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Persistent Proarrhythmic Neural Remodeling Despite Recovery From Premature Ventricular Contraction-Induced Cardiomyopathy.

持续性致心律失常性神经重构尽管由室性早搏诱发的心肌病恢复。

  • 影响因子:6.43
  • DOI:10.1016/j.jacc.2019.10.046
  • 作者列表:"Tan AY","Elharrif K","Cardona-Guarache R","Mankad P","Ayers O","Joslyn M","Das A","Kaszala K","Lin SF","Ellenbogen KA","Minisi AJ","Huizar JF
  • 发表时间:2020-01-07
Abstract

BACKGROUND:The presence and significance of neural remodeling in premature ventricular contraction-induced cardiomyopathy (PVC-CM) remain unknown. OBJECTIVES:This study aimed to characterize cardiac sympathovagal balance and proarrhythmia in a canine model of PVC-CM. METHODS:In 12 canines, the investigators implanted epicardial pacemakers and radiotelemetry units to record cardiac rhythm and nerve activity (NA) from the left stellate ganglion (SNA), left cardiac vagus (VNA), and arterial blood pressure. Bigeminal PVCs (200 ms coupling) were applied for 12 weeks to induce PVC-CM in 7 animals then disabled for 4 weeks to allow complete recovery of left ventricular ejection fraction (LVEF), versus 5 sham controls. RESULTS:After 12 weeks of PVCs, LVEF (p = 0.006) and dP/dT (p = 0.007) decreased. Resting SNA (p = 0.002) and VNA (p = 0.04), exercise SNA (p = 0.01), SNA response to evoked PVCs (p = 0.005), heart rate (HR) at rest (p = 0.003), and exercise (p < 0.04) increased, whereas HR variability (HRV) decreased (p = 0.009). There was increased spontaneous atrial (p = 0.02) and ventricular arrhythmias (p = 0.03) in PVC-CM. Increased SNA preceded both atrial (p = 0.0003) and ventricular (p = 0.009) arrhythmia onset. Clonidine suppressed SNA and abolished all arrhythmias. After disabling PVC for 4 weeks, LVEF (p = 0.01), dP/dT (p = 0.047), and resting VNA (p = 0.03) recovered to baseline levels. However, SNA, resting HR, HRV, and atrial (p = 0.03) and ventricular (p = 0.03) proarrhythmia persisted. There was sympathetic hyperinnervation in stellate ganglia (p = 0.02) but not ventricles (p = 0.2) of PVC-CM and recovered animals versus sham controls. CONCLUSIONS:Neural remodeling in PVC-CM is characterized by extracardiac sympathetic hyperinnervation and sympathetic neural hyperactivity that persists despite normalization of LVEF. The altered cardiac sympathovagal balance is an important trigger and substrate for atrial and ventricular proarrhythmia.

摘要

背景: 室性期前收缩诱导的心肌病 (pvc-二1212) 中神经重构的存在和意义仍然未知。 目的: 本研究旨在描述犬PVC二1212模型的心脏交感迷走神经平衡和心律失常。 方法: 在12只犬中,研究人员植入心外膜起搏器和无线电遥测装置,记录左星状神经节 (SNA) 、左心迷走神经 (VNA) 和动脉血压的心律和神经活动。与5个假对照相比,在7只动物中应用双嵌合PVCs (200 ms偶联) 12周以诱导pvc-二1212,然后禁用4周以允许左心室射血分数 (LVEF) 的完全恢复。 成果: PVCs术后12周,LVEF (p = 0.006) 和dP/dT (p = 0.007) 降低。静息SNA (p = 0.002) 和VNA (p = 0.04) 、运动SNA (p = 0.01) 、SNA对诱发PVCs的反应 (p = 0.005) 、静息时心率 (HR) (p = 0.003) 和运动 (p < 0.04) 增加,而心率变异性 (HRV) 降低(p = 0.009)。PVC二1212组自发性心房 (p = 0.02) 和室性心律失常 (p = 0.03) 增加。SNA增加先于心房 (p = 0.0003) 和心室 (p = 0.009) 心律失常发作。可乐定抑制SNA并消除所有心律失常。禁用PVC 4周后,LVEF (p = 0.01) 、dP/dT (p = 0.047) 和静息VNA (p = 0.03) 恢复至基线水平。然而,SNA、静息心率、HRV和心房 (p = 0.03) 和心室 (p = 0.03) 前心律失常持续存在。与假对照相比,pvc-二1212和康复动物的星状神经节 (p = 0.02) 中存在交感神经过度支配,但心室中不存在 (p = 0.2)。 结论: PVC二1212的神经重塑以心外交感神经过度支配和交感神经过度活跃为特征,尽管LVEF正常化,但仍持续存在。改变的心脏交感迷走神经平衡是心房和室性心律失常的重要触发和底物。

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心律失常方向

心律失常(arrhythmia)是由于窦房结激动异常或激动产生于窦房结以外,激动的传导缓慢、阻滞或经异常通道传导,即心脏活动的起源和(或)传导障碍导致心脏搏动的频率和(或)节律异常。心律失常是心血管疾病中重要的一组疾病,可单独发病,亦可与其他心血管病伴发。其预后与心律失常的病因、诱因、演变趋势、是否导致严重血流动力障碍有关,可突然发作而致猝死,亦可持续累及心脏而致其衰竭。

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