Cardiovascular Disease in Spinal Cord Injury

Abstract

Cardiovascular disease is a growing concern for the spinal cord-injured (SCI) population. For long-term SCI, morbidity and mortality from cardiovascular causes now exceeds that caused by renal and pulmonary conditions, the primary causes of mortality in previous decades. Although risk estimates commonly used for ambulatory individuals have not been established from follow-up studies in SCI, nearly all risk factors tend to be more prevalent in SCI subjects compared with ambulatory subjects. These risks include a greater prevalence of obesity, lipid disorders, metabolic syndrome, and diabetes. Daily energy expenditure is significantly lower in SCI individuals, not only because of a lack of motor function, but also because of a lack of accessibility and fewer opportunities to engage in physical activity. Autonomic dysfunction caused by SCI is also associated with several conditions that contribute to heightened cardiovascular risk, including abnormalities in blood pressure, heart rate variability, arrhythmias, and a blunted cardiovascular response to exercise that can limit the capacity to perform physical activity. Thus, screening, recognition, and treatment of cardiovascular disease should be an essential component of managing individuals with SCI, and judicious treatment of risk factors can play an important role in minimizing the incidence of cardiovascular disease in these individuals. This article reviews the cardiovascular consequences of chronic SCI, including the prevalence of cardiovascular disease and risk factors unique to these individuals, and provides a synopsis of management of cardiovascular disease in this population.

Immune dysfunction and chronic inflammation following spinal cord injury

“…Together, this places the SCI population at a higher risk for the development of metabolic disorders such as obesity, type 2 diabetes and atherosclerosis; 12-14 each of which are independently associated with a chronic inflammatory status. 12,35 Obesity is now classified as an inflammatory disorder due to the discovery that adipose tissue acts as an endocrine organ, possessing the ability to secrete proinflammatory mediators, termed adipokines, such as TNF (tumor necrosis factor)-α, IL (interleukin)-1 and IL-6. 36 As such, an abundance of adipose tissue, as seen in obesity, may result in the overproduction of proinflammatory mediators and contribute to a low-grade inflammatory state.…”

“…6,10,11 The loss of motor and sensory function also contribute to this population's greater susceptibility to a number of acute infections, including urinary tract infection (UTI) and pressure ulcers, as well as metabolic disorders associated with a more sedentary lifestyle such as obesity, atherosclerosis and type 2 diabetes. [12][13][14] A number of related disorders found to be significantly more prevalent following SCI such as depression and neuropathic pain may also contribute to a heightened systemic inflammatory state. [15][16][17] It has yet to be definitively established whether or not such elevations in proinflammatory mediators are beneficial to this population or if they are in fact surrogate markers of further neurological and endocrinal impairment.…”

Increasing heat storage by wearing extra clothing during upper body exercise up-regulates heat shock protein 70 but does not modify the cytokine response

“…Such populations are at a higher risk of developing chronic disease associated with chronic low-grade inflammation (Myers, Lee, & Kiratli, 2007). This may be a result of a smaller physical capacity, a smaller active muscle mass that may affect cytokine production and reduced access to and therefore participation in sports.…”

Validation of an RPE-based submaximal oxygen consumption test using a total body recumbent stepper for individuals with spinal cord injury : a proof of concept study.

“…Spinal cord injury often reduces participation in physical activity (Buchholz, McGillivray, & Pencharz, 2003;Buchholz & Pencharz, 2004;Dallmeijer, Hopman, van As, & van der Woude, 1996;Fernhall, Heffernan, Jae, & Hedrick, 2008;Hoffman, 1986;Jacobs & Nash, 2004;Janssen, Dallmeijer, Veeger, & van der Woude, 2002;Lavis, Scelza, & Bockenek, 2007;Myers et al, 2007;Phillips et al, 1998) and decreases an individual's resting metabolic rate (Buchholz et al, 2003;Buchholz & Pencharz, 2004;Hayes et al, 2005;McCully et al, 2011;Myers et al, 2007;Phillips et al, 1998;Price, 2010) which causes a major decrease in total daily energy expenditure. This decrease in total daily energy expenditure, combined with disorders of the autonomic nervous system commonly found in SCI patients (Garstang & Miller-Smith, 2007;Karlsson, 2006;Krassioukov, 2009;Krassioukov & Claydon, 2006;Teasell, Arnold, Krassioukov, & Delaney, 2000;Theisen, 2012;West et al, 2012), causes an increase in percent body fat (Buchholz & Pencharz, 2004;Flank, Wahman, Levi, & Fahlstrom, 2012;Gorgey et al, 2012), as well as places this population at a much higher risk of chronic diseases like cardiovascular disease (Cowan & Nash, 2010;Fernhall et al, 2008;Flank et al, 2012;Garshick et al, 2005;Myers et al, 2007;Svircev, 2009), obesity ...…”

“…Additional secondary complications include pulmonary emboli, pain, and reduced mobility (Walter et al, 2002). Individuals with chronic SCI have lower resting metabolic rates (RMR), resting energy expenditure (REE), and VO 2 peak (Buchholz & Pencharz, 2004;Coutts, Rhodes, & McKenzie, 1983;Myers, Lee, & Kiratli, 2007;Phillips et al, 1998;Zurlo, Larson, Bogardus, & Ravussin, 1990). Spinal cord injury may also impact autonomic function (Krassioukov, 2006(Krassioukov, , 2009Krassioukov et al, 2012;Krassioukov & Claydon, 2006;Sisto et al, 2012;West et al, 2012).…”