Recanalisation therapy in patients with acute ischaemic stroke caused by large artery occlusion: choice of therapeutic strategy according to underlying aetiological mechanism?

Abstract

Various mechanisms underlie causative large artery occlusion (LAO) in patients with acute ischaemic stroke. Cardioembolic and atherosclerotic occlusions are the two most common types. The pathophysiological changes and responses to mechanical thrombectomy (MT) and antithrombotic treatments including thrombolysis, antiplatelet and anticoagulation therapy may vary among patients with different aetiological mechanisms of occlusion. Atherosclerotic occlusion is inclined to have relatively abundant collaterals and larger area of penumbra, hence a relatively wider time window for reperfusion therapy, while poor response to medical thrombolysis and MT. Severe residual stenosis and reocclusion occurred frequently after MT in atherosclerotic LAO. Angioplasty and stenting as rescue or the first-line therapy and more intensified antiplatelet therapy beyond related recommendations in the current guidelines are sometimes used in managing acute causative LAO because of poor recanalisation after recommended standard thrombolysis or MT therapy, which are usually based on individual experience. Standard protocol to establish emergent aetiological diagnosis of causative LAO and individualised aetiology-specific treatment strategy is needed.

Utility of Leptomeningeal Collaterals in Predicting Intracranial Atherosclerosis-Related Large Vessel Occlusion in Endovascular Treatment

“…This study was originally contrived from the necessity to enhance the preprocedural determination of occlusion pathomechanism in endovascular treatment of LVO. Because the optimal endovascular strategy—which includes selection of the most effective endovascular modality and when to switch from one modality to another—depends on the type of occlusion pathomechanism, the earlier determination of occlusion pathomechanism can be crucial in attaining significant recanalization [ 18 , 19 ]. However, unfortunately, there have been only a few practical factors identified that we can rely on to identify occlusion pathomechanism before an endovascular procedure.…”

Eprosartan: A closer insight into its neuroprotective activity in rats with focal cerebral ischemia–reperfusion injury

“…[8] Early reperfusion following ischemia triggers several oxidative, apoptotic, and inflammatory cellular responses leading to reperfusion injury. [9] Oxidative stress is believed to be the major event during this process because reperfusion stimulates an overproduction of a series of reactive oxygen species. [10] The inflammatory response following ischemic brain injury also plays a vital role in the pathogenesis of stroke.…”

Intracranial Atherosclerosis Burden and Stroke Recurrence for Symptomatic Intracranial Artery Stenosis (sICAS)

“…Therefore, recurrent risks in patients with mild stenosis need to be fully appreciated in future studies, so that high-risk patients would not be missed because of artificially graded severity of ICAS by the degree of luminal stenosis [13]. And then, different stroke mechanisms accompany with ICAS, and different aetiological mechanisms has significant clinical implications [15]. Recently study show Interleukin-33 (IL-33) and levels of fibrinogen after anticoagulation were related to ischemic stroke [16,17].…”