Investigating Biological Mechanisms of Post-Thrombectomy Cerebral Hypoperfusion

In the case of acute ischemic stroke related to proximal occlusion of a cerebral artery, the standard current treatment is mechanical thrombectomy, which allows arterial recanalization in 85% of patients. However, approximately half of the patients with effective arterial recanalization still experience significant neurological sequelae or die. One potential explanation for this poor prognosis is the persistence of post-thrombectomy parenchymal hypoperfusion despite arterial recanalization, a phenomenon which is well-studied and potentially treatable in animals but poorly understood in humans. The aim of my work in the Stanford Stroke Center will be to identify biological markers associated with the occurrence of cerebral hypoperfusion after mechanical thrombectomy in humans. Biological and radiological data from a prospective cohort of patients treated for ischemic stroke by thrombectomy, who underwent pre- and post-thrombectomy blood sampling and systematic cerebral perfusion imaging by MRI immediately and at 24 hours post-thrombectomy, will be analyzed. I will also analyze the clinical impact of the cerebral hypoperfusion and biological markers on the three-month functional prognosis of the stroke. This study could help better understand the pathophysiology of post-thrombectomy cerebral hypoperfusion and eventually lead to the development of adjunctive treatments to thrombectomy aimed at improving the clinical prognosis of stroke patients.