Role of Endothelin-1 and Nitric Oxide in Acute Ischemic Stroke Leptomeningeal Collaterals Activation

Le résumé fourni par la source

Good leptomeningeal collaterals (LMC) after large vessel occlusion (LVO) extend the time window for endovascular therapy. The mechanisms regulating LMC activation are not fully understood. The aim of this study was to investigate the potential role of two vasoactive molecules Endothelin-1 (ET1) – vasoconstrictor agent - and nitric oxide (NO) – vasodilator agent - in the regulation of post-stroke LMC. Ischemic stroke patients within 6 hours of LVO were included. Collateral status was assessed using the Menon scoring system based on Computed Tomography Angiography scans. Patients were accordingly divided into three groups: poor, intermediate, and good LMC. Recanalization was evaluated using the modified Thrombolysis in Cerebral Infarction (mTICI) score. Serum levels of ET1 and NO were measured at three time points: T0 (<6 hours), T1 (24 hours), and T2 (48 hours). A total of 105 patients were enrolled (mean age 76 ± 12.8 years): 44 with good (46.2%), 36 with intermediate (37.8%), and 22 with poor LMCs (23.1%). NO values decreased whereas ET1 values increased from T0 to T1 in all groups of patients. No significant association was found between serum ET-1 levels and collateral status. Higher ET-1 levels at T1 correlated with poor outcome regardless the LMC status and the degree of recanalization (p = 0.030). A significant linear positive correlation was revealed at T0 between high levels of ET-1 and neutrophils count (Spearman’s rho = 0.236; p=0.035). Subgroup analysis showed a significant inverse correlation at T1 between NO and the collateral score (Spearman’s rho= -0.251, p=0.021). Although we observed no significant association between LMC score and serum ET-1 concentrations, at 24 hours higher ET-1 serum levels were predictive of poor outcome and higher NO levels were correlated with poor collateral status. These findings may indicate an inadequate microvascular reperfusion possibly due to ET-1 mediated vasoconstriction, neutrophil activation and NO mediated oxidative stress, suggesting their potential role in no-reflow phenomenon.

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