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Syndecan-1, endocan and non-culprit coronary plaque composition following non-ST elevation myocardial infarction

Naomi E Wattchow1,2,3, Thalia Salagaras1, Mau T Nguyen1,2,4

  • 1Vascular Research Centre, Lifelong Health Theme, South Australian Health and Medical Research Institute (SAHMRI), Adelaide, Australia.

International Journal of Cardiology. Heart & Vasculature
|May 11, 2026
PubMed

Insights

Serum levels of syndecan-1 and endocan decrease after myocardial infarction (MI). While syndecan-1 showed modest links to plaque composition, endocan did not, suggesting limited roles in mediating MI outcomes.

Area of Science:

  • Cardiovascular Research
  • Biomarker Discovery
  • Atherosclerosis Research

Background:

  • Syndecan-1 and endocan are established biomarkers associated with endothelial damage and poorer outcomes following myocardial infarction (MI).
  • The precise mechanisms linking these biomarkers to adverse cardiovascular events remain incompletely understood.
  • Investigating their association with the composition of non-culprit coronary atherosclerotic plaques is crucial for elucidating their role post-MI.

Purpose of the Study:

  • To investigate the association between serum syndecan-1 and endocan levels and the characteristics of non-culprit coronary atherosclerotic plaques in patients post-MI.
  • To determine if changes in these biomarkers correlate with plaque composition over time.
  • To explore potential relationships between these biomarkers and inflammatory markers.

Main Methods:

  • A post hoc analysis of the COCOMO-ACS trial involving 45 patients with non-ST elevation MI.
  • Serum samples collected at baseline and follow-up (median 17.8 months) were analyzed for syndecan-1 and endocan concentrations using ELISA.
  • Optical coherence tomography (OCT) was used to assess the composition of non-culprit, lipid-rich coronary plaques.

Main Results:

  • Serum levels of both syndecan-1 and endocan significantly decreased from baseline to follow-up post-MI.
  • A strong correlation was observed between the changes in syndecan-1 and endocan levels.
  • Syndecan-1 showed weak correlations with fibrous cap thickness and lipid arc, while endocan did not demonstrate significant associations with plaque composition. Weak associations were found between syndecan-1 and IL-1β, and endocan and IL-6.

Conclusions:

  • Serum syndecan-1 and endocan levels decrease over time following MI with guideline-directed therapy.
  • Syndecan-1, but not endocan, exhibited modest associations with specific compositional features of lipid-rich, rupture-prone plaques.
  • These findings suggest a limited direct relationship between these biomarkers and the structural characteristics of non-culprit plaques in the context of MI outcomes.
Abstract

Keywords:
Acute coronary syndromeBiomarkerCoronary artery diseaseEndocanGlycocalyxPlaque ruptureSyndecan-1

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