Use of Imaging to Select Patients for Late Window Endovascular Therapy

Gregory W. Albers, MD


Stroke. 2018;49(9):2256-2260. 

In This Article


Collaterals can be assessed noninvasively with either CT angiography or perfusion imaging. CT angiography was used in conjunction with Alberta Stroke Program Early CT (ASPECT) scores to select patients for the ESCAPE study (Endovascular Treatment for Small Core and Anterior Circulation Proximal Occlusion with Emphasis on Minimizing CT to Recanalization Times).[14] This trial enrolled 49 patients beyond 6 hours after stroke onset. The treatment effect in this group favored the endovascular thrombectomy group but was not statically significant in this small group of patients.

Studies have shown that both MRI and CTP maps can estimate the adequacy of the collateral circulation in acute stroke patients. Substantial delays in Tmax are typically because of poor collateral flow. For example, brain regions with >10 seconds of delay on Tmax are likely to have poor collateral flow. The ratio of the volume of tissue with Tmax >10 seconds compared with the Tmax >6 seconds volume is referred to as the hypoperfusion intensity ratio. A high hypoperfusion intensity ratio, such as ≈≥50%, correlates with poor angiographic collaterals, and these patients have larger baseline ischemic core volumes and more rapid infarct growth.[15] For thrombectomy candidates who are being transferred from a primary center to a comprehensive center, repeat imaging may be warranted for patients with poor collaterals, significant changes in neurological examination, or those with long transfer times. Recent data suggest that an hypoperfusion intensity ratio of >50% can identify patients who are likely to have substantial core growth during transfer.

Assessing the CBV within the ischemic lesion can also predict angiographic collaterals. By comparing the CBV within the Tmax lesion to the CBV in normally perfused brain regions, a relative CBV ratio can be obtained. Relative CBV has been shown to predict with angiographic collaterals and infarct growth.[16]