去肾交感神经术对心肌梗死后 心脏保护机制的 研究进展

Research Progress on the Cardioprotective Mechanisms of Renal Denervation after Myocardial Infarction

摘要: 心肌梗死(Myocardial Infarction, MI)是严重威胁人类生命健康的重大心血管疾病。尽管经皮冠状动脉介入治疗(Percutaneous Coronary Intervention, PCI)及现代药物治疗显著改善了心肌梗死患者的预后，但缺血再灌注损伤、心室重构、恶性心律失常及心力衰竭等问题仍是影响远期结局的重要因素。心肌梗死后交感神经系统(Sympathetic Nervous System, SNS)过度激活可促进肾素–血管紧张素–醛固酮系统激活、氧化应激增强、炎症反应放大、心肌细胞凋亡及电重构，进而加重心肌损伤和心室重构。去肾交感神经术(Renal Denervation, RDN)作为一种介入性神经调控策略，可通过消融肾动脉周围交感神经纤维，调节肾交感传入和传出信号，从上游抑制全身交感神经过度激活。近年来，临床前研究及少量早期临床探索提示，去肾交感神经术可能通过抑制交感神经活性、调节肾素–血管紧张素–醛固酮系统、减轻氧化应激和炎症反应、抑制心肌纤维化与细胞凋亡、改善自主神经失衡及降低室性心律失常风险等途径发挥心脏保护作用。本文对去肾交感神经术在心肌梗死后心脏保护中的潜在机制及研究进展进行综述，并讨论其临床转化面临的问题与未来研究方向。

Abstract: Myocardial Infarction (MI) remains a major cardiovascular disease that seriously threatens human health. Although Percutaneous Coronary Intervention (PCI) and contemporary pharmacological therapy have substantially improved patient outcomes, ischemia-reperfusion injury, ventricular remodeling, malignant arrhythmias, and heart failure continue to contribute to adverse long-term prognosis. Excessive activation of the Sympathetic Nervous System (SNS) after myocardial infarction can promote activation of the renin-angiotensin-aldosterone system, increase oxidative stress, amplify inflammatory responses, and induce cardiomyocyte apoptosis and electrical remodeling, thereby exacerbating myocardial injury and ventricular remodeling. Renal Denervation (RDN) is an interventional neuromodulation strategy that ablates sympathetic nerve fibers surrounding the renal arteries and modulates both renal afferent and efferent sympathetic signaling, thereby suppressing excessive systemic sympathetic activation at an upstream level. In recent years, preclinical studies and limited early clinical investigations have suggested that renal denervation may exert cardioprotective effects after myocardial infarction by inhibiting sympathetic overactivity, regulating the renin-angiotensin-aldosterone system, alleviating oxidative stress and inflammation, reducing cardiomyocyte apoptosis and myocardial fibrosis, improving autonomic imbalance, and decreasing the risk of ventricular arrhythmias. This review summarizes the potential cardioprotective mechanisms and research progress of renal denervation after myocardial infarction, and further discusses the current challenges and future directions for its clinical translation.