Introduction The interplay between thrombectomy-related infarct volume reduction, post-acute neurological improvement and functional outcome has been described[1-4]. However, pathophysiological mechanisms might be different in patients with large established infarcts.

Aim of Study To evaluate how much of the thrombectomy-related treatment effect is explained by follow-up infarct volume and the post-acute neurological status in patients with large ischemic core enrolled in the TENSION RCT[5]. We hypothesize that the proportion of the treatment effect explained by infarct volume reduction is lower in patients with established large infarctions.

Methods Main inclusion criteria of the TENSION RCT were anterior circulation stroke and ASPECTS 3-5. All patients with availability of relevant data points were included. Two causal treatment effect models (ordinal logistic regression) were defined to quantify the effect of endovascular therapy on improvement in functional outcome (90d-mRS) explained by a) follow-up infarct volume and b) 24h-NIHSS.

Results 188 patients were included (table 1). For both models, MT was associated with a 25 percentage-points higher probability of 90d-mRS 1-4 (cumulative treatment effects mRS 1-4, figure 1). Follow-up infarct volume explained 28% and 24h-NIHSS explained 64% of the MT-related improvement in functional outcome.

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Abstract P018 Figure 1

Causal treatment effect model results with mediation through follow-up infarct volume and 24h NIHSS

Conclusion In patients with large established infarct core, follow-up infarct volume explained 28% of the MT-related improvement in functional outcome, while NIHSS at 24h reflected 64% of the effect. Compared to follow-up infarct volume, other pathophysiological factors such as topography, selective neuronal loss, neural plasticity and effectivness of rehabilitation may play a more important role in outcomes of patients with large established infarct cores.