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• W1996603208 abstract "Objective Reduced soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) levels have been related with cardiovascular disease. However, there are no data on the relationship between sTWEAK and atherosclerotic burden in subjects with or without cardiovascular risk factors but free from clinical disease. We have analyzed the association between circulating sTWEAK levels and the presence of carotid and/or femoral atherosclerotic plaques in subjects without known vascular disease. Methods A multicenter, cross-sectional study was conducted in 448 subjects free from clinical CVD. B-mode ultrasound was performed to detect the presence of carotid and/or femoral atherosclerotic plaques. sTWEAK concentrations were measured by enzyme-linked immunosorbent assay. Results sTWEAK serum levels were reduced in parallel with an increment in cardiovascular risk factors. sTWEAK concentrations were independently and negatively associated with carotid intima/media thickness. Subjects with atherosclerotic plaques showed a reduction in sTWEAK levels [808 (645–963) vs 993 (830–1278); p < 0.001]. A gradual decrease in sTWEAK levels was observed as the number of atherosclerotic plaques increased in our studied population. When we analyzed sTWEAK levels according to the vascular territory affected, we observed that sTWEAK concentrations were only diminished in subjects with carotid atherosclerotic plaques but not in those with femoral plaques. Following adjustment for various confounders, the OR for presenting carotid atherosclerotic plaque in subjects in lower vs higher tertile of sTWEAK levels was 8.09 [4.30–15.23; median (IQR); p < 0.001]. Conclusions Diminished sTWEAK concentrations were significantly and independently associated with the presence of carotid atherosclerotic plaques in asymptomatic subjects." @default.
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• W1996603208 date "2015-04-01" @default.
• W1996603208 modified "2023-10-16" @default.
• W1996603208 title "Soluble TWEAK levels predict the presence of carotid atherosclerotic plaques in subjects free from clinical cardiovascular diseases" @default.
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• W1996603208 doi "https://doi.org/10.1016/j.atherosclerosis.2015.01.040" @default.
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