Microcirculatory failure after successful recanalization in ischemic stroke: insights into mechanisms, imaging, and therapeutic strategies.

Early, effective reopening of an occluded large artery is a cornerstone of modern ischemic stroke care. Yet angiographic success does not consistently translate into tissue level reperfusion, nor does it reliably forecast good neurological recovery. Futile recanalization is multifactorial, and in many patients poor outcome may also reflect extensive irreversible injury already present at the time of recanalization because reopening is achieved too late to rescue substantial tissue. A growing body of work suggests that persistent microcirculatory dysfunction after recanalization may represent one important contributor to this discordance. In the post-recanalization setting, microvascular failure reflects intertwined ischemia-reperfusion processes: oxidative stress, inflammatory activation, endothelial injury, microthrombosis, and pericyte-driven capillary constriction, that together degrade capillary perfusion and exchange. As a result, tissue hypoxia can persist and the infarct core may continue to expand even when large-vessel patency has been restored. Experimental studies and emerging clinical observations, including trials of adjunct intra-arterial thrombolysis, increasingly support the idea that resolving residual microvascular obstruction can yield functional benefits beyond macrorecanalization alone. In parallel, progress in microcirculation imaging and monitoring, ranging from high-resolution optical tools in experimental models to angiography- and perfusion-derived metrics in patients, has strengthened