Key result
Renal denervation performed 1 day before acute myocardial infarction significantly reduced the number of ventricular tachycardia events compared to the AMI control group (112 vs 331.2, P<0.001).
Why the study?
Renal denervation can reduce ventricular arrhythmia after acute myocardial infarction, but the underlying mechanism remains unclear.
Does renal denervation reduce ventricular arrhythmia in a rat model of acute myocardial infarction?
Does renal denervation reduce ventricular arrhythmia in a rat model of acute myocardial infarction?
Absolute Event Rate: 112% vs 331.2%
p-value: p=<0.001
Renal denervation reduces ventricular arrhythmias after acute myocardial infarction in rats by inhibiting central sympathetic nerve discharge.
RDN may suppress post-AMI arrhythmias via central sympathetic inhibition in rats; leaves open translation to human practice.
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.
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Ye et al. (2022) studied Acute myocardial infarction and ventricular arrhythmia (n=32). Renal denervation vs. Acute myocardial infarction without renal denervation was evaluated on Number of ventricular tachycardia events over 1 hour (p=<0.001). Renal denervation performed 1 day before acute myocardial infarction significantly reduced the number of ventricular tachycardia events compared to the AMI control group (112 vs 331.2, P<0.001).
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