Percutaneous left stellate ganglion block to increase ventricular fibrillation threshold and defibrillation success rate in acute fulminant myocarditis with electrical storm

Abstract Introduction Acute fulminant myocarditis represents a predisposing substrate for life–threatening ventricular arrhythmias (VAs). Percutaneous left stellate ganglion block (PLSGB) usage has been reported for the prevention of recurrent VAs, but clinical data on its acute effect on ongoing ventricular fibrillation (VF) are missing. Case A 57–years–old man suffering gastroenteritis and fever in the past week presented in the ED with typical chest pain. ECG depicted infero–lateral ST–segment elevation, cardiac ultrasound showed a mildly reduced LVEF and coronary angiography ruled out coronary lesions. In the following hours the patient developed frequent premature ventricular complexes with R on T phenomenon triggering short coupled torsade de pointes with rapid degeneration into VF. VAs episodes, initially responsive to single DC shock, kept recurring despite intravenous (iv) amiodarone, iv lidocaine and iv correction of potassium and magnesium. The patient was therefore treated with deep sedation, intubation and ECMO VA placement; still, he reached a status of persistently ongoing VF, refractory even to DC shocks (n=20). Therefore, ultrasound–guided PLSGB using a local bolus of lidocaine 150 mg + ropivacaine 50 mg was performed. After 5 minutes, a single DC shock was delivered, effective in achieving a stable sinus rhythm at 35 bpm with no more recurrences. Despite electrical stabilization, the patient developed a severe cardiogenic shock due to bradycardia and severe biventricular disfunction, treated with vasopressin and dobutamine. In the next 48 hours we observed a significant improvement, resumption of biventricular contractility and absence of VAs recurrences, so the patient was slowly weaned off ECMO and vasopressors. Immunological tests showed Enterovirus IgM positivity, while endomyocardial biopsy was negative for inflammatory infiltrates in the analyzed sections. Cardiac MRI (performed 10 days after onset) showed edema and non–ischemic LGE in the antero–lateral and infero–lateral basal subepicardial regions of the left ventricle, LVEF was 55%. After 15 days from admission, despite ongoing amiodarone and bisoprolol, the patient developed a run of monomorphic VA of 30 beats at 170 bpm, therefore he underwent sICD implantation. Conclusion PLSGB played a key role for the acute management of refractory VF unresponsive to DC shocks, allowing for acute stabilization. More clinical data are needed on acute neuromodulation for electrical storm.