Persistent Proarrhythmic Neural Remodeling Despite Recovery From Premature Ventricular Contraction-Induced Cardiomyopathy,Journal of the American College of Cardiology

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Persistent Proarrhythmic Neural Remodeling Despite Recovery From Premature Ventricular Contraction-Induced Cardiomyopathy
Journal of the American College of Cardiology ( IF 21.7 ) Pub Date : 2020-01-01 , DOI: 10.1016/j.jacc.2019.10.046
Alex Y Tan ₁ , Khalid Elharrif ₁ , Ricardo Cardona-Guarache ₁ , Pranav Mankad ₁ , Owen Ayers ₂ , Martha Joslyn ₂ , Anindita Das ₃ , Karoly Kaszala ₁ , Shien-Fong Lin ₄ , Kenneth A Ellenbogen ₁ , Anthony J Minisi ₁ , Jose F Huizar ₁

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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.

中文翻译：

尽管从室性早搏诱发的心肌病中恢复，但持续的促心律失常神经重塑

背景神经重塑在室性早搏诱发的心肌病（PVC-CM）中的存在和意义仍然未知。目的本研究旨在表征 PVC-CM 犬模型中心脏交感神经平衡和致心律失常的特征。方法研究人员在 12 只犬科动物中植入心外膜起搏器和无线电遥测装置，以记录心律和左星状神经节 (SNA)、左心迷走神经 (VNA) 的神经活动 (NA) 和动脉血压。在 7 只动物中应用二联 PVC（200 ms 耦合）12 周来诱导 PVC-CM，然后禁用 4 周，以使左心室射血分数 (LVEF) 完全恢复，而 5 只假手术对照。结果 PVC 治疗 12 周后，LVEF (p = 0.006) 和 dP/dT (p = 0.007) 下降。静息 SNA (p = 0.002) 和 VNA (p = 0.04)、运动 SNA (p = 0.01)、SNA 对诱发 PVC 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) 减少 (p = 0.009)。PVC-CM 中自发性房性心律失常 (p = 0.02) 和室性心律失常 (p = 0.03) 增加。SNA 增加先于房性 (p = 0.0003) 和室性 (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 HR、HRV 以及心房 (p = 0.03) 和心室 (p = 0.03) 致心律失常持续存在。与假手术对照组相比，PVC-CM 和康复动物的星状神经节（p = 0.02）存在交感神经支配过度，但心室（p = 0.2）则不然。结论 PVC-CM 的神经重塑的特点是心外交感神经过度神经支配和交感神经过度活跃，尽管 LVEF 正常化，但这种情况仍然存在。心脏交感神经平衡的改变是房性和室性心律失常的重要触发因素和基础。

更新日期：2020-01-01

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