Tumour necrosis factor like cytokine 1A levels and lesion complexity in non-smoking patients with coronary artery disease

Background: Tumour necrosis factor like cytokine 1A (TL1A), which is a member of tumour necrosis factor alpha superfamily (TNF-α), is a novel indicator of atherosclerosis. Objective: Smoking is an established stimulant of TNF-α. We aimed to investigate whether TLA1 plays a role in the presence and c...

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Published in:Biomarkers Vol. 24; no. 8; pp. 764 - 770
Main Authors: Akyüz, Aydın, Özkaramanlı Gür, Demet, Alpsoy, Şeref, Güzel, Savaş
Format: Journal Article
Language:English
Published: England Taylor & Francis 17-11-2019
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Summary:Background: Tumour necrosis factor like cytokine 1A (TL1A), which is a member of tumour necrosis factor alpha superfamily (TNF-α), is a novel indicator of atherosclerosis. Objective: Smoking is an established stimulant of TNF-α. We aimed to investigate whether TLA1 plays a role in the presence and complexity of coronary artery atherosclerosis, exclusively in non-smoking patients with CAD. Methods: We enrolled 103 participants in the study, who underwent coronary angiography for stable angina pectoris. We divided the study population into 2 groups: The CAD group consisted of 62 patients with CAD and the control group consisted of 41 subjects with non-CAD. SYNTAX and Gensini scores, indicating CAD severity and complexity, were analysed as well as TLA1 levels. Results: TLA1 levels was higher in patients with CAD than those in controls (228[119-824] vs 178[15-418]pg/ml, p < 0.001). Presence of CAD (β ± SE = 106.29 ± 33.11, p = 0.002), Syntax score (β ± SE= 6.57 ± 1.75, p = 0.012), and Gensini score (β ± SE = 2.30 ± 0.65, p = 0.001) were found to be predictors of TL1A levels. Gensini score and Syntax score were positively correlated with TL1A levels (r = 0.420, p < 0.001, and r = 0.402, p < 0.001, respectively). Conclusions: Non-smoker CAD patients have higher TLA1 levels that are promising biomarker for diagnosing CAD and indicating CAD lesion complexity.
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ISSN:1354-750X
1366-5804
DOI:10.1080/1354750X.2019.1685004