PVI + RSD is a safe treatment that is superior to PVI alone for treatment of paroxysmal AF in CKD patients.
BackgroundAtrial fibrillation (AF) commonly occurs in association with chronic kidney disease (CKD), resulting in adverse outcomes. Combining pulmonary vein isolation (PVI) and renal sympathetic denervation (RSD) may reduce the recurrence of AF in patients with CKD and hypertension. We considered that RSD could reduce the recurrence of AF in patients with CKD by modulating sympathetic hyperactivity. Our goal was to compare the impact of PVI + RSD with that of PVI alone in patients with concurrent AF and CKD.MethodsThis was a single-center, prospective, longitudinal, randomized, double-blind study. Forty-five patients with controlled hypertension, symptomatic paroxysmal AF and/or persistent AF, stage 2 or 3 CKD, and a dual-chamber pacemaker were enrolled from January 2014 to January 2015. We assessed the 30-second recurrence of AF recorded by the pacemaker, 24-hour ambulatory blood pressure measurements, estimated glomerular filtration rate, albuminuria, echocardiographic parameters, and safety of RSD.ResultsNo patient developed procedural or other complications. The ambulatory blood pressure measurements did not differ within the PVI + RSD group or between the PVI + RSD and PVI groups throughout the study. Significantly more patients in the PVI + RSD group than in the PVI group were free of AF at the 12-month follow-up evaluation. The PVI group had an unacceptable response to ablation with respect to changes in echocardiographic parameters, whereas these parameters improved in the PVI + RSD group.ConclusionPVI + RSD were associated with a lower AF recurrence rate than PVI alone; it also improved renal function and some echocardiographic parameters. These encouraging data will serve as baseline information for further long-term studies on larger patient populations.
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.
Premature ventricular complexes 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, Armaganijan et al reported the relevance of sympathetic activation in patients with ventricular arrhythmias and suggested a potential role for catheter-based renal sympathetic denervation in reducing the arrhythmic burden.In this report, we describe a 32-year-old hypertensive male patient presenting with a high incidence of polymorphic premature ventricular complexes on a 24 hour Holter monitor. Beginning 1 year prior, the patient experienced episodes of presyncope, syncope, and tachycardia palpitations. The patient was taking losartan 100 mg/day, which kept his blood pressure (BP) under control, and sotalol 160 mg twice daily. Bisoprolol 10 mg/day was used previously but was not successful for controlling the episodes. The 24 hour Holter performed after the onset of sotalol 160 mg twice daily showed a heart rate ranging between 48 (minimum)–78 (average)–119 (maximum) bpm; 14,286 polymorphic premature ventricular complexes; 3 episodes of nonsustained ventricular tachycardia, the largest composed of 4 beats at a rate of 197 bpm; and 14 isolated atrial ectopic beats. Cardiac magnetic resonance imaging with gadolinium perfusion performed at rest and under pharmacological stress with dipyridamole showed increased left atrial internal volume, preserved systolic global biventricular function, and an absence of infarcted or ischemic areas. The patient underwent bilateral renal sympathetic denervation.The only drug used postprocedure was losartan 25 mg/day. Three months after the patient underwent renal sympathetic denervation, the mean BP value dropped to 132/86 mmHg, the mean systolic/diastolic 24 hour ambulatory BP measurement was reduced to 128/83 mmHg, and the 24 hour Holter monitor showed a heart rate ranging between 51 (minimum)–67 (average)–108 (maximum) bpm, 854 polymorphic premature ventricular complexes, and no episodes of nonsustained ventricular tachycardia.
Chronic kidney disease (CKD) patients on stage 4 present greater risk rates for malignant ventricular arrhythmia events. This study examined patients with CKD in stages 1, 2, 3 and 4, left ventricular dysfunction and automatic implantable cardioverter-defibrillator (ICD). Our goal was to record the appropriate therapies, “Anti-tachycardia Therapy Pacing” (ATP) and shock events during the 18 months of follow-up and compare the incidence and severity of these at different stages of CKD, mainly in patients with CKD stage 4 underwent renal sympathetic denervation (RSD) guided by renal nerve stimulation (RNS). One hundred and fifteen patients were evaluated once every three months till 18 months of follow-up. The arrhythmic events were assessed at each follow-up visit. Comparing the groups, we can see the number of ATP and shock events recorded by ICD during 18 months of follow-up, and differences in the number of therapeutic events between the various stages of CKD. The hazard ratio (HR), 95% confidence interval (CI) and P value for ATP and shock events between all the CKD stages were evaluated by the log-rank/Mantel-Haenszel test. At the 18th month of follow-up, 75% of patients with CKD stage 4 received ATP, and 70% were treated with shock while only 20% of the subjects with CKD stage 4 that were submitted to RSD received ATP and 20% were treated with shock, P<0.0001 and P=0.0002, respectively. In our study, a decline occurred in the incidence of arrhythmias, and therefore, appropriate ICD therapies in advanced stages of CKD, reducing the risk rates for these events in patients with CKD on stage 4 after RSD guided by RNS in comparison to the other CKD stages. Our results suggest that RSD can control the higher incidence of malignant arrhythmias in advanced CKD stages.
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