Immunothrombosis may drive futile reperfusion in stroke

Mechanical thrombectomy has made angiographic reperfusion routine for large-vessel occlusion stroke, yet functional recovery remains inconsistent. Growing evidence links this therapeutic ceiling to the no-reflow phenomenon, defined as persistent tissue-level hypoperfusion despite proximal patency. No-reflow may arise from ischemia-reperfusion microvascular injury and distal microembolization, creating conditions that may promote immunothrombotic obstruction. Neutrophil-platelet cooperation, endothelial activation, and neutrophil extracellular traps represent candidate mechanisms linking capillary failure to futile reperfusion. Future trials should prospectively phenotype no-reflow with early perfusion imaging, integrate mechanistic biomarkers, and test microvascular-facing adjuncts that convert macrovascular recanalization into durable tissue reperfusion.