Abstract

See related article, pages 2379–2383. Unlike in acute myocardial infarction, the underlying pathophysiological mechanism of vascular arterial occlusion in acute stroke is heterogeneous. Composition of cerebral embolic material may vary, depending on specific endothelial and flow conditions of the embolic source. Old, platelet-rich, and well-organized thrombi formed under flow conditions have been shown to be more resistant to thrombolysis than fresh, fibrin- and red cell–rich clots formed under conditions of stasis.1 Moreover, clot structure may differ depending on whether the embolic source is a thrombus engrafted in a proximal atherosclerotic lesion or a clot formed in cardiac cavities. In this context, stroke subtypes may represent a surrogate of the composition of offending clot. Efforts to image intravascular thrombus in acute ischemic stroke have been increasingly done in the last years. In acute ischemic stroke, the presence of hyperattenuated middle cerebral artery sign on computed tomography indicates intraluminal clot with a high specificity but low sensitivity (47%).2 On MRI, vessel signs of arterial occlusion have been described as hyperintense vessel sign on fluid-attenuated …

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