Abstract
Nonstenotic plaque (NSP) of a cervical artery feeding the territory of acute cerebral infarction is increasingly recognized as a cause of cryptogenic stroke. While these atherosclerotic lesions are not associated with significant luminal stenosis (<50%), the probability of finding such plaque exceeds chance and is more common in parent vessels rather than vessels supplying brain regions remote from infarction. More than 20%–30% of patients with unilateral hemispheric embolic stroke of undetermined source may be attributable to cervical internal or common carotid NSP. For these patients, randomized clinical trials have not shown a significant benefit of revascularization (endarterectomy or stenting), and optimal secondary prevention strategies rely on risk factor modification and antiplatelet therapy. Heightened awareness of this subtle finding may inform second‐tier diagnostic testing recommendations for occult stroke mechanisms (eg, monitoring for paroxysmal atrial fibrillation or hypercoagulability testing). Furthermore, recognition of NSP as a culprit lesion may lead to more targeted pharmacologic strategies aimed at stabilizing plaque. Recent guidelines have also incorporated evidence of plaque vulnerability (eg, intraplaque hemorrhage or lipid‐rich necrotic core) in decision making regarding revascularization approaches. In this review, the epidemiology and management of NSP in patients with cryptogenic embolic infarction is summarized, with an emphasis on recognition of NSP such that future clinical trials can be designed to test novel interventional strategies against current medical management of embolic stroke of undetermined source.
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