Metabolically healthy obesity and subclinical atherosclerosis in persons with spinal cord injury.

Abstract

Despite preserved metabolic function, metabolically healthy obesity may increase the risk of subclinical atherosclerosis. Given the high prevalence of cardiometabolic diseases in individuals with spinal cord injury, the aim of this study was to investigate the association of insulin resistance, systemic low-grade inflammation, and markers of subclinical atherosclerosis with metabolically healthy obesity in individuals with spinal cord injury. Insulin resistance index (HOMA-IR), high-sensitivity C-reactive protein, carotid artery intima-media thickness and carotid-femoral pulse wave velocity were measured in individuals with spinal cord injury classified with metabolically healthy obesity (n = 12), metabolically unhealthy obesity (n = 8), or metabolically healthy normal-weight (n = 18). Metabolically healthy obesity was defined as spinal cord injury-specific cut-off of body mass index ≥ 22 kg/m2 with < 3 metabolic abnormalities. There were no differences in HOMA-IR or high-sensitivity C-reactive protein in metabolically healthy obesity compared with metabolically healthy normal-weight (p > 0.05). Pulse wave velocity was higher in metabolically healthy obesity than in metabolically healthy normal-weight (p ≤ 0.05), but lower than in metabolically unhealthy obesity (p ≤ 0.05). Metabolically healthy obesity had similar carotid artery intima-media thickness vs metabolically healthy normal-weight (p > 0.05), but lower carotid artery intima-media thickness compared with metabolically unhealthy obesity (p ≤ 0.05). Despite a somewhat preserved metabolic and inflammatory status, individuals with spinal cord injury with metabolically healthy obesity present with an intermediate subclinical atherosclerotic phenotype, as evidenced by increased aortic stiffness but not carotid thickness.