Ischemia-Reperfusion Injury After Endovascular Thrombectomy for Ischemic Stroke

But you didn't keep going and determine the neuronal cascade of death injury in the first week. You missed the elephant in the room. You also didn't quantify how many millions of neurons are in that .9 ml area that expanded the lesion. You put that off as inconsequential.  Good, let's take that many millions from your brain and see how you feel about it then. 

Ischemia-Reperfusion Injury After Endovascular Thrombectomy for Ischemic Stroke

Maxime Gauberti

,

Bertrand Lapergue

,

Sara Martinez de Lizarrondo

,

Denis Vivien

,

Sébastien Richard

,

Serge Bracard

,

Michel Piotin

, and

Benjamin Gory

Originally published24 Oct 2018Stroke. 2018;0:STROKEAHA.118.022015

Abstract

Background and Purpose—

In experimental models of ischemic stroke, abrupt reperfusion is associated with secondary brain damages, responsible for up to 70% of the final lesion size. Whether this remains true in humans is unknown.

Methods—

Using data from the ASTER randomized trial (Aspiration vs Stent Retriever for Successful Revascularization), we investigated the effect of complete reperfusion (defined as a modified Thrombolysis In Cerebral Infarction 3) after endovascular thrombectomy on early lesion growth as assessed by diffusion-weighted imaging at baseline and 1 day after reperfusion.

Results—

Among 381 patients included in the trial, 35 achieved complete reperfusion, benefited from both baseline and day 1 diffusion-weighted imaging, lacked significant hemorrhagic transformation, and were, therefore, included in the present study. We found that the median growth of the ischemic lesion between baseline and day 1 was only 0.9 mL after complete reperfusion, representing <4% of the mean lesion size. The actual lesion growth occurring after reperfusion is probably even smaller because this lesion growth occurred, at least in part, between baseline imaging and complete reperfusion, as demonstrated by a statistically significant positive correlation between imaging-to-reperfusion time and lesion growth (R²=0.116; P=0.048).

Conclusions—

There is no significant lesion growth after complete reperfusion in most patients. This important discrepancy between clinical and preclinical pathophysiologies should be considered during preclinical evaluation of neuroprotective strategies.