Endothelial glycocalyx (eGC) was composed of proteoglycan polymers and found in the endothelium’s surface layer. Syndecan-1, heparan sulfate, and hyaluronic acid were important components of eGC, and the rising detection of these molecules in serum indicated that eGC was actively degrading. Patients without heart failure (non-HF) and with HF with reduced ejection fraction (HFrEF) of less than 40%, either stable chronic HF (CHF) or acute decompensated HF (ADHF), had their sera collected. Syndecan-1, heparan sulfate, and hyaluronic acid were tested for group comparisons, with clinical and laboratory data considered. Researchers enrolled 51 non-HF, 66 ADHF, and 72 CHF patients in the study cohort. Left ventricular (LV) mass index, LV ejection fraction, and pulmonary capillary wedge pressure did not differ between ADHF and CHF. However, ADHF patients had considerably greater eGC components than CHF and non-HF patients. During the follow-up period, 21 patients with HF passed away, and the mortality rate was greater in those with elevated serum syndecan-1 or heparan sulfate (log-rank P=0.007 and 0.016, respectively). In multivariate analysis, a doubling of serum heparan sulfate concentration was associated with an increase of 31.5% in all-cause mortality (hazard ratio=1.31, CI=1.012−1.709, P=0.040). In conclusion, serum indicators of eGC were higher in ADHF (but not in CHF) in patients with HFrEF, suggesting that eGC degradation and endothelial dysfunction might play a role in HF decompensation. Only elevated heparin sulfate was related to increased all-cause mortality in patients with HFrEF after adjustment for conventional risk factors.
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