The addition of renal sympathetic denervation to pulmonary vein isolation reduces recurrence of paroxysmal atrial fibrillation in chronic kidney disease patients.

BACKGROUND: Atrial fibrillation (AF) frequently complicates chronic kidney disease (CKD). AF treatment is challenging and requires complete pulmonary vein isolation (PVI). Recently, renal sympathetic denervation (RSD) has been reported to reduce AF recurrence when performed alongside PVI. METHODS: A prospective therapeutic study of patients with controlled hypertension and paroxysmal AF was undertaken. Renal function was evaluated using estimated glomerular filtration rate. Outcomes for patients with normal renal function who underwent PVI (n = 101) were compared with those for CKD patients who underwent either PVI alone (n = 96) or PVI + RSD (n = 39). The primary endpoint was recurrence of AF recorded by 24-h Holter monitoring. RESULTS: During the 22.4 ± 12.1 months following intervention, the incidence of AF recurrence was higher in CKD patients treated with PVI alone (61.5 %) than in CKD patients treated with PVI + RSD (38.5 %; HR 1.86, 95 % CI 1.14-3.03, P = 0.0251) or patients without CKD subjected to PVI (35.6 %; hazard ratio (HR) 2.27, 95 % confidence interval (CI) 1.51-3.42, P < 0.0001). In particular, the addition of RSD to PVI significantly reduced AF recurrence in CKD stage 4, but not stage 2 or 3, patients. Ambulatory blood pressure and mean heart rate were not different between groups or time points. No complications of either procedure were observed. CONCLUSIONS: PVI + RSD is a safe treatment that is superior to PVI alone for treatment of paroxysmal AF in CKD patients.

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

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 < 0.0001 to all the comparisons between the mean of each time point with the mean of every other time point. No changes in mean 24-h ABPM and renal function in both groups were observed at 12th month of follow-up. However, 24-h Holter mean heart rate decreased in control group at 12th month of follow-up, which did not happen with the RSD group. At the sixth month post-RSD in comparison to baseline, a significant reduction in the number of polymorphic PVCs (∆ = -34,817 ± 3590, P < 0.0001) was observed, as well as, in CRM parameters such as left ventricular mass/body surface area (∆ = -5.4 ± 2.1 g/m2, P < 0.0001) and left ventricular ejection fraction (∆ = +3.0 ± 1.8 %, P < 0.0001). In comparison to control group at the same time point, these findings were statistically superior in RSD group (P > 0.05). A significant correlation was found between the Δ number of polymorphic PVCs at the sixth month (r = -0.6723, P = 0.0012) after the RSD and the total number of RSD ablated spots. CONCLUSIONS: Polymorphic PVCs refractory to medication therapy may be modifiable by RSD in patients without structural heart disease. Although encouraging, our data are preliminary and need to be validated in a large population and in long term.