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Editorial
November 1999

Strategic Location of Large-Vessel Atherothrombotic Cerebral Vascular Disease

Author Affiliations
 

Copyright 1999 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.1999

Arch Neurol. 1999;56(11):1329-1330. doi:10.1001/archneur.56.11.1329

STROKE IS A heterogeneous disorder. Ischemic stroke, as identified in the National Institutes of Health Stroke Data Bank,1 can be classified into 3 basic pathologic stroke subtypes.2-5 They include embolic, accounting for 60% of all ischemic strokes; small-vessel lacunar, accounting for 25%; and large-vessel atherothrombotic, accounting for 15%. Large-vessel atherothrombotic stroke, or transient ischemic attack (TIA), is caused by either hemodynamic "low-flow" ischemia or "artery-to-artery" embolism, in which there is an interplay between local and systemic hemostatic mechanisms6-8 and the atheromatous plaque, similar to the interplay in atherothrombotic coronary artery disease. Vascular-bed–specific hemostasis6 may play a role in thrombosis of the intracranial and extracranial vessels; however, in embolic stroke, it operates only at the site of thrombus formation (ie, the heart or aortic arch). Therefore, it becomes important to think about large-vessel atherothrombotic disease leading to TIA or stroke as occurring at strategically important loci,2-5 just as in the coronary circulation. Acute therapies and preventive therapeutic strategies can and should be designed with specific pathophysiologic mechanisms in mind.

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