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.
Kistler JP, Furie KL. Strategic Location of Large-Vessel Atherothrombotic Cerebral Vascular Disease. Arch Neurol. 1999;56(11):1329-1330. doi:10.1001/archneur.56.11.1329