Enhancing SCI Care: Using Wearable Technologies for Physical Activity, Sleep, and Cardiovascular Health.

Wearable devices have the potential to advance healthcare by enabling real-time monitoring of biobehavioral data and facilitating the management of an individual's health conditions. Individuals living with spinal cord injury (SCI) have impaired motor function, which results in deconditioning and worsening cardiovascular health outcomes. Wearable devices may promote physical activity and allow the monitoring of secondary complications associated with SCI, potentially improving motor function, sleep, and cardiovascular health. However, several challenges remain to optimize the application of wearable technologies within this population. One is striking a balance between research-grade and consumer-grade devices in terms of cost, accessibility, and validity. Additionally, limited literature supports the validity and use of wearable technology in monitoring cardio-autonomic and sleep for individuals with SCI. Future directions include conducting performance evaluations of wearable devices to precisely capture the additional variation in movement and physiological parameters seen in those with SCI. Moreover, efforts to make the devices small, lightweight, and inexpensive for consumer ease of use may impact those with severe motor impairments. Overcoming these challenges holds the potential for wearable devices to help individuals living with SCI receive timely feedback to manage their health conditions and help clinicians gather comprehensive patient health information to aid in diagnosis and treatment.

Temporal Changes of Cardiac Structure, Function, and Mechanics During Sub-acute Cervical and Thoracolumbar Spinal Cord Injury in Humans: A Case-Series.

Individuals with cervical spinal cord injury (SCI) experience deleterious changes in cardiac structure and function. However, knowledge on when cardiac alterations occur and whether this is dependent upon neurological level of injury remains to be determined. Transthoracic echocardiography was used to assess left ventricular structure, function, and mechanics in 10 male individuals (median age 34 years, lower and upper quartiles 32-50) with cervical (n = 5, c-SCI) or thoracolumbar (n = 5, tl-SCI) motor-complete SCI at 3- and 6-months post-injury. Compared to the 3-month assessment, individuals with c-SCI displayed structural, functional, and mechanical changes during the 6-month assessment, including significant reductions in end diastolic volume [121 mL (104-139) vs. 101 mL (99-133), P = 0.043], stroke volume [75 mL (61-85) vs. 60 mL (58-80), P = 0.042], myocardial contractile velocity (S') [0.11 m/s (0.10-0.13) vs. 0.09 m/s (0.08-0.10), P = 0.043], and peak diastolic longitudinal strain rate [1.29°/s (1.23-1.34) vs. 1.07°/s (0.95-1.15), P = 0.043], and increased early diastolic filling over early myocardial relaxation velocity (E/E') ratio [5.64 (4.71-7.72) vs. 7.48 (6.42-8.42), P = 0.043]. These indices did not significantly change in individuals with tl-SCI between time points. Ejection fraction was different between individuals with c-SCI and tl-SCI at 3 [61% (57-63) vs. 54% (52-55), P < 0.01] and 6 months [58% (57-62) vs. 55% (52-56), P < 0.01], though values were considered normal. These results demonstrate that individuals with c-SCI exhibit significant reductions in cardiac function from 3 to 6 months post-injury, whereas individuals with tl-SCI do not, suggesting the need for early rehabilitation to minimize cardiac consequences in this specific population.

Spinal cord injury impairs cardiac function due to impaired bulbospinal sympathetic control.

Spinal cord injury chronically alters cardiac structure and function and is associated with increased odds for cardiovascular disease. Here, we investigate the cardiac consequences of spinal cord injury on the acute-to-chronic continuum, and the contribution of altered bulbospinal sympathetic control to the decline in cardiac function following spinal cord injury. By combining experimental rat models of spinal cord injury with prospective clinical studies, we demonstrate that spinal cord injury causes a rapid and sustained reduction in left ventricular contractile function that precedes structural changes. In rodents, we experimentally demonstrate that this decline in left ventricular contractile function following spinal cord injury is underpinned by interrupted bulbospinal sympathetic control. In humans, we find that activation of the sympathetic circuitry below the level of spinal cord injury causes an immediate increase in systolic function. Our findings highlight the importance for early interventions to mitigate the cardiac functional decline following spinal cord injury.

Accidental boosting in an individual with tetraplegia - considerations for the interpretation of cardiopulmonary exercise testing.

