Orthostatic Blood Pressure and Arterial Stiffness in Persons with Spinal Cord Injury: The Effect of the Renin Angiotensin Aldosterone System

With advances in acute medical care, longevity has increased in persons with SCI; however, morbidity due to cardiovascular disease (CVD) occurs at an earlier age compared to the general population. Arterial stiffness (AS) is recognized as an independent risk factor for CVD and, specifically, pulse wave velocity (PWV) has been proven to be a valid tool to predict and track structural arterial changes that reflect arteriosclerosis. Evidence has shown that persons with SCI have increased AS compared to uninjured able-bodied controls; however, possible contributors to this increase are not yet fully understood. After a SCI, sympathetic control in the regions below the lesion level are severely disrupted; however, parasympathetic function is preserved. Due to the dissociation between the two systems, those with lesions above T6 experience low resting blood pressure (BP) and further decreases in BP when changing postures (orthostatic hypotension (OH)). As a consequence, individuals with high-level injuries have a heightened reliance on the renin-angiotensin-aldosterone system (RAAS) to maintain and stabilize BP. A mechanism for increased AS in the uninjured population is over activation of the RAAS. In this study, individuals with high-level SCI (injured above T1) and low-level SCI (injured between T6-T12) had increased AS compared to age-matched controls. The change in renin from supine rest to 60-degree head-up tilt (HUT) was a significant predictor to the change in systolic BP; however, the group predictor was not significant. Additionally, group and change in renin were significant predictors to AS. The data indicate that individuals with high-level injuries rely heavily on RAAS to maintain and normalize BP during OH, which is correlated to increased AS. A better way to treat asymptomatic OH in the SCI population is needed to decrease CVD

Orthostatic Blood Pressure and Arterial Stiffness in Persons with Spinal Cord Injury: The Effect of the Renin Angiotensin Aldosterone System

With advances in acute medical care, longevity has increased in persons with SCI; however, morbidity due to cardiovascular disease (CVD) occurs at an earlier age compared to the general population. Arterial stiffness (AS) is recognized as an independent risk factor for CVD and, specifically, pulse wave velocity (PWV) has been proven to be a valid tool to predict and track structural arterial changes that reflect arteriosclerosis. Evidence has shown that persons with SCI have increased AS compared to uninjured able-bodied controls; however, possible contributors to this increase are not yet fully understood. After a SCI, sympathetic control in the regions below the lesion level are severely disrupted; however, parasympathetic function is preserved. Due to the dissociation between the two systems, those with lesions above T6 experience low resting blood pressure (BP) and further decreases in BP when changing postures (orthostatic hypotension (OH)). As a consequence, individuals with high-level injuries have a heightened reliance on the renin-angiotensin-aldosterone system (RAAS) to maintain and stabilize BP. A mechanism for increased AS in the uninjured population is over activation of the RAAS. In this study, individuals with high-level SCI (injured above T1) and low-level SCI (injured between T6-T12) had increased AS compared to age-matched controls. The change in renin from supine rest to 60-degree head-up tilt (HUT) was a significant predictor to the change in systolic BP; however, the group predictor was not significant. Additionally, group and change in renin were significant predictors to AS. The data indicate that individuals with high-level injuries rely heavily on RAAS to maintain and normalize BP during OH, which is correlated to increased AS. A better way to treat asymptomatic OH in the SCI population is needed to decrease CVD