Longitudinal assessment of endothelial glycocalyx in ST-elevation myocardial infarction: Interplay with oxidative stress and inflammation

BACKGROUND: Microvascular dysfunction (MVD) after ST-elevation myocardial infarction (STEMI) is common and contributes to adverse left ventricular remodeling and reduced survival. Endothelial glycocalyx (eGC) shedding during STEMI has been proposed as a potential mechanism for MVD. This study evaluated eGC shedding during STEMI, its recovery over time, and its correlations with oxidative stress, inflammation, and endothelial injury. METHODS: In this before-after clinical study, STEMI patients were assessed in the acute phase and again six months later. Circulating biomarkers of eGC shedding (syndecan-1 [SDC-1], hyaluronan [HYAL], sulfated glycosaminoglycans [GAGs]); endothelial injury (thrombomodulin [TBML], tissue plasminogen activator [tPA], vascular endothelial growth factor [VEGF], nitrite); oxidative stress (malondialdehyde [MDA], total hydroperoxides [H₂O₂], superoxide dismutase [SOD], reduced glutathione [GSH], total antioxidant capacity [TAC]); and inflammatory mediators (IL-6, TNF-α) were quantified. Sublingual microcirculation was evaluated using GlycoCheck to estimate the perfused boundary region (PBR), an inverse parameter of eGC thickness. RESULTS: Twenty patients were included, with a mean interval of 188 ± 31 days between assessments. PBR and flow-adjusted PBR decreased significantly from the acute phase to follow-up, indicating eGC restoration. Acute elevations in SDC-1, HYAL, GAGs, MDA, H₂O₂, SOD, tPA, and nitrite were attenuated at six months. Biomarkers of eGC shedding and PBR values correlated positively with indices of oxidative stress, endothelial injury and inflammation. CONCLUSION: eGC shedding occurs during STEMI and shows evidence of recovery in the subsequent months. Correlations between eGC shedding and oxidative stress, endothelial injury and inflammation support a mechanistic interplay contributing to MVD development after STEMI.