Management of electrical storm of unstable ventricular tachycardia in post myocardial infarction patients: A single centre experience

Abstract

Objective: This is a case series of consecutive patients with past myocardial infarction presenting with Electrical Storm (ES) of unstable ventricular tachycardia (VT) treated by a protocol directed algorithm.

Methods: Management protocol involved treatment of reversible causes, ventilatory & hemodynamic support, administration of antiarrhythmic drugs (AAD) & maximally tolerated doses of beta-blockers, stellate ganglionectomy and Radiofrequency ablation (RFA) guided by Electro Anatomic Mapping (EAM). Patients were followed up periodically with review of device data logs.

Results: There were 12 patients (mean age=61.38±6.48years & mean LVEF=31.92±4.23%). Presentation was recurrent ICD shocks (n=5) or VT (n=7). All were mechanically ventilated. Reversible causes were identified in 4 patients and appropriately addressed. Totally 8 patients underwent endocardial substrate modification by EAM & RFA. Endocardial LV Voltage mapping demonstrated a mean scar area of 70.04±17.63 sq.cm (27.04±6.20% of mapped area). The electrograms targeted for ablation included late potentials, fractionated electrograms, double potentials and channels within the scar. Two patients had stellate ganglionectomy in addition. Ten patients (83.3%) survived to discharge, all of whom are alive at a follow up of 30.12±19months free of ES. VT free survival at end of follow up was 80%. No patient had hospitalization related to VT. Single episode of VT recurrence was seen in 2 patients at 7 months and 1year of follow up respectively.

Conclusion: In post myocardial infarction patients presenting with ES and unstable VT, a protocol driven approach involving substrate modification targeting abnormal electrograms improves outcomes.

Keywords: Catheter ablation; Electrical storm; Electro anatomic mapping; Substrate modification; Ventricular tachycardia.

Fig. 1

Panel A: LV Voltage map in sinus rhythm of a patient in AP view showing areas of scar (denoted in red, with voltage of <0.5 mV) and normal myocardium (denoted in pink, with voltage of >1.5 mV). The areas between the scar and the normal myocardium are low voltage corridors containing abnormal electrograms. The fine white dots indicate the points mapped. Each abnormal electrogram is tagged with a different colour (blue: double potentials; yellow/orange: late potentials; white: fractionated signals; pink: continuous electrical activity) which are targets for ablation. Panel B: shows a substrate map of the LV in LAO view where voltage thresholds have been adjusted to identify low voltage channels (multicoloured zones seen between pink areas) within the scar. The figure shows a late potential within a channel (blue tag and arrow) that was targeted for ablation. Panel C: shows abnormal electrograms targeted for ablation. QRS complex in ECG lead V1, and corresponding LV electrogram on mapping catheter are shown. 1 to 3 are examples of isolated late potentials (ILPs), 1 is an ILP that is identified as a high frequency discrete potential separated from the ventricular electrogram by 50 msec, 2 shows an ILP which is fractionated,3 is a double-component or fractionated late potential that is formed by the almost fusion of two late potentials. 4 is a double potential having two component electrograms of low voltage separated by an isoelectric interval. 5shows low voltage pluricomponent signals without intervening isoelectric intervals that appears as continuous electrical activity (CEA).

Fig. 2

12 lead ECG recordings of one of the patients who had 4 different morphologies of VT (A to D) during procedure. The cycle length of the VTs was variable 260–300 ms (280.75 ± 19.38). All the VTs were hemodynamically unstable and unmappable.