Objectives: Spinal cord injury (SCI) often results in severe dysfunction of the autonomic nervous system. C1-C8 SCI affects the supraspinal control to the heart, T1-T5 SCI affects the spinal sympathetic outflow to the heart, and T6-T12 SCI leaves sympathetic control to the heart intact. Heart rate variability (HRV) analysis can serve as a surrogate measure of autonomic regulation. The aim of this study was to investigate changes in HRV patterns and alterations in patients with acute traumatic SCI. Methods: As soon as possible after SCI patients who met the inclusion criteria had 24 h Holter monitoring of their cardiac rhythm, additional Holter monitoring were performed 1, 2, 3 and 4 weeks after SCI. Results: Fifty SCI patients were included. A significant increase in standard deviation of the average normal-to-normal (SDANN) sinus intervals was seen in the first month after injury (P = 0.008). The increase was only significant in C1-T5 incomplete patients and in patients who did not experience one or more episodes of cardiac arrest. Significant lower values of Low Frequency Power, Total Power and the Low Frequency over High Frequency ratio were seen in the C1-T5 SCI patients compared with T6-T12 SCI patients. Conclusions: The rise in SDANN in the incomplete C1-T5 patients could be due to spontaneous functional recovery caused by synaptic plasticity or remodelling of damaged axons. That the autonomic nervous system function differs between C1-C8, T1-T5 and T6-T12 patients suggest that the sympathovagal balance in both the C1-C8 and T1-T5 SCI patients has yet to be reached. INTRODUCTIONSpinal cord injury (SCI) patients with tetraplegia and high level paraplegia are known to suffer from dysfunction of the autonomic nervous system (ANS) including the autonomic regulation of the heart. 1 The severity and the neurological level of the SCI have major impact on ANS function. 2 Patients with SCI above T1 often have intact efferent vagal and sympathetic neural pathways innervating the heart. However, they are deprived of the supraspinal control causing reduced sympathetic activity below the level of SCI. Furthermore, the loss of supraspinal control causes morphological changes in sympathetic preganglionic neurons and peripheral alpha-adrenoceptor hyperresponsiveness. 1 Patients with T1-T5 SCI lose cardiac sympathetic preganglionic neurons as the injury occurs corresponding to the sympathetic outflow to the heart, and likewise the postganglionic sympathetic innervation to the heart undergoes plastic changes. 3 Individuals with SCI at T6 and below have intact cardiac spinal sympathetic neurons and intact innervation of the heart.In tetraplegic individuals with complete lesions, the disconnection of the spinal sympathetic neurons from cerebral control represents a unique possibility for analysis of the sympathetic influence on the heart rate (HR) variability (HRV).
Objective: Cardiovascular complications including cardiac arrest and arrhythmias remain a clinical challenge in the management of acute traumatic spinal cord injury (SCI). Still, there is a lack of knowledge regarding the characteristics of arrhythmias in patients with acute traumatic SCI. The aim of this prospective observational study was to investigate the occurrence of cardiac arrhythmias and cardiac arrests in patients with acute traumatic SCI. Methods: As early as possible after SCI 24-hour Holter monitoring was performed. Additional Holter recordings were performed 1, 2, 3, and 4 weeks after SCI. Furthermore, 12-lead electrocardiograms (ECGs) were obtained shortly after SCI and at 4 weeks. Results: Thirty patients were included. Bradycardia (heart rate (HR) <50 b.p.m.) was present in 17-35% of the patients with cervical (C1-C8) SCI (n = 24) within the first 14 days. In the following 14 days, the occurrence was 22-32%. Bradycardia in the thoracic (Th1-Th12) SCI group (n = 6) was present in 17-33% during the observation period. The differences between the two groups were not statistically significant. The mean minimum HR was significantly lower in the cervical group compared with the thoracic group both on 12-lead ECGs obtained shortly after SCI (P = 0.030) and at 4 weeks (P = 0.041). Conclusion: Many patients with cervical SCI experience arrhythmias such as bradycardia, sinus node arrest, supraventricular tachycardia, and more rarely cardiac arrest the first month after SCI. Apart from sinus node arrests and limited bradycardia, no arrhythmias were seen in patients with thoracic SCI. Standard 12-lead ECGs will often miss the high prevalence these arrhythmias have.
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