Dynamic Changes and Clinical Significance of Plasma Galectin-3 in Patients with Acute Ischemic Stroke Undergoing Endovascular Therapy.

Purpose: Galectin-3 is a key regulator of microglial proliferation and activation and may have dual and time-dependent effects on ischemic stroke. This study aimed to prospectively investigate the dynamic changes in Galectin-3 levels in patients with acute ischemic stroke receiving endovascular therapy and its clinical significance. Patients and Methods: A total of 105 patients with acute ischemic stroke who underwent endovascular therapy were prospectively enrolled. Plasma Galectin-3 was quantitatively detected by an enzyme-linked immunosorbent assay before the operation and at 1 day, 3 days and 7 days after the operation. A linear mixed-effect model, Pearson correlation analysis and receiver operating characteristic (ROC) curve analysis were used to evaluate the dynamic changes in the plasma Galectin-3 concentration and its relationship with clinical outcomes. Results: Increases in plasma Galectin-3 levels at 1 day and 3 days after surgery were associated with early neurological deterioration and death (both P <0.05). Increased Galectin-3 levels before surgery and at 1 day and 3 days after surgery were associated with poor prognosis (P <0.05). Pearson correlation analysis revealed that Galectin-3 levels before surgery (r =0.318, P =0.002), at 1 day (r =0.318, P =0.001), 3 days (r =0.429, P < 0.001) and 7 days after surgery (r =0.340, P =0.001) were positively correlated with NIHSS scores. The ROC curve results showed that Galectin-3 concentration had a certain predictive value for death at 1 day (AUC=0.707, P=0.013), 3 days (AUC=0.708, P=0.016) and 7 days after the operation (AUC=0.708, P=0.016), but this predictive value was lower than that of the NIHSS score. Conclusion: In acute ischemic stroke patients receiving endovascular therapy, an increase in the plasma Galectin-3 levels were associated with death, poor prognosis, and early neurological deterioration. Galectin-3 levels were significantly correlated with the NIHSS score and had a certain predictive value for death.

Stroke recurrence is associated with unfavorable intracranial venous outflow in patients with symptomatic intracranial atherosclerotic large vessel severe stenosis or occlusion.

Objective: The purpose of this study was to investigate the predictive value of intracranial venous outflow for recurrent cerebral ischemic events (RCIE) in patients with symptomatic intracranial atherosclerotic large-vessel severe stenosis or occlusion (sICAS-S/O). Methods: This retrospective study included sICAS-S/O patients with anterior circulation who underwent dynamic computed tomography angiography (dCTA) and computed tomography perfusion (CTP). Arterial collaterals were evaluated using the pial arterial filling score for dCTA data, tissue-level collaterals (TLC) were assessed using the high-perfusion intensity ratio (HIR, Tmax >10 s/Tmax >6 s), and cortical veins were evaluated using the multi-phase venous score (MVS) for the vein of Labbé (VOL), sphenoparietal sinus (SPS), and superficial cerebral middle vein (SCMV). The relationships between multi-phase venous outflow (mVO), TLC, and 1-year RCIE were analyzed. Results: Ninety-nine patients were included, 37 of whom had unfavorable mVO (mVO-) and 62 of whom had favorable mVO (mVO+). Compared with the mVO+ patients, mVO- patients had a higher admission National Institutes of Health Stroke Scale (NIHSS) score (median, 4 [interquartile range (IQR), 0-9] vs. 1 [IQR, 0-4]; p = 0.048), larger ischemic volume (median, 74.3 [IQR, 10.1-177.9] vs. 20.9 [IQR, 5-86.4] mL; p = 0.042), and worse tissue perfusion (median, 0.04 [IQR, 0-0.17] vs. 0 [IQR, 0-0.03]; p = 0.007). Multivariate regression analysis showed that mVO- was an independent predictor of 1-year RCIE. Conclusion: For patients with sICAS-S/O of the anterior circulation, unfavorable intracranial venous outflow is a potential imaging indicator for predicting higher 1-year RCIE risk.

Dynamic changes in the glycocalyx and clinical outcomes in patients undergoing endovascular treatments for large vessel occlusion.

Purpose: We aimed to verify the prognostic value of the glycocalyx as a marker of blood-brain barrier damage in patients with acute ischemic stroke undergoing endovascular therapy. Methods: We recruited patients with large vessel occlusion who were undergoing recanalization and tested their glycocalyx at multiple time points. On the basis of the 90-day follow-up data, the patients were divided into a survivor group and a nonsurvivor group. In addition, neurological function was tracked, and patients were divided into a neurological deterioration group and a group without neurological deterioration. Associations between outcomes and dynamic changes in the glycocalyx were determined using a linear mixed model, and significant factors were used as covariates. Results: Nonsurvivors and patients with neurological deterioration had significantly higher syndecan-1 concentrations than survivors and patients without neurological deterioration, and syndecan-1 tended to decline after endovascular therapy (p < 0.05). The increased level of syndecan-1 at 36 h after endovascular treatment was positively correlated with the National Institute of Health Stroke Scale score for neurological deterioration (r = 0.702, p = 0.005). However, there was no significant difference in the level of hyaluronic acid or heparan sulfate in the plasma of patients with different clinical outcomes. Conclusion: Pre-reperfusion syndecan-1 levels in patients with large vessel occlusion stroke are associated with 90-day mortality and the re-degradation of syndecan-1 is positively associated with neurological deterioration.