Renal sympathetic denervation guided by renal nerve stimulation to treat ventricular arrhythmia in CKD patients with ICD.

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.

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.

Registro de arritmias em pacientes com marcapassos e doença renal crônica de leve a moderada (RYCKE): resultados de um estudo de coorte observacional / Register of arrhythmias in patients with pacemakers and mild to moderate chronic kidney disease (RYCKE): results from an observational cohort study

O presente estudo examinou pacientes submetidos a implante de marcapasso dupla-câmara em decorrência de doença do nó sinusal ou bloqueio atrioventricular de 3o ou 2o graus do tipo 2 na doençarenal crônica em estágios 2, 3 e 4. O estudo teve como objetivo registrar os eventos arrítmicos durante 12 mesesde acompanhamento e comparar a incidência e a gravidade deles nas diferentes fases da doença renal crônica.Método: No total, 305 pacientes foram avaliados a cada 4 meses até 12 meses de acompanhamento. Os eventosarrítmicos foram avaliados em cada visita de acompanhamento. Resultados: Dentro do mesmo grupo de estágio da doença renal crônica não houve diferença entre as causas doença do nó sinusal e bloqueio atrioventricular, a respeito da ocorrência de qualquer arritmia. No entanto, menor incidência de taquicardia atrial/fibrilação atrial foi observada para todas as comparações entre todos os pacientes e os mesmos subgrupos em pacientes no estágio 2 (total: 58%; doença do nó sinusal: 63%; bloqueio atrioventricular: 51%), comparativamente aos estágios 3 (total:87%, P < 0,0001; doença do nó sinusal: 89%, P = 0,0020; bloqueio atrioventricular: 84%, P = 0,0019) e 4 (total: 85%, P < 0,0001; doença do nó sinusal: 81%, P = 0,0409; bloqueio atrioventricular: 90%, P < 0,0001). Em relação à taquicardia ventricular não sustentada/taquicardia ventricular sustentada, foi observada incidência mais elevada para todas as comparações entre todos os pacientes e os mesmos subgrupos em pacientes no estágio 4 (total: 32%; doença do nó sinusal: 16%; bloqueio atrioventricular: 16%), comparativamente aos estágios 3 (total: 11%, P = 0,0007; doença do nó sinusal: 9%, P = 0,0110; bloqueio atrioventricular: 14%, P = 0,0441) e 2 (total: 3%, P < 0,0001; doença do nó sinusal: 3%, P < 0,0001; bloqueio atrioventricular: 4%, P < 0,0001). Conclusão: Nossos resultados sugerem que quanto mais avançado o estágio da doença renal crônica maior a incidência de arritmias malignas...

The present study evaluated patients who had received a dual chamber pacemaker implant due to sinus node disease or 3rd/2nd degree type 2 atrioventricular block in chronic kidney disease stages 2, 3 and 4. The study was aimed at registering arrhythmic events for 12 months of follow-up and comparing their incidence and severity in different stages of chronic kidney disease. Method: Three hundred and five patients were evaluated every 4 months up to 12 months of follow-up. Arrhythmic events were assessed at each follow-up visit. Results: Within the same chronic kidney disease stage group there was no difference between the causes ofsinus node disease and atrioventricular block for the occurrence of any arrhythmia. However, a lower incidence of atrial fibrillation/tachycardia was observed for all comparisons among all patients and the same subgroups in stage 2 patients (total: 58%; sinus node disease: 63%; atrioventricular block: 51%) compared to stages 3 (total: 87%,P < 0.0001; sinus node disease: 89%, P = 0.0020; atrioventricular block: 84%, P = 0.0019) and 4 (total: 85%,P < 0.0001; sinus node disease: 81%, P = 0.0409; atrioventricular block: 90%, P < 0.0001). Regarding nonsustained/ sustained ventricular tachycardia, a higher incidence was observed for all comparisons among all patients and the same subgroups in stage 4 patients (total: 32%; sinus node disease: 16%; atrioventricular block: 16%) compared to stages 3 (total: 11%, P = 0.0007; sinus node disease: 9%, P = 0.0110; atrioventricular block: 14%, P = 0.0441) and 2 (total: 3%, P < 0.0001; sinus node disease: 3%, P < 0.0001; atrioventricular block: 4%,P < 0.0001). Conclusion: Our findings suggest that the more advanced the stage of chronic kidney disease, thegreater the incidence of malignant arrhythmias...

A Case Report of Renal Sympathetic Denervation for the Treatment of Polymorphic Ventricular Premature Complexes: Expanding Horizons.

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.

Pulmonary artery ablation to treat pulmonary arterial hypertension: a case report.

INTRODUCTION: Idiopathic 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 PRESENTATION: We 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. CONCLUSIONS: At 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.