The underlying pathophysiology and determinants of the velocity of infarction are complex and multifactorial, but cumulative evidence suggests that an interplay between energy supply and energy demand in the hypoperfused tissue sets the pace of the infarct growth. Thus, large potential exists for creative diagnostics, therapeutics, and ideally, theranostics for ELVO. In this paradigm, it is critical to identify factors associated with slow vs fast infarct growth, and to deliver early individualized therapeutics to slow penumbral loss. It should also be recognized that some patients achieve favorable outcomes despite large volumes of infarct, whereas some patients develop significant disability despite small infarct volumes. Furthermore, about 50% of patients undergoing EVT do not achieve good outcome despite successful recanalization, mainly due to fast progression of penumbral tissue loss. However, a considerable number of patients with stroke with ELVO are not candidates for EVT at the time of presentation due to a large core infarct. The more recent DAWN and DEFUSE-3 trials extended the endovascular treatment window up to 24 hours following symptom onset based on advanced imaging studies. 1 Endovascular therapy (EVT) is a highly effective treatment that has dramatically affected outcomes following ELVO. Glossary CBF = cerebral blood flow CTA = CT angiography ELVO = emergent large vessel occlusion EVT = endovascular therapy MCA = middle cerebral artery SPGS = sphenopalatine ganglion stimulationĮmergent large vessel occlusion (ELVO) comprises about 30%–40% of acute ischemic strokes and is responsible for 90% rate of functional loss and 20% mortality in 3 months if left untreated.
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