Schnekenberg Luiz, Sedghi Annahita, Schoene Daniela, Pallesen Lars-Peder, Barlinn Jessica, Woitek Felix, Linke Axel, Puetz Volker, Barlinn Kristian, Mangner Norman, Siepmann Timo
Department of Neurology, Faculty of Medicine Carl Gustav Carus, Technische Universität Dresden, 01307 Dresden, Germany.
Dresden Heart Center, Medical Faculty Carl Gustav Carus, Technische Universität Dresden, 01307 Dresden, Germany.
J Cardiovasc Dev Dis. 2023 Jul 12;10(7):297. doi: 10.3390/jcdd10070297.
Cardiac damage has been attributed to SARS-CoV-2-related pathology contributing to increased risk of vascular events. Heart rate variability (HRV) is a parameter of functional neurocardiac integrity with low HRV constituting an independent predictor of cardiovascular mortality. Whether structural cardiac damage translates into neurocardiac dysfunction in patients infected with SARS-CoV-2 remains poorly understood. Hypothesized mechanisms of possible neurocardiac dysfunction in COVID-19 comprise direct systemic neuroinvasion of autonomic control centers, ascending virus propagation along cranial nerves and cardiac autonomic neuropathy. While the relationship between the autonomic nervous system and the cytokine cascade in general has been studied extensively, the interplay between the inflammatory response caused by SARS-CoV-2 and autonomic cardiovascular regulation remains largely unclear. We reviewed the current literature on the potential diagnostic and prognostic value of autonomic neurocardiac function assessment via analysis of HRV including time domain and spectral analysis techniques in patients with COVID-19. Furthermore, we discuss potential therapeutic targets of modulating neurocardiac function in this high-risk population including HRV biofeedback and the impact of long COVID on HRV as well as the approaches of clinical management. These topics might be of particular interest with respect to multimodal pandemic preparedness concepts.
心脏损伤被认为与SARS-CoV-2相关病理有关，从而增加了血管事件的风险。心率变异性（HRV）是功能性神经心脏完整性的一个参数，低HRV是心血管死亡率的独立预测指标。感染SARS-CoV-2的患者心脏结构损伤是否会转化为神经心脏功能障碍仍知之甚少。COVID-19中可能的神经心脏功能障碍的假设机制包括自主控制中心的直接全身神经侵袭、病毒沿颅神经的上行传播和心脏自主神经病变。虽然一般来说自主神经系统与细胞因子级联反应之间的关系已得到广泛研究，但SARS-CoV-2引起的炎症反应与自主心血管调节之间的相互作用仍基本不清楚。我们回顾了当前关于通过分析HRV（包括时域和频谱分析技术）评估COVID-19患者自主神经心脏功能的潜在诊断和预后价值的文献。此外，我们讨论了在这一高风险人群中调节神经心脏功能的潜在治疗靶点，包括HRV生物反馈、长期COVID对HRV的影响以及临床管理方法。就多模式大流行防范概念而言，这些主题可能特别令人感兴趣。
