Why the study?
Does a high spinal cord lesion increase arterial stiffness compared to low lesions or uninjured controls in individuals with chronic spinal cord injury?
Does a high spinal cord lesion increase arterial stiffness compared to low lesions or uninjured controls in individuals with chronic spinal cord injury?
Higher spinal cord injury lesions are associated with greater arterial stiffness, likely driven by autonomic disruption, orthostatic hypotension, and physical inactivity.
Higher lesions may signal greater AI-related CVD risk in SCI; leaves open whether lesion-specific interventions modify stiffness.
Individuals with chronic spinal cord injury (SCI) are at a heightened risk of cardiovascular disease (CVD) resulting from autonomic nervous system dysfunction, physical inactivity, and increased inflammatory processes. Arterial stiffness (AS) is recognized as an independent risk factor for CVD and, specifically, pulse wave analysis (PWA) has proven to be a useful tool to predict and track structural arterial changes that reflect arteriosclerosis. The augmentation index (AI) can be used to estimate AS and is derived from the amplitude and timing of the blood pressure (BP) wave reflection in a peripheral artery. Recently, AS has been shown to be increased in persons with SCI compared with the uninjured population; however, possible contributors to increased AS in the SCI population have not been fully explored. In this study, increased radial artery AI is demonstrated in persons with high cord lesions (above T6) compared with individuals with low cord lesions (T7 and below) and uninjured controls. The association between age and AI was not significant in the SCI population; however, there was a direct association between AI and level of injury. Further, AI was inversely associated with seated systolic blood pressure (SBP) and was increased in individuals who reported orthostatic hypotension (OH) and in those who were physically inactive. In conclusion, individuals with higher cord lesions have more severe cardiovascular autonomic disruption, leading to orthostatic BP dysregulation and physical inactivity, which appear to contribute independently to increased AS in these individuals.
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Katzelnick et al. (2017) studied this question.
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