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

Syndecan-1 and endocan are biomarkers of endothelial damage, which associate with worse outcomes after myocardial infarction (MI). As it is unclear how this is mediated, we investigated how they associate with the composition of residual, non-culprit coronary atherosclerotic plaques following acute MI. This post hoc analysis of the COCOMO-ACS trial used serum samples from forty-five patients with non-ST elevation MI who underwent blood collection and optical coherence tomography (OCT) imaging of non-culprit, lipid-rich coronary plaques at baseline and after a median of 17.8 months. Serum syndecan-1 and endocan concentrations at both time-points were measured by ELISA. Relationships between these biomarkers and OCT parameters of rupture-prone plaque were examined. Serum levels of syndecan-1 (median 161.0 ng/mL at baseline vs 93.5 ng/mL at follow-up, P < 0.0001) and endocan (225.7 pg/mL vs 191.2 pg/mL, P = 0.003) both decreased from time of MI to follow-up, with strong correlation between their changes (R 2 = 0.64, P < 0.0001). Only syndecan-1 showed a weak negative correlation with minimum fibrous cap thickness at baseline (R 2 = 0.10, P = 0.03) and a weak positive correlation with maximum lipid arc at follow-up (R 2 = 0.14, P = 0.01). While syndecan-1 and endocan showed no relationship with plasma lipid concentrations, there were weak associations between follow-up syndecan-1 and interleukin-1-beta (R 2 = 0.21, P = 0.001), and follow-up endocan and interleukin-6 (R 2 = 0.15, P = 0.008). Although serum syndecan-1 and endocan levels decreased in peripheral blood over time post-MI on guideline-directed therapy, this study identified only modest relationships between syndecan-1 (and not endocan) and OCT compositional characteristics of lipid-rich, rupture-prone plaque.