Abstract
Approximately 15% of patients undergoing endovascular thrombectomy for anterior circulation acute ischemic stroke have a tandem lesion, defined as a severe stenosis or occlusion of the cervical internal carotid artery ipsilateral to its intracranial occlusion. Patients with tandem lesions have worse outcomes than patients with isolated intracranial occlusions, but the optimal management of their carotid lesions during endovascular thrombectomy remains controversial. The main options commonly used in current practice include acute stent placement in the carotid lesion versus thrombectomy alone without definitive revascularization of the carotid artery. While treatment decisions for these patients are often complex and strategies vary according to clinical, anatomic, and technical considerations, only results from randomized trials comparing these approaches are likely to strengthen current recommendations and optimize patient care.
Highlights
Studies of patients with tandem lesion (TL) have generally included more men than women,[2] which likely reflects a true difference in the prevalence of carotid atherosclerosis according to sex.[3]
Ischemia, usually due to impaired carotid artery territory perfusion rather than intracranial clot embolization. These patients are infrequent in the setting of acute ischemic stroke (AIS), generally have a more favorable prognosis than patients with TLs, and are less often considered for endovascular thrombectomy (EVT), given the absence of an intracranial occlusion.[14]
In cases of chronic cervical internal carotid artery (c-ICA) occlusions with recurrent embolic or hemodynamic ischemia, randomized trials have demonstrated that extracranial-to-intracranial arterial bypass procedures are not useful, so this delayed approach is not recommended.[49,50]
Summary
Received February 23, 2020; accepted after revision March 17. From the Departments of Medicine (Neurology) (A.Y.P., G.J., C.S.), and Radiology (Neuroradiology) (D.R.), Centre Hospitalier de l’Université de Montréal, Montréal, Québec, Canada; Neurovascular Group (A.Y.P., G.J., C.S.), Axe Neurosciences, Centre de Recherche du Centre Hospitalier de l’Université de Montréal, Montréal, Québec, Canada; Stroke Center (L.D.), Department of Neurology, Neurological Hospital, Hospices Civils de Lyon, Lyon, France; and EA 7425 HESPER (L.D.), Health Services and Performance Research, Claude Bernard Lyon 1 University, Lyon, France. Published series of acute TLs suggest that about 60%–70% are due to atherosclerotic plaque; 20%–30%, due to dissection; and the remainder, attributable to carotid webs and cardiac emboli.[2,7] In this last group, a large cardiac embolus presumably lodges in the c-ICA (possibly due to underlying atherosclerotic stenosis) and fragments to embolize in the intracranial circulation. Radiologic differentiation of these various etiologies of carotid stenosis is possible and does not necessarily require conventional angiography. Patients with dissection may be distinguished from those with atherosclerotic plaque as having different pathologies with potentially different treatment approaches and prognoses.[15]
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