tachycardia, and premature ventricular contractions in the absence of structural heart disease are >85–90%, intermediate freedom from recurrent VT at experienced centers has been shown to be ~50% at 6–12 months [1,2]. While the vast majority of patients at risk for recurrent VT have implantable cardioverter-defibrillators (ICD), ICD therapy is only abortive and does not prevent VT. ICD shocks are strongly associated with diminished quality of life and increased mortality [3]. While antiarrhythmics have been shown to reduce ICD therapies, side effects can be significant, prompting discontinuation in a substantial proportion of patients [4]. At present, surgical and catheter ablation remains the most effective method to eliminate VT, although further progress in the field is necessary. The reasons for ablation failure and recurrence are multifactorial. The underlying patient substrate with scar-mediated monomorphic VT has multiple comorbidities and the severity of heart failure is associated with increased risk for recurrent VT [1]. Changes in scar biology and the inherent nature of VT, which can be inconsistently inducible or hemodynamically unstable to preclude activation mapping are important factors. As opposed to other arrhythmias, the induction of multiple VT morphologies within scar is common. Importantly, biophysical limitations of radiofrequency ablation exist in thick ventricular walls that have transmural circuits, where trabeculations, calcification, layered thrombus, and epicardial coronary vessels and fat can all serve as barriers to effective power delivery into scar.
    Methods to localize the origin of VT: ECG and Imaging The most common method to localize the origin of VT is analysis of the 12-lead electrocardiogram [5,6]. VTs are characterized by the QRS morphology and left bundle branch morphologies originate from the RV or LV septum and right bundle branch VTs originate from the LV. Sites that originate from superior sites (anterior wall and outflow tracts) exhibit inferior axis and sites from the diaphragmatic surface of the heart exhibit a superior axis. Akin to accessory pathway localization, leftward sites of origin are commonly negative in lead I and septal sites have a tendency to have leftward vector. The precordial transition is useful in determining basal versus apical locations, where the mitral annulus is the most posterior structure (R dominant, early transition) and the apex is anatomically most anterior (S dominant, late transition) (Fig. 1).