Background Renal denervation (RDN) can reduce ventricular arrhythmia after acute myocardial infarction (AMI), but the mechanism is not clear. The purpose of this study is to study its mechanism. Methods Thirty-two Sprague–Dawley rats were divided into four groups: control group, AMI group, RDN-1d + AMI group, RDN-2w + AMI group. The AMI model was established 1 day after RDN in the RDN-1d + AMI group and 2 weeks after RDN in the RDN-2w + AMI group. At the same time, 8 normal rats were subjected to AMI modelling (the AMI group). The control group consisted of 8 rats without RDN intervention or AMI modelling. Results The study confirmed that RDN can reduce the occurrence of ventricular tachycardia in AMI rats, reduce renal sympathetic nerve discharge, and inhibit the activity of local sympathetic nerves and cell growth factor (NGF) protein expression in the heart after AMI. In addition, RDN decreased the expression of norepinephrine (NE) and glutamate in the hypothalamus,and NE in cerebrospinal fluid, and increased the expression level of γ aminobutyric acid (GABA) in the hypothalamus after AMI. Conclusion RDN can effectively reduce the occurrence of ventricular arrhythmia after AMI, and its main mechanism may be via the inhibition of central sympathetic nerve discharge.

Objective To explore the blood pressure response to different ablation points of renal denervation (RDN) in patients with resistant hypertension Methods A total of 42 cases with resistant hypertension treated by RDN in our center from 2013 to 2015 were retrospectively analyzed. The patients were divided into two groups according to the different ablation points of RDN: the standard treatment group (spiral ablation from near to proximal, with less than 8 points per artery) and the intensive treatment group (from near to far by spiral ablation, with at least 8 points per artery), with 21 patients in each group. The ablation parameters, including points, impedance, actual wattage, and actual temperature, were recorded intraoperatively. Renal angiography was performed again after RDN. Ambulatory blood pressure (ABP) images were taken for all patients at the baseline and 6 months after operation. Results The mean 24-h blood pressure of the standard treatment group was lower than that of the baseline (24-h systolic blood pressure decreased by 7.4 ± 10.6 mmHg and 24-h diastolic blood pressure decreased by 4.6  ± 6.1 mmHg), and the mean 24-h blood pressure decreased significantly from baseline to 6 months in the intensive treatment group (24–h systolic blood pressure decreased by 27.4 ±  11.4 mmHg, P < 0.0001; 24–h diastolic blood pressure decreased by 10.9 ±  9.6 mmHg, P = 0.005). There was a positive correlation between the decrease of systolic/diastolic 24-hour mean and the number of ablation points used in the procedure. The mean value of systolic and diastolic blood pressure was positively correlated with ablation points at 24-hour (R2 = 0.777 and 0.633 respectively, P < 0.01). There were no adverse events in either group after the operation and during the follow-up. Conclusions RDN could significantly reduce BP in patients with resistant hypertension. Our study showed that the antihypertensive effect appeared to be positively correlated with the number of ablation points.

Background: Renal denervation (RDN) can reduce ventricular arrhythmia after acute myocardial infarction(AMI), but the mechanism is not clear. The purpose of this study is to study its mechanism. Methods: Thirty-two Sprague-Dawley rats were divided into four groups: control group, AMI group, RDN-1d+AMI group, RDN-2w+AMI group. The AMI model was established 1 day after RDN in the RDN-1d+AMI group and 2 weeks after RDN in the RDN-2w+AMI group. At the same time, 8 normal rats were subjected to AMI modelling (the AMI group). The control group consisted of 8 rats without RDN intervention or AMI modelling. Results：The study confirmed that RDN can reduce the occurrence of ventricular tachycardia in AMI rats, reduce renal sympathetic nerve discharge, and inhibit the activity of local sympathetic nerves and cell growth factor (NGF) protein expression in the heart after AMI. In addition, RDN decreased the expression of norepinephrine (NE) and glutamate in the hypothalamus ,and NE in cerebrospinal fluid, and increased the expression level of γ -aminobutyric acid (GABA) in the hypothalamus after AMI. Conclusion: RDN can effectively reduce the occurrence of ventricular arrhythmia after AMI, and its main mechanism may be via the inhibition of central sympathetic nerve discharge.