Subclinical atherosclerosis is related to injury level but not to inflammatory parameters in spinal cord injury subjects.
METHODS
Cross-sectional.


OBJECTIVE
Individuals with spinal cord injury (SCI) exhibit increased carotid intima-media thickness (IMT) and are reported to be exposed to higher circulating levels of inflammatory mediators. This study evaluated the relationship between inflammatory markers and carotid surrogates of cardiovascular risk in subjects with SCI.


METHODS
São Paulo, Brazil.


METHODS
A total of 65 nondiabetic, nonhypertensive, sedentary, nonsmoker men (34 with SCI; 31 healthy subjects) were evaluated by medical history, anthropometry, routine laboratory tests, analysis of hemodynamic, inflammatory parameters and ultrasound examination of carotid arteries.


RESULTS
Subjects with SCI (18 tetraplegic and 16 paraplegic) had lower systolic blood pressure (P = 0.009), higher serum C-reactive protein (P = 0.001), tumor necrosis factor (TNF) receptor-II (P = 0.02) and TNF receptor-I (P = 0.04) levels and increased in vitro production of interleukin-6 by mononuclear cells (P = 0.04), compared to able-bodied individuals. No differences in serum interleukin-6, e-selectin, intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and transforming growth factor-β levels, or in vitro release of interleukin-10, interleukin-17 and interferon-γ by mononuclear cells, were detected between the studied groups. Common carotid IMT, but not internal carotid resistive index, was significantly higher in subjects with SCI (P<0.0001 adjusted for C-reactive protein and TNF receptor-II levels). In addition, tetraplegic subjects exhibited increased IMT (P = 0.002 adjusted for systolic blood pressure and body mass index), but similar levels of inflammatory mediators compared to paraplegic ones.


CONCLUSIONS
Individuals with SCI exhibit a clustering of vascular and inflammatory surrogates of increased cardiovascular risk. Nevertheless, subclinical carotid atherosclerosis is related to injury level but not to increased inflammatory status in these subjects.
Matos-Souza
J R
JR
Department of Internal Medicine, School of Medicine, University of Campinas, Campinas, São Paulo, Brazil.
Pithon
K R
KR
Ozahata
T M
TM
Oliveira
R T
RT
Téo
F H
FH
Blotta
M H
MH
Cliquet
A
A
Nadruz
W
W
D000328:Adult; D000886:Anthropometry; D050197:Atherosclerosis / Q000209:etiology*; D002097:C-Reactive Protein / Q000378:metabolism; D002339:Carotid Arteries / Q000473:pathology*; D017536:Carotid Artery, Common / Q000473:pathology; D002343:Carotid Artery, Internal / Q000473:pathology; D015815:Cell Adhesion Molecules / Q000378:metabolism; D003430:Cross-Sectional Studies; D016207:Cytokines / Q000097:blood; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000209:etiology*; D008297:Male; D013119:Spinal Cord Injuries / Q000150:complications* / Q000473:pathology*
D015815:Cell Adhesion Molecules; D016207:Cytokines; D002097:C-Reactive Protein