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No-reflow after recanalization in ischemic stroke: From pathomechanisms to therapeutic strategies
Abstract
Endovascular
reperfusion therapy is the primary strategy for acute ischemic stroke.
No-reflow is a common phenomenon, which is defined as the failure of
microcirculatory reperfusion despite clot removal by thrombolysis or
mechanical embolization. It has been reported that up to 25% of ischemic
strokes suffer from no-reflow, which strongly contributes to an
increased risk of poor clinical outcomes. No-reflow is associated with
functional and structural alterations of cerebrovascular
microcirculation, and the injury to the microcirculation seriously
hinders the neural functional recovery following macrovascular
reperfusion. Accumulated evidence indicates that pathology of no-reflow
is linked to adhesion, aggregation, and rolling of blood components
along the endothelium, capillary stagnation with neutrophils, astrocytes
end-feet, and endothelial cell edema, pericyte contraction, and
vasoconstriction. Prevention or treatment strategies aim to alleviate or
reverse these pathological changes, including targeted therapies such
as cilostazol, adhesion molecule blocking antibodies, peroxisome
proliferator-activated receptors (PPARs) activator, adenosine, pericyte
regulators, as well as adjunctive therapies, such as extracorporeal
counterpulsation, ischemic preconditioning, and alternative or
complementary therapies. Herein, we provide an overview of
pathomechanisms, predictive factors, diagnosis, and intervention
strategies for no-reflow, and attempt to convey a new perspective on the
clinical management of no-reflow post-ischemic stroke.
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