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.

IntroductionIdiopathic pulmonary arterial hypertension is defined as a group of diseases characterized by a progressive increase in pulmonary vascular resistance that results in right heart failure and premature death. Although therapies exist to improve hemodynamic instability and symptoms, there is no cure for pulmonary arterial hypertension and it remains a life-threatening condition. A recent study performed in China reported, for the first time, the effect of pulmonary arterial denervation on functional capacity and hemodynamics in patients with refractory idiopathic pulmonary arterial hypertension.Case presentationWe report a case of a 60-year-old white Brazilian man, with controlled hypertension and stage 2 obesity who complained of progressive fatigue with moderate to light exertion of approximately 1 year’s duration. During this period, he underwent myocardial perfusion scintigraphy without evidence of obstructive ischemic disease. He had no clinical evidence of systolic heart failure. He had undergone biological mitral valve replacement 3 years previously for mitral valve stenosis and ablation of atrioventricular nodal reentry tachycardia 18 months previously. At the time of valve replacement, he had no reported evidence of pulmonary arterial hypertension. His echocardiogram showed normal function of a mitral prosthesis, normal global left ventricular systolic function (left ventricular ejection fraction 62 % measured using the Teichholz method), stage I diastolic dysfunction, and a mean systolic pulmonary arterial blood pressure of 50 mmHg. In the 6-minute walk test, the patient walked 104 meters. Catheterization of his right heart chambers and pulmonary arteries confirmed the diagnosis of pulmonary hypertension. Electroanatomic reconstruction of the right ventricular outflow tract and pulmonary artery was performed under direct fluoroscopic visualization, and a merger was made with a formatted image of cardiac computed tomography angiography. Then we performed irrigated cardiac catheter ablation of the pulmonary trunk.ConclusionsAt the patient’s 3-month follow-up, he showed improvement in functional class for fatigue on major exertion, increased distance walked in the 6-minute walk test, and reductions in pressure of both the right cavities and the pulmonary artery. Currently, with 6 months of clinical follow-up, the patient has maintained his functional classification and is pedaling his bicycle.

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<p><strong>Background:</strong> The implantation of ICDs left pectorally is the conventional normal practice, but pathological reasons may obly to insert the devices on the right side. The aim of our evaluation was to define the outcome of right-sided implantation (n=52) on defibrillation effectiveness in comparison to the left-sided ICD implantation (n=210).</p><p><strong>Methods: </strong>A cohort of patients received standard therapy for primary or secondary prevention of sudden cardiac death (SCD) in patients with the structural cardiac disease, lay open to the ICD-DR implantation. The 262 individuals who had all the inclusion criteria were comprised in the assessment.</p><p><strong>Results: </strong>The defibrillation threshold testing (DFT), at the end of implantation showed that the mean energy to revert a programmed induced sustained ventricular tachycardia/ventricular fibrillation was 33.4±6.3 J for the patients that had the ICD implanted on the right side, and 23.9±5.3 J for the ones that presented the ICD positioned on the left side, P&lt;0.0001. However the mean and the sum of shock events recorded by ICD during 1 year of monitoring, according to the side of ICD implantation, did not show any difference.</p><p><strong>Conclusion: </strong>Our results show that ICD implantation on the right side caused an elevated DFT in comparison to the left side insertion. This study also reported that there is no difference regarding safety and effectiveness about the amount of appropriate and inappropriate shock therapies, the mean and the sum of shock events recorded by ICD during 1 year of monitoring, according to the side of ICD implantation.</p>