Abstract
Ventricular arrhythmias (VAs) are the leading cause of sudden cardiac death in patients with myocardial infarction (MI). We sought to compare effects of renal denervation (RDN) and metoprolol on VAs after MI. Fifty-four male Sprague-Dawley rats underwent ligation of left anterior descending coronary artery to induce MI, while 6 rats served as Control. Metoprolol was given 20 mg/kg/day for 5 weeks after MI surgery. RDN/Sham-RDN procedure was performed at 1 week after MI. At 5 weeks after MI, electrical programmed stimulation (EPS) was performed in all groups for evaluation of VAs. After EPS, heart and kidneys were harvested. Compared with MI group, RDN and metoprolol significantly decreased the incidence of VAs, and RDN is superior to metoprolol. Compared with metoprolol group, Masson staining showed that RDN significantly reduced the myocardial fibrosis. Both RDN and metoprolol decreased the protein expression of connexin43 (Cx43) compared with MI group, while only RDN lighted this decrease remarkably. Immunohistochemical staining of Tyrosine hydroxylase (TH) and growth associated protein 43 (GAP43) revealed that RDN and metoprolol had similar effect on reducing densities of sympathetic nerve in infarction border zone. According to this study, RDN is more effective in reducing VAs than metoprolol in ischemic cardiomyopathy model.
Highlights
According to World Health Organization statistics, Myocardial infarction (MI) is the leading cause of death in human[1]
At 1 week post-myocardial infarction (MI), echocardiography revealed that MI significantly decreased left ventricular ejection fraction (LVEF MI 44.77 ± 3.66% vs. Control 67.80 ± 1.14%, P = 0.0012) and left ventricular fractional shortening (LVFS MI 24.08 ± 1.24% vs. Control 38.96 ± 0.92%, P < 0.0001) compared with control group (Fig. 1)
We found that Renal denervation (RDN) is superior to metoprolol in reducing cardiac fibrosis[12,30], which may explain the lower incidence of ventricular arrhythmias (VAs)
Summary
According to World Health Organization statistics, Myocardial infarction (MI) is the leading cause of death in human[1]. Sympathetic nerve remodeling[6,7] refers to a series of pathophysiological changes after MI, including myocardial denervation, nerve sprouting, sympathetic over-regeneration and high domination, developing into electrophysiological heterogeneity. This may form the basis for increased susceptibility of VAs in rats with ischemic cardiomyopathy[8]. Several clinical studies have shown that RDN can reduce the incidence of arrhythmias[14], including ventricular electrical storm[15], atrial fibrillation[16] and other types of arrhythmias[17]. We established MI model to investigate the effect and mechanism of RDN on VAs after MI and compared with metoprolol
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