title: Arterial stiffening, wave reflection, and inflammation in habitually exercising systemic lupus erythematosus patients.
abstract: BACKGROUND
  Chronic systemic inflammation has been implicated in the pathogenesis of hypertension and cardiovascular disease. Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by chronic inflammation and an increased risk for cardiovascular disease. Currently few studies have evaluated the potential cardiovascular benefits of exercise in SLE. It is unknown whether the favorable effect of habitual exercise on arterial stiffness observed in healthy adults can be extended to SLE. Therefore, as an initial step, we determined the association between habitual exercise, inflammatory markers, central arterial compliance, and aortic wave reflection in healthy adults and SLE patients.
  
  
  METHODS
  We studied 41 adults, aged 33 ± 11 years (15 healthy controls, 12 sedentary SLE, and 14 physically active SLE patients).
  
  
  RESULTS
  Age, body mass index, and metabolic risk factors were not different between the three groups. Carotid arterial compliance was lower whereas augmentation index (AI) and inflammatory markers (C-reactive protein (CRP), interleukin (IL)-12, tumor necrosis factor-α (TNF-α)) were higher in sedentary SLE patients compared with healthy controls, but were not different between physically active SLE patients and healthy controls. Cardiac ejection fraction was lower in sedentary SLE than physically active SLE or healthy controls. In the pooled population, carotid arterial compliance was inversely associated with TNF-α (r = -0.38; P < 0.01), and AI was positively associated with both CRP (r = 0.33; P < 0.05) and intercellular adhesion molecule-1 (r = 0.28; P < 0.05).
  
  
  CONCLUSIONS
  SLE-associated stiffening of the central artery and wave reflection were not observed in habitually exercising adults with SLE. Furthermore, greater arterial stiffness was associated with higher inflammatory markers, suggesting that need for studies on inflammation and SLE-associated arterial stiffening.
authors.affiliation: Cardiovascular Aging Research Laboratory, Department of Kinesiology and Health Education, University of Texas at Austin, USA. Barnes.Jill@mayo.edu
authors.forename: Jill N
authors.initials: JN
authors.lastname: Barnes
authors.forename: Nantinee
authors.initials: N
authors.lastname: Nualnim
authors.forename: Jun
authors.initials: J
authors.lastname: Sugawara
authors.forename: Shawn M
authors.initials: SM
authors.lastname: Sommerlad
authors.forename: Christopher P
authors.initials: CP
authors.lastname: Renzi
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Tanaka
mesh_terms: D000328:Adult; D001158:Arteries / Q000503:physiopathology; D001783:Blood Flow Velocity; D002097:C-Reactive Protein / Q000378:metabolism; D002339:Carotid Arteries / Q000502:physiology*; D003187:Compliance / Q000502:physiology; D015444:Exercise; D005260:Female; D006801:Humans; D007249:Inflammation / Q000209:etiology*; D018664:Interleukin-12 / Q000378:metabolism; D008180:Lupus Erythematosus, Systemic / Q000150:complications / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D057185:Sedentary Behavior; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014655:Vascular Resistance; D059289:Vascular Stiffness
chemical_list: D014409:Tumor Necrosis Factor-alpha; D018664:Interleukin-12; D002097:C-Reactive Protein