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      Intracranial Artery Calcification and Its Clinical Significance

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          Abstract

          Intracranial arterial calcification (IAC) is an easily identifiable entity on plain head computed tomography scans. Recent studies have found high prevalence rates for IAC worldwide, and this may be associated with ischemic stroke and cognitive decline. Aging, traditional cardiovascular risk factors, and chronