Proof of concept study: renal sympathetic denervation for treatment of polymorphic premature ventricular complexes

• Published in: Journal of interventional cardiac electrophysiology 2016-11, Vol.47 (2), p.221-229
• Main Authors: Kiuchi, Márcio Galindo, e Silva, Gustavo Ramalho, Paz, Luis Marcelo Rodrigues, Chen, Shaojie, Souto, Gladyston Luiz Lima
• Format: Article
• Language: English
• Subjects: Anti-Arrhythmia Agents - therapeutic use; Cardiology; Feasibility Studies; Female; Humans; Kidney - innervation; Kidney - surgery; Male; Medicine; Medicine & Public Health; Middle Aged; Pilot Projects; Sympathectomy - methods; Treatment Outcome; Ventricular Premature Complexes - diagnosis; Ventricular Premature Complexes - therapy
• ISSN: 1383-875X; 1572-8595
• DOI: 10.1007/s10840-016-0146-1

Background or Purpose Polymorphic premature ventricular complexes (PVCs) are very common, appearing most frequently in patients with hypertension, obesity, sleep apnea, and structural heart disease. Sympathetic hyperactivity plays a critical role in the development, maintenance, and aggravation of ventricular arrhythmias. Recently, the relevance of sympathetic activation in patients with ventricular arrhythmias was reported, and this finding suggested a potential role for catheter-based renal sympathetic denervation in reducing the arrhythmic burden. Methods We evaluated the effectiveness of the renal sympathetic denervation (RSD) in comparison to antiarrhythmic pharmacologic therapy in reducing polymorphic PVCs refractory to medication therapy and cardiac parameters assessed by 24-h Holter monitoring and cardiac magnetic resonance (CRM), respectively, in patients with structurally normal heart. Results Thirty-four patients were included in this study, 14 served as control, and 20 were treated with an ablation cardiac catheter with open irrigated tip. RSD was performed by a single operator following the standard technique. All the patients included had polymorphic PVCs and structurally normal heart. Data were obtained at baseline at the 12th month of follow-up (sixth month after RSD or adjustment of antiarrhythmic dosage). In RSD group, we observed a significant decrease in the number of polymorphic PVCs from baseline 36,091 ± 3327 to 3, 6, 7 (first month after RSD, without drugs), and 12 months (sixth month after RSD, without drugs) of follow-up, 31,009 ± 3251, 20,411 ± 3820, 7701 ± 1549, and 1274 ± 749, respectively, in all patients, P