Abstract

Abstract Introduction Perioperative management of advanced patients with indication to ventricular tachycardia (VT) ablation is complex. A PAINESD score ≥ 15 was proposed to identify those who might benefit from pre–emptive mechanical cardiopulmonary support (MCS). We present a case successfully managed with continuous percutaneous left stellate ganglion block (C–PLSGB). Case A 71–year–old diabetic man with severe post–ischemic cardiomyopathy (LVEF 24%, NYHA Class III) and chronic pulmonary disease was admitted for electrical storm with multiple ICD shocks due to poorly tolerated monomorphic VT (MMVT) at 176 bpm resistant to anti–tachycardia pacing (ATP), despite ongoing chronic oral therapy with amiodarone and carvedilol. Poorly tolerated and ATP–resistant MMVTs at 170–180 bpm recurred despite intravenous (iv) amiodarone and lidocaine (20 mcg/kg/min) and oral propranolol. Ultrasound guided C–PLSGB was therefore started; lidocaine was chosen for the continuous infusion due to the short half–life, at the initial dose of 10 mg/h; 6 hours later, his poorly tolerated MMVT recurred at 167 bpm. Therefore, at first we increased iv lidocaine to 30 mcg/kg/min, without benefit, then we increased C–PLSGB at 37.5 mg/h and decreased iv lidocaine to 20 mcg/kg/min due to neurological symptoms. With this regimen, the patient stayed VT free for 2 hours, then the clinical VT recurred at 130 bpm, with good hemodynamic tolerability and ATP–response. C–PLSGB infusion was than increased to 75 mg/h, with no more VT. Endocardial VT ablation was planned. Despite a very high PAINESD score (31) we decided to avoid pre–emptive MCS. We stopped lidocaine (both iv and as C–PLSGB) 2 hours before ablation. As soon as the patient came in the EP room (before instrumentation), the clinical MMVT recurred at 133 bpm. C–PLSGB was then resumed (initially at 100 mg/h for 30 minutes, then at 37.5 mg/h). The MMVT then spontaneously recurred at 133 bpm: it was mapped and ablated in the medio–apical anterior wall, with acute VT interruption. A second VT morphology then appeared, that was mapped and ablated at a more basal site, despite a partial epicardial component of the circuit was identified. C–PLSGB was then stopped and no more VT occurred nor were induced 1 hour later. At 8 months the patient is still alive with no more VT. Conclusion C–PLSGB with individually tailored infusion rates could be used during VT ablation as a mean to reduce VT cycle length and allow for mapping without MCS.

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