CONTEXT: Autonomic dysreflexia (AD), characterized by a transient increase in systolic blood pressure (BP), is experienced by individuals with spinal cord injury (SCI) and can be purposefully induced ('boosting') to counteract autonomic dysfunction that impairs cardiovascular responses to exercise. Herein, we demonstrate the impact of unintentional boosting observed during cardiopulmonary exercise testing (CPET) in an inactive male with SCI (C5, motor-complete). FINDINGS: On two separate occasions the individual performed a standard arm-crank CPET (1-min stages, 7W increase in resistance) following by a longer CPET (4-min stages, 12W increase in resistance), both to volitional exhaustion. The second CPET was performed to confirm the accuracy of exercise intensity prescription and verify peak exercise parameters. Immediately following the second CPET on the initial visit, the individual reported symptoms of AD, verified as a 58mmHg increase in systolic BP from baseline. Relative to the first CPET, performed only 35 min earlier, there were pronounced differences in peak exercise responses. In comparison to the longer CPET performed on the second visit without a concomitant episode of AD (thereby controlling for the type of CPET protocol administered), peak exercise outcomes were considerably elevated: power output (Δ19W), oxygen uptake (Δ3.61 ml·â€…kg·-1min-1), ventilation (Δ11.4 L ·min-1) and heart rate (Δ9 b·min-1). CONCLUSION/CLINICAL RELEVANCE: This case raises important considerations around the nuances of CPET in this population. In individuals susceptible to BP instability, the physiologically boosted state may explain a significant proportion of the variance in peak aerobic capacity and should be closely monitored before and after clinical CPET.

Cardiac arrhythmias six months following traumatic spinal cord injury.

OBJECTIVE: To investigate the incidence of cardiac arrhythmias at six months following traumatic spinal cord injury (SCI) and to compare the prevalence of arrhythmias between participants with cervical and thoracic SCI. DESIGN: A prospective observational study using continuous twenty-four-hour Holter monitoring. SETTING: Inpatient rehabilitation unit of a university research hospital and patient home setting. PARTICIPANTS: Fifty-five participants with acute traumatic SCI were prospectively included. For each participant, the SCI was characterized according to the International Standards for Neurological Classification of SCI by the neurological level and severity according to the American Spinal Injury Association Impairment Scale. OUTCOME MEASURES: Comparisons between demographic characteristics and arrhythmogenic occurrences as early as possible after SCI (4 ± 2 days) followed by 1, 2, 3, 4 weeks and 6 month time points of Holter monitoring. RESULTS: Bradycardia (heart rate [HR] <50 bpm) was present in 29% and 33% of the participants with cervical (C1-C8) and thoracic (T1-T12) SCI six months after SCI, respectively. The differences in episodes of bradycardia between the two groups were not significant (P < 0.54). The mean maximum HR increased significantly from 4 weeks to 6 months post-SCI (P < 0.001), however mean minimum and maximum HR were not significantly different between the groups at the six-month time point. There were no differences in many arrhythmias between recording periods or between groups at six months. CONCLUSIONS: At the six-month timepoint following traumatic SCI, there were no significant differences in occurrences of arrhythmias between participants with cervical and thoracic SCI compared to the findings observed in the first month following SCI.

Associations between left ventricular structure and function with cardiorespiratory fitness and body composition in individuals with cervical and upper thoracic spinal cord injury.

STUDY DESIGN: Cross-sectional. OBJECTIVE: It is known that left ventricular mass (LVM) and cardiorespiratory fitness (CRF) are associated to fat-free mass (FFM).  It is unknown if these factors associated with left ventricular (LV) structure and function outcomes in individuals with spinal cord injury (SCI). SETTING: University-based laboratory.Vancouver, BC, Canada. METHODS: Thirty-two individuals (aged 40 ± 11 years) with chronic, motor-complete SCI between the fourth cervical and sixth thoracic levels were recruited. Echocardiographic LV parameters and body composition were assessed at rest, as per the recommended guidelines for each technique. CRF was assessed during an incremental arm-cycle exercise test until volitional fatigue. The appropriate bivariate correlation coefficients [i.e., Pearson's (r) and Spearman's rank (Rs)] tests were used for normal and non-normal distributed variables, respectively. RESULTS: LV structure and function parameters were not associated with the indexed peak oxygen consumption (V̇O2peak) [i.e., relative to body weight or FFM] (Rs values ranged from -0.168 to 0.134, all P values > 0.223). The association between peak oxygen pulse and the resting echocardiographic-obtained SV was medium sized (Rs = 0.331, P = 0.069). The LVM associations with FFM and fat mass (FM) were large and small (r = 0.614, P < 0.001 and r = 0.266, P = 0.141, respectively). Associations of absolute V̇O2peak were medium- positive with FFM (Rs = 0.414, P = 0.021) but negative with FM (Rs = -0.332, P = 0.068). CONCLUSION: LV parameters measured at rest are not associated with V̇O2peak in individuals with cervical and upper-thoracic SCI. Given the observed associations between LVM and V̇O2peak with FFM, future studies may consider utilizing FFM for indexing cardiovascular measures following SCI.