Endothelial glycocalyx dysfunction in the setting of mechanical thrombectomy: a conceptual link between cardiometabolic vulnerability and microvascular reperfusion failure
www.frontiersin.org
Nov. 3, 2026, 1:25 p.m.
Mechanical thrombectomy has revolutionized acute ischemic stroke treatment by enabling reopening of large vessels, yet angiographic success does not guarantee effective tissue-level reperfusion or oxygen delivery to brain tissue. This narrative review synthesizes literature from major databases through April 2026 to explore endothelial glycocalyx dysfunction as a critical interface linking pre-existing cardiometabolic vulnerabilities to post-thrombectomy microvascular complications. The authors examined evidence across human mechanical thrombectomy studies, biomarker analyses, imaging findings, and experimental models to elucidate how multiple stressors—including ischemic priming, reperfusion injury, oxidative stress, complement activation, and device-induced trauma—may converge on the endothelial surface. Glycocalyx dysfunction could amplify leukocyte adhesion, platelet aggregation, and blood-brain barrier destabilization, yet direct causal evidence in human mechanical thrombectomy remains absent. Circulating biomarkers such as syndecan-1, heparan sulfate, and hyaluronan represent systemic signals rather than direct cerebral glycocalyx measurements. The review emphasizes that post-thrombectomy microcirculatory rescue remains therapeutically targetable but requires integrated approaches combining compartment-specific biomarkers, advanced perfusion imaging, and tissue endpoints while accounting for individual cardiometabolic risk factors and competing microvascular mechanisms.