Cardiac sympathectomy in humans: Rationale, results & mechanistic insights

The autonomic nervous system plays a critical role in the genesis and maintenance of ventricular arrhythmias. Pharmacological anti-adrenergic interventions, such as beta-blockers are a cornerstone of therapeutic management of ventricular arrhythmias. However, ventricular arrhythmias that remain refractory to standard medical management are associated with a high mortality. Neuraxial modulation using thoracic epidural anesthesia (TEA) and surgical removal of the stellate ganglia and thoracic sympathetic ganglia (cardiac sympathetic denervation, CSD) are therapeutic options for such cases. The protective effects of CSD have been demonstrated in long QT syndrome (LQTS) and catecholaminergic polymorphic ventricular tachycardia. CSD has also been shown to lengthen ventricular refractoriness and raise the ventricular fibrillation threshold without impairing cardiac contractility. Analysis of data from patients with VT refractory to medical therapy and catheter ablation referred for CSD between 4/2009 and 8/2012 was performed. Thirty eight patients (32 males, 6 females, age 60 ± 12 years, EF 30 ± 15%) with recurrent VT or VT underwent CSD. One patient was referred for idiopathic VF. Patients had experienced a median of 2 catheter ablation procedures and 13 (range 7-55) implantable cardiac defibrillator (ICD) shocks in the 6 months prior to the procedure. At a mean follow up of 356 ± 300 days (median = 160 days), 4 patients (12.5%) underwent heart transplantation and 15 (39%) patients died, two after heart transplantation, one after lead extraction, one from renal failure, and 11 from worsening heart failure or multi-organ failure. Incidence of recurrent arrhythmias from ICD logs was available in 31 patients (82%), 10 with left CSD and 21 with bilateral CSD. Three (30%) of the left CSD patients and 11 (52%) of bilateral CSD patients were completely free of ICD shocks (P < 0.05 for bilateral vs. left). Bilateral CSD demonstrates long-term benefit in reducing ICD shocks in patients with recurrent VT and cardiomyopathy refractory to medical therapy.