Endothelial dysfunction as a predictor of post-reperfusion complications in acute ischemic stroke: a literature review
Abstract
Acute ischemic stroke remains one of the leading causes of mortality and long-term disability worldwide. Although reperfusion therapies, including thrombolysis and mechanical thrombectomy, have demonstrated efficacy, a substantial proportion of patients fail to achieve the expected functional recovery, highlighting the need to identify additional pathogenetic factors that may influence stroke outcomes. Among these, endothelial dysfunction plays a particularly important role. Objective: To summarize current evidence regarding the role of endothelial dysfunction in the development of complications following reperfusion therapy in acute ischemic stroke and to assess the prospects of endothelium-protective strategies. Materials and methods: A literature review of publications from the last five years was conducted, including clinical studies, meta-analyses, and systematic reviews. Contemporary concepts of vascular endothelial injury, disruption of the blood–brain barrier, reperfusion injury, hemorrhagic transformation, and the “no-reflow” phenomenon (failure of microcirculation restoration) were analyzed. Laboratory and functional methods for evaluating endothelial function, including the EASIX index, were examined, and perspectives on endothelium-protective therapeutic approaches were outlined. Results: Endothelial dysfunction was associated with an increased risk of hemorrhagic transformation, cerebral edema, and microcirculatory failure following thrombolysis and mechanical thrombectomy. Patients with elevated soluble E‑selectin, von Willebrand factor, and symmetric dimethylarginine had worse functional outcomes, with favorable recovery (modified Rankin Scale 0–2) in 38 % compared with 64 % for lower biomarker levels (p < 0.01). In 325 patients undergoing thrombectomy, 12.6 % developed parenchymal hematoma, and higher endothelial dysfunction scores were independently associated with its occurrence (adjusted odds ratio 1.43; 95 % CI 1.03–1.99; p = 0.032), improving predictive performance of conventional risk models. These findings highlight endothelial dysfunction as a clinically relevant predictor of post-reperfusion complications. Conclusions: Endothelial dysfunction is an important pathogenetic factor influencing the risk of complications and the effectiveness of reperfusion interventions. Integrating endothelial function assessment into clinical protocols may contribute to personalized treatment strategies, improved therapeutic outcomes, and better prognosis in patients with acute ischemic stroke.