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      Intracranial atherosclerosis: Review of imaging features and advances in diagnostics

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          Abstract

          Intracranial atherosclerotic disease is one of the leading causes of ischemic strokes and poses a moderate risk of recurrence. Diagnosis is currently limited to stenosis on luminal imaging, which likely underestimates the true prevalence of the disease. Detection of non-stenosing intracranial atherosclerosis is important in order to optimize secondary stroke prevention strategies. This review collates findings from the early seminal trials and the latest studies in advanced radiological techniques that characterize symptomatic intracranial atherosclerotic disease across various imaging modalities. While computed tomography angiography (CTA) and magnetic resonance angiography (MRA) comprise diagnostic mainstays in identifying stenotic changes secondary to atherosclerosis, emerging techniques such as high-resolution MRA, quantitative MRA, and computational fluid dynamics may reveal a myriad of other underlying pathophysiological mechanisms.

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          Mechanisms of plaque formation and rupture.

          Jacob Fog Bentzon, Fumiyuki Otsuka, Renu Virmani … (2014)
          Atherosclerosis causes clinical disease through luminal narrowing or by precipitating thrombi that obstruct blood flow to the heart (coronary heart disease), brain (ischemic stroke), or lower extremities (peripheral vascular disease). The most common of these manifestations is coronary heart disease, including stable angina pectoris and the acute coronary syndromes. Atherosclerosis is a lipoprotein-driven disease that leads to plaque formation at specific sites of the arterial tree through intimal inflammation, necrosis, fibrosis, and calcification. After decades of indolent progression, such plaques may suddenly cause life-threatening coronary thrombosis presenting as an acute coronary syndrome. Most often, the culprit morphology is plaque rupture with exposure of highly thrombogenic, red cell-rich necrotic core material. The permissive structural requirement for this to occur is an extremely thin fibrous cap, and thus, ruptures occur mainly among lesions defined as thin-cap fibroatheromas. Also common are thrombi forming on lesions without rupture (plaque erosion), most often on pathological intimal thickening or fibroatheromas. However, the mechanisms involved in plaque erosion remain largely unknown, although coronary spasm is suspected. The calcified nodule has been suggested as a rare cause of coronary thrombosis in highly calcified and tortious arteries in older individuals. To characterize the severity and prognosis of plaques, several terms are used. Plaque burden denotes the extent of disease, whereas plaque activity is an ambiguous term, which may refer to one of several processes that characterize progression. Plaque vulnerability describes the short-term risk of precipitating symptomatic thrombosis. In this review, we discuss mechanisms of atherosclerotic plaque initiation and progression; how plaques suddenly precipitate life-threatening thrombi; and the concepts of plaque burden, activity, and vulnerability. © 2014 American Heart Association, Inc.
          Article 0 comments Cited 468 times – based on 0 reviews     Review now
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            Stenting versus aggressive medical therapy for intracranial arterial stenosis.

            Marc I Chimowitz, Michael J Lynn, Colin Derdeyn … (2011)
            Atherosclerotic intracranial arterial stenosis is an important cause of stroke that is increasingly being treated with percutaneous transluminal angioplasty and stenting (PTAS) to prevent recurrent stroke. However, PTAS has not been compared with medical management in a randomized trial. We randomly assigned patients who had a recent transient ischemic attack or stroke attributed to stenosis of 70 to 99% of the diameter of a major intracranial artery to aggressive medical management alone or aggressive medical management plus PTAS with the use of the Wingspan stent system. The primary end point was stroke or death within 30 days after enrollment or after a revascularization procedure for the qualifying lesion during the follow-up period or stroke in the territory of the qualifying artery beyond 30 days. Enrollment was stopped after 451 patients underwent randomization, because the 30-day rate of stroke or death was 14.7% in the PTAS group (nonfatal stroke, 12.5%; fatal stroke, 2.2%) and 5.8% in the medical-management group (nonfatal stroke, 5.3%; non-stroke-related death, 0.4%) (P=0.002). Beyond 30 days, stroke in the same territory occurred in 13 patients in each group. Currently, the mean duration of follow-up, which is ongoing, is 11.9 months. The probability of the occurrence of a primary end-point event over time differed significantly between the two treatment groups (P=0.009), with 1-year rates of the primary end point of 20.0% in the PTAS group and 12.2% in the medical-management group. In patients with intracranial arterial stenosis, aggressive medical management was superior to PTAS with the use of the Wingspan stent system, both because the risk of early stroke after PTAS was high and because the risk of stroke with aggressive medical therapy alone was lower than expected. (Funded by the National Institute of Neurological Disorders and Stroke and others; SAMMPRIS ClinicalTrials.gov number, NCT00576693.).
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              Intracranial Vessel Wall MRI: Principles and Expert Consensus Recommendations of the American Society of Neuroradiology.

              D.M. Mandell, M Mossa-Basha, Y Qiao … (2017)
              Intracranial vessel wall MR imaging is an adjunct to conventional angiographic imaging with CTA, MRA, or DSA. The technique has multiple potential uses in the context of ischemic stroke and intracranial hemorrhage. There remain gaps in our understanding of intracranial vessel wall MR imaging findings and research is ongoing, but the technique is already used on a clinical basis at many centers. This article, on behalf of the Vessel Wall Imaging Study Group of the American Society of Neuroradiology, provides expert consensus recommendations for current clinical practice.
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                Author and article information

                Contributors
                Journal
                Title: International Journal of Stroke
                Abbreviated Title: International Journal of Stroke
                Publisher: SAGE Publications
                ISSN (Print): 1747-4930
                ISSN (Electronic): 1747-4949
                Publication date Created: July 2022
                Publication date (Electronic): January 05 2022
                Publication date (Print): July 2022
                Volume: 17
                Issue: 6
                Pages: 599-607
                Affiliations
                [1 ]Vascular Neurology and Neurocritical Care, Sutter Health Comprehensive Stroke Care Center, San Francisco, CA, USA
                [2 ]Cardiovascular Research Institute of Vermont, The University of Vermont, Colchester, VT, USA
                [3 ]Neurosciences and Rehabilitation, Baystate Health, Springfield, MA, USA
                [4 ]Neurovascular Imaging Research Core and UCLA Stroke Center, Los Angeles, CA, USA
                Article
                DOI: 10.1177/17474930211066427
                PubMed ID: 34983259
                SO-VID: 2b9682a8-a436-4821-9271-ec19d9c29677
                Copyright © © 2022
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                http://journals.sagepub.com/page/policies/text-and-data-mining-license

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