Intracranial Atherosclerotic Disease: An Update

Zeenat Qureshi Stroke Research Center, University of Minnesota, Minneapolis, MN 55455, USA.
Annals of Neurology (Impact Factor: 9.98). 12/2009; 66(6):730-8. DOI: 10.1002/ana.21768
Source: PubMed


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
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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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    ABSTRACT: Intracranial atherosclerotic disease (ICAD) represents a major cause of stroke and transient ischemic attacks. The prevalence and natural course of ICAD are closely related to race and ethnicity. The best treatment for ICAD is a crucial issue; data from recent trials indicate that aggressive medical management and life style modifications are better than endovascular treatments for prevention of recurrent stroke in high-risk patients with ICAD. Endovascular treatment is still an option for subgroup of patients who are not responded to optimal medical therapy.
    Full-text · Article · Jun 2014 · World Journal of Cardiovascular Diseases
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    • "Knowledge of the epidemiology of ICAD is limited.8 There have been no data on the prevalence of ICAD in large clinical trials, and data are limited regarding the prevalence of asymptomatic ICAD in the general population. "
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    ABSTRACT: The importance of intracranial atherosclerotic disease (ICAD) as a cause of stroke is underscored as compared to that of extracranial carotid stenosis and nonvalvular atrial fibrillation. Recent large clinical trials of ICAD, which evaluated the effectiveness of anticoagulation and stenting to prevent thromboembolism and restore hemodynamic compromise, failed to reduce major vascular events in patients with ICAD. These trials showed the importance of optimal control of risk factors to reduce major vascular events in these patients. Recent advances in risk factors for ICAD are summarized, together with possible reasons for race-ethnic differences in the prevalence of ICAD. In addition, the failure of the major clinical trials of ICAD may be caused by limitations in the understanding of ICAD. Unlike in patients with extracranial carotid stenosis or atrial fibrillation, stroke associated with ICAD occurs in association with various stroke mechanisms such as in situ thrombotic occlusion, artery-to-artery embolism, hemodynamic insufficiency, and branch occlusion. In clinical trials of ICAD, patients with all these types of ICAD were included. However, treatment effects may differ among the different types of ICAD. Treatment strategies might be selected based on clinical features (including the time after onset) and serologic and neuroimaging biomarkers (including diffusion-weighted image pattern and plaque images). Additional clinical trials considering these features are needed.
    Full-text · Article · Jan 2014
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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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    ABSTRACT: This review will focus on the strengths and limitations associated with the current standard of care for primary prevention of ischaemic strokes in children with sickle cell anaemia (SCA) - transcranial Doppler ultrasound (TCD) screening followed by regular blood transfusion therapy when TCD measurement is above a threshold defined by a randomized clinical trial (RCT). The theoretical basis for potential alternative strategies for primary prevention of neurological injury in SCA is also discussed. These strategies will include, but will not be limited to: immunizations to prevent bacterial infections, particularly in low income countries; management of elevated blood pressure; and targeted strategies to increase baseline haemoglobin levels with therapies such as hyroxycarbamide or potentially definitive haematopoietic stem cell transplant.
    Full-text · Article · Jan 2012 · British Journal of Haematology
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