High-level spinal cord injury (SCI) can disrupt cardiovascular autonomic function. However, the evolution of cardiovascular autonomic function in the acute phase following injury is unknown. We evaluated the timing, severity, progression, and implications of cardiovascular autonomic injury following acute SCI. We tested 63 individuals with acute traumatic SCI (aged 48 ± 2 years) at five time-points: <2 weeks, and 1, 3, 6–12, and >12 months post-injury. Supine beat-to-beat systolic arterial pressure (SAP) and R-R interval (RRI) were recorded and low-frequency variability (LF SAP and LF RRI) determined. Cross-spectral analyses were used to determine baroreflex function (low frequency) and cardiorespiratory interactions (high frequency). Known electrocardiographic (ECG) markers for arrhythmia and self-reported symptoms of cardiovascular dysfunction were determined. Comparisons were made with historical data from individuals with chronic SCI and able-bodied controls. Most individuals had high-level (74%) motor/sensory incomplete (63%) lesions. All participants had decreased LF SAP at <2 weeks (2.22 ± 0.65 mm Hg²). Autonomic injury was defined as high-level SCI with LF SAP <2 mm Hg². Two distinct groups emerged by 1 month: autonomically complete SCI with sustained low LF SAP (0.76 ± 0.17 mm Hg²) and autonomically incomplete SCI with increased LF SAP (5.46 ± 1.0 mm Hg², p < 0.05). Autonomically complete injuries did not recover over time. Cardiovascular symptoms were prevalent and worsened with time, especially in those with autonomically complete lesions, and chronic SCI. Baroreflex function and cardiorespiratory interactions were impaired after SCI. Risk of arrhythmia increased immediately after SCI, and remained elevated throughout the acute phase. Acute SCI is associated with severe cardiovascular dysfunction. LF SAP provides a simple, non-invasive, translatable, quantitative assessment of autonomic function, and is most informative 1 month after injury.

中文翻译：

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脊髓损伤急性期自主神经功能的纵向评估：使用低频血压变异性作为自主神经功能的定量测量

高水平脊髓损伤 (SCI) 会破坏心血管自主神经功能。然而，损伤后急性期心血管自主神经功能的演变尚不清楚。我们评估了急性 SCI 后心血管自主神经损伤的时间、严重程度、进展和影响。我们在五个时间点测试了 63 名患有急性创伤性 SCI（年龄 48 ± 2 岁）的个体：<2 周，以及受伤后 1、3、6-12 和 >12 个月。记录仰卧逐次收缩动脉压 (SAP) 和 RR 间期 (RRI)，并确定低频变异性（LF SAP 和 LF RRI）。交叉光谱分析用于确定压力反射功能（低频）和心肺相互作用（高频）。确定已知的心律失常心电图 (ECG) 标志物和自我报告的心血管功能障碍症状。与来自慢性 SCI 和健全对照者的历史数据进行了比较。大多数人有高水平 (74%) 运动/感觉不完全 (63%) 病变。所有参与者的 LF SAP 在 <2 周（2.22 ± 0.65 mm Hg²）。自主神经损伤被定义为LF SAP <2 mm Hg ²的高水平SCI 。1 个月后出现了两个不同的组：具有持续低 LF SAP (0.76 ± 0.17 mm Hg ² ) 的自主神经完全 SCI 和具有增加的 LF SAP (5.46 ± 1.0 mm Hg ² , p < 0.05)。随着时间的推移，自主神经完全损伤没有恢复。心血管症状普遍存在并随着时间的推移而恶化，尤其是在具有自主神经完全病变和慢性 SCI 的患者中。SCI 后压力反射功能和心肺相互作用受损。脊髓损伤后心律失常的风险立即增加，并在整个急性期保持升高。急性 SCI 与严重的心血管功能障碍有关。LF SAP 提供了一种简单的、非侵入性的、可翻译的、对自主神经功能的定量评估，并且在受伤后 1 个月提供的信息最多。