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Войти в исследования Brain sciences · 2026
Plasma Biomarkers of the Glycocalyx in Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage.
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Aslankurt Karmen, Schenck Hanna, van Kuijk Sander M J, Hoogland Govert, de Ridder Inger, Teernstra Onno, Dings Jim, Aries Marcel, Veldeman Michael, Vink Hans, Temel Yasin, van Lanen Rick, Haeren Roel
Аннотация
BACKGROUND: An aneurysmal subarachnoid hemorrhage (aSAH) is a life-threatening neurovascular emergency. Among survivors, the most dreaded complication is delayed cerebral ischemia (DCI), affecting approximately one third of aSAH patients. Several mechanisms contributing to DCI have been described, yet the pathophysiology remains unclear. Disruption of the endothelial glycocalyx plays a key role in these pathomechanisms and is therefore of particular interest. This study aimed to explore changes in plasma glycocalyx breakdown products following aSAH and in relation to the development of DCI.
METHODS: In this prospective study, plasma samples were collected during a two-week follow-up period after aSAH diagnosis. Baseline plasma samples were collected within 72 h after ictus, followed by two additional samples in the first week and three samples in the second week. In patients who developed DCI, additional daily samples were obtained. DCI was defined using its clinical definition. Glycocalyx breakdown products syndecan-1 and hyaluronan concentrations were measured using enzyme-linked immunosorbent assays (ELISA) kits.
RESULTS: Twenty-nine aSAH patients were included, of whom six developed DCI. Overall, median syndecan-1 concentrations increased significantly from baseline (33.72 ng/mL, IQR 23.29-42.55 ng/mL) to the day 14 measurements (44.83 ng/mL, IQR 32.52-62.68) (p = 0.002). This increase was more prominent in the DCI group (baseline: 34.35 ng/mL, IQR 33.77-50.99, final measurement: 52.31 ng/mL, IQR 44.98-170.62, p = 0.031) compared to the non-DCI group (baseline: 33.07 ng/mL, IQR 23.29-42.32, final measurement: 37.97 ng/mL, IQR 32.52-52.14, p = 0.028), and mainly occurred at DCI onset. Median baseline hyaluronan concentrations were increased at baseline (148.81 ng/mL, IQR 90.61-178.93) and subsequently decreased (final measurement 115.96 ng/mL, IQR 99.15-140.35, p = 0.263). A comparable decrease in hyaluronan levels was noted in the DCI (baseline: 147.82 ng/mL, IQR 80.63-169.63, final measurement: 117.02 ng/mL, IQR 96.73-200.68, p = 0.893) and non-DCI group (baseline: 149.81 ng/mL, IQR 109.16-178.92, final measurement: 114.91 ng/mL, IQR 102.26-136.63, p = 0.156).
CONCLUSIONS: The results from this explorative study indicate that aSAH is associated with glycocalyx breakdown. While hyaluronan levels were high in the acute phase and decreased thereafter, syndecan-1 levels increased during the first two weeks following aSAH in DCI patients. For syndecan-1, this change was more pronounced in DCI patients. Our findings suggest an involvement of glycocalyx breakdown in the pathophysiology of DCI. This study requires validation in larger cohorts to strengthen our results, and establishes the potential of glycocalyx breakdown products as biomarkers for DCI.
METHODS: In this prospective study, plasma samples were collected during a two-week follow-up period after aSAH diagnosis. Baseline plasma samples were collected within 72 h after ictus, followed by two additional samples in the first week and three samples in the second week. In patients who developed DCI, additional daily samples were obtained. DCI was defined using its clinical definition. Glycocalyx breakdown products syndecan-1 and hyaluronan concentrations were measured using enzyme-linked immunosorbent assays (ELISA) kits.
RESULTS: Twenty-nine aSAH patients were included, of whom six developed DCI. Overall, median syndecan-1 concentrations increased significantly from baseline (33.72 ng/mL, IQR 23.29-42.55 ng/mL) to the day 14 measurements (44.83 ng/mL, IQR 32.52-62.68) (p = 0.002). This increase was more prominent in the DCI group (baseline: 34.35 ng/mL, IQR 33.77-50.99, final measurement: 52.31 ng/mL, IQR 44.98-170.62, p = 0.031) compared to the non-DCI group (baseline: 33.07 ng/mL, IQR 23.29-42.32, final measurement: 37.97 ng/mL, IQR 32.52-52.14, p = 0.028), and mainly occurred at DCI onset. Median baseline hyaluronan concentrations were increased at baseline (148.81 ng/mL, IQR 90.61-178.93) and subsequently decreased (final measurement 115.96 ng/mL, IQR 99.15-140.35, p = 0.263). A comparable decrease in hyaluronan levels was noted in the DCI (baseline: 147.82 ng/mL, IQR 80.63-169.63, final measurement: 117.02 ng/mL, IQR 96.73-200.68, p = 0.893) and non-DCI group (baseline: 149.81 ng/mL, IQR 109.16-178.92, final measurement: 114.91 ng/mL, IQR 102.26-136.63, p = 0.156).
CONCLUSIONS: The results from this explorative study indicate that aSAH is associated with glycocalyx breakdown. While hyaluronan levels were high in the acute phase and decreased thereafter, syndecan-1 levels increased during the first two weeks following aSAH in DCI patients. For syndecan-1, this change was more pronounced in DCI patients. Our findings suggest an involvement of glycocalyx breakdown in the pathophysiology of DCI. This study requires validation in larger cohorts to strengthen our results, and establishes the potential of glycocalyx breakdown products as biomarkers for DCI.