Innate immunity is linked to the severity of stable coronary artery disease through sCD40L pathway

Abstract Introduction Soluble CD40 ligand (sCD40L) activates different cell types involved in innate immunity, including macrophages and platelets. The influence of innate immunity, particularly of sCD40L pathway, on stable coronary artery disease (SCAD) expression is not fully understood. We evalua...

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Veröffentlicht in:European heart journal 2020-11, Vol.41 (Supplement_2)
Hauptverfasser: Silva, T.P.D, Napoleao, P, Pinheiro, T, Selas, M, Silva, F, Ferreira, V, Goncalves, A, Reis, J, Castelo, A, Bras, P, Cruz Ferreira, R, Mota Carmo, M
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Sprache:eng
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Zusammenfassung:Abstract Introduction Soluble CD40 ligand (sCD40L) activates different cell types involved in innate immunity, including macrophages and platelets. The influence of innate immunity, particularly of sCD40L pathway, on stable coronary artery disease (SCAD) expression is not fully understood. We evaluated if sCD40L expression is related to the presence of SCAD and to its clinical and anatomical severity. Methods We prospectively recruited two groups of age- and sex-matched participants: 1) without coronary artery disease (CAD) (calcium score=0, no soft plaques on coronary angioCT scan) (controls); and 2) with stable obstructive CAD (≥50% for the left main, ≥70% for other epicardial vessels, on invasive coronary angiography). Acute atherosclerotic events or coronary artery bypass grafting (CABG) within 12 months, previous percutaneous coronary intervention, heart failure, infection, malignancy and severe renal dysfunction were exclusion criteria. Clinical, laboratorial and anatomical data were prospectively collected. Serum was stored at −80°C and measurements were performed in a blinded fashion, by ELISA (sCD40L Human Quantikine). Results Sixty-three participants were included: 14 controls and 49 patients with SCAD. In SCAD patients, classical cardiovascular risk factors were globally more prevalent and the serum levels of sCD40L (5553±3356 vs 3099±644 ng/mL, p
ISSN:0195-668X
1522-9645
DOI:10.1093/ehjci/ehaa946.1298