Abstract
Introduction
Ventricular tachycardia (VT) storm in patients with advanced structural heart disease remains a challenging clinical problem, particularly when ventricular arrhythmias persist despite antiarrhythmic therapy and catheter ablation. Cardiac sympathetic denervation (CSD) is an adjunctive neuromodulatory strategy that reduces sympathetic input contributing to ventricular arrhythmogenesis. We describe successful robotic left cardiac sympathetic denervation (LCSD) for refractory VT storm in a patient with severe ischemic cardiomyopathy.
Case Info
A 69-year-old man with severe ischemic cardiomyopathy (left ventricular ejection fraction 15%), prior coronary artery bypass grafting, mechanical aortic valve replacement, mitral valve repair, permanent atrial fibrillation, and a cardiac resynchronization therapy defibrillator (CRT-D) developed recurrent VT requiring multiple ICD therapies. Despite extensive substrate-based VT ablation, he subsequently experienced recurrent VT and nonsustained ventricular arrhythmias while receiving mexiletine. Amiodarone had been discontinued because pulmonary function testing demonstrated reduced diffusing capacity and a restrictive ventilatory defect concerning for underlying parenchymal lung disease. Several months later, he presented with VT storm requiring multiple ICD therapies, including 11 shocks in a single day. He remained hemodynamically stable without evidence of acute ischemia and was initially treated with intravenous lidocaine.
Disc Clinical
Given recurrent ventricular arrhythmias despite antiarrhythmic therapy and prior catheter ablation, CSD was pursued. The patient underwent robotic-assisted LCSD under general anesthesia. The left sympathetic chain was mobilized from immediately below the stellate ganglion through the T4 level and transected, with cauterization of surrounding tissue to interrupt accessory sympathetic fibers, including the nerves of Kuntz. The procedure was uncomplicated.
Sympathetic activation can facilitate ventricular arrhythmias by increasing myocardial excitability and dispersion of repolarization. Recurrent VT and ICD shocks may further increase adrenergic activation, creating a self-perpetuating cycle of ventricular arrhythmias. CSD targets this autonomic contribution without eliminating the underlying scar-mediated substrate and therefore represents a complementary strategy to catheter ablation. Following LCSD, the patient continued mexiletine. Subsequent device interrogation demonstrated no recurrent ventricular high-rate events, VT, or ICD therapies. At one-year follow-up, he remained free of recurrent ventricular tachyarrhythmias and ICD therapies.
Conclusion
Robotic LCSD may provide effective and durable suppression of ventricular arrhythmias in carefully selected patients with advanced structural heart disease and refractory VT despite antiarrhythmic therapy and catheter ablation. This case adds to the existing literature supporting cardiac sympathetic denervation as an adjunctive strategy for refractory ventricular arrhythmias, particularly given the limited evidence from large prospective trials.