Mechanisms of renal sympathetic denervation on improving ventricular arrhythmias after acute myocardial infarction in rats

Background: More than 50% of acute myocardial infarction (MI) survivors died from malignant ventricular arrhythmias (VA). Renal sympathetic denervation (RSD) has been demonstrated to exert remarkable effects on VA, but the mechanism remains unclear. Methods: Thirty Sprague Dawley rats were divided into three groups randomly, that is Sham, MI (ligation of left anterior descending artery) and MI+RSD (ethanol ablation). Six hours after modeling, electrocardiogram was recorded. Four weeks later, the left ventricular function indexes were obtained through echocardiography, and cardiac tissues were stained by Masson trichrome for fibrotic analysis. Whole-cell patch-clamp recordings were performed to record the transient outward K+ current (I-to) and the protein expression of Kv4.2 and Kv4.3 in the left ventricle were detected using Western blot. Results: Compared to that in MI group, RSD group showed reduced incidence of premature ventricular contractions and ventricular tachycardia, increased left ventricular ejection fraction and fractional shortening, and decreased left ventricular end diastolic diameter and left ventricular end systolic diameter. RSD attenuated collagen deposition in the cardiac tissue. RSD group alleviated prolonged action potential duration (p < 0.05) especially APD(20). The I-to current density was significantly decreased in the MI group compared to the sham group, and was reversed by RSD. MI-induced a decreased cardiac protein expression of Kv4.2, but not that of Kv4.3, and it was restored by RSD. Conclusions: RSD reduced the incidence of VA after MI in rats. This may be due to the improvement of left ventricular function, the recovery of cardiac I-to density and Kv4.2 protein expression.