Intracranial Atherosclerotic Disease: An Update

Zeenat Qureshi Stroke Research Center, University of Minnesota, Minneapolis, MN 55455, USA.
Annals of Neurology (Impact Factor: 11.91). 12/2009; 66(6):730-8. DOI: 10.1002/ana.21768
Source: PubMed

ABSTRACT The consensus conference on intracranial atherosclerosis provides a comprehensive review of the existing literature relevant to the epidemiology, diagnosis, prevention, and treatment of intracranial atherosclerosis, and identifies principles of management and research priorities. Patients who have suffered a stroke or transient ischemic attack attributed to stenosis (50-99%) of a major intracranial artery face a 12 to 14% risk for subsequent stroke during the 2-year period after the initial ischemic event, despite treatment with antithrombotic medications. The annual risk for subsequent stroke may exceed 20% in high-risk groups. In patients with intracranial atherosclerotic disease, short-term and long-term anticoagulation is not superior to antiplatelet treatment. Overall, the subgroup analyses from randomized trials provide evidence about benefit of aggressive atherogenic risk factor management. Intracranial angioplasty with or without stent placement has evolved as a therapeutic option for patients with symptomatic intracranial atherosclerotic disease, particularly those with high-grade stenosis with recurrent ischemic symptoms, medication failure, or both. A multicenter randomized trial is currently under way to compare stent placement with intense medical management for patients with high-grade symptomatic intracranial atherosclerotic disease.

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Available from: M. Fareed K Suri, Aug 11, 2015
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    • "Patients who experience a stroke or transient ischaemic attack due to a stenosis of 50% -99% have traditionally been treated with antithrombotic medication. Even with this treatment there remains a 12% -14% risk of further stroke in the subsequent 2 years, increasing to 20% in at-risk individuals [4]. Trials comparing antithrombotic medications with anticoagulants for prevention of stroke or vascular events have not generated satisfactory results and, worse still, have been associated with high rates of bleeding [5]. "
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    • "The cause of cerebral vasculopathy in children with SCA is not known, but pathologically, endothelial damage with intimal thickening and/or smooth muscle proliferation are seen within the larger arteries, with fibrin deposition, inflammatory changes and thrombus formation(Merkel, et al 1978, Rothman, et al 1986). Pathologically, this is quite different from the typical causes of cerebral vasculopathy in adult stroke, where there is intracranial atherosclerosis due to cholesterol-containing plaques(Qureshi, et al 2009). The most common locations for the vascular changes seen in SCA are branch points in the cerebral circulation, such as the supraclinoid (distal) ICA as it branches into the anterior cerebral and middle cerebral arteries(Kandeel, et al 1996). "
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    • "Neointima formation is an early step in the development of atherosclerotic plaques [13] [14]. Atherogenic lesions progress through a prolonged process of lipid accumulation and can trigger ischemic attack or stroke [15]. Recent studies indicate that PPARc antagonists are able to inhibit adipocyte differentiation. "
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