Effect of Renal Sympathetic Denervation on Ventricular Electrical Activity in Myocardial Infarction

Coronary artery blockage causes myocardial infarction (MI), a frequent and serious cardiovascular disease. The early recurrence of post-MI ventricular fibrillation after defibrillation has been widely investigated and treated. This research investigated the relationship between electrophysiological indicators of early recurrence following defibrillation in post-MI ventricular fibrillation and sympathetic renal denervation's therapeutic benefits and probable causes. Animal models were used for experiments. Electrophysiological indications of early recurrence were reported after MI and defibrillation in ventricular fibrillation patients. After that, a selection of rats received sympathetic renal denervation, and the therapeutic results were compared to the control group. Electrocardiogram monitoring, myocardial histology, and neurotransmitter assays were done. Defibrillation therapy causes an early recurrence in ventricular fibrillation patients. Electrophysiological measures showed increased ST segment elevation and T wave alterations in the early recurrence group. In the sympathetic renal denervation intervention group, early recurrence was greatly decreased and the electrocardiogram (ECG) was more stable and regular. Myocardial histology showed decreased cellular damage and fibrosis in the sympathetic renal denervation group. Sympathetic renal denervation intervention significantly reduced sympathetic nerve activity, according to neurotransmitter measures. Electrophysiological indications of early recurrence following defibrillation in post-MI ventricular fibrillation are linked to sympathetic renal denervation's therapeutic benefits. Myocardial damage and fibrosis may be reduced, ECG features improved, and the early recurrence rate reduced by sympathetic renal denervation. One possible method of sympathetic renal denervation intervention is reduced sympathetic nerve activity.