Introducere: We present the case of a 60-year old man, drinker, smoker, hypertensive, with a history of an an-tero-lateral myocardial infarction treated conservatory with evolution towards dilation and severe left ventri-cular (LV) systolic dysfunction, under treatment with Amiodarone for paroxysmal AF. He was admitted in our hospital for the investigation of 3 syncopes, docu-mented as VT on the surface ECG.
Methods: Laboratory tests showed a serum creatini-ne level of 1.5 mg/dl, a BNP value of 1020 pg/ml and normal values of myocardial enzymes (CK-MB, TGO, LDH, troponine) and TSH. The ECG documented si-nus rhythm 60 bpm, left axis deviation, both intraatri-al and intraventricular conduction disturbances, with left bundle branch block and chronic antero-lateral myocardial infarction. Echocardiography revealed a severely dilated left ventricle, with akinesia of the in-terventricular septum and anterior wall (ejection frac-tion=15%) and severe secondary mitral regurgitation. Coronarography showed lesions with no indication for PTCA. An ICD was implanted for the secondary pre-vention of SCD. Three days later, the patient developed incessant VT, unresponsive to electrical shocks and pharmacological therapy.
Results: We performed urgent electrophysiological, which confirmed VT of septoapical origin, irresponsive to ATP, so we proceeded with urgent catheter ablation. Activation mapping was performed using the CARTO 3D electroanatomical mapping system, unveiling the best activation time at the septal region of the LV, where we ablated with radiofrequency, leading to interrupti-on of the tachycardia. Moreover, we performed voltage mapping and substrate ablation, guided by the aspect of the intracardiac electrograms (entrance points, exit points and mid-diastolic potentials), the result being non-inducibility of any VT by programmed ventricu-lar stimulation. At the 1 month follow-up, the device interrogation documented one sustained VT episode, successfully treated by the ICD by administering 1 in-ternal electrical shock of 20J. Nevertheless, at 5 months device follow-up, the patient remained arrhythmia-free under a small dose of Amiodarone (100 mg/day). Furt-hermore, the 9 months device follow-up showed no sustained VT episodes and the patient was referred for cardiac transplantation.
Conclusions: Catheter ablation should be considered early in patients presenting with electrical storm after the correction of reversible causes/triggers and especi-ally when Amiodarone fails. Moreover, catheter abla-tion has good results when the VT is monomorphic, the procedural end-point being the non-inducibility at the end of the procedure, which is associated with less recurrences and improved survival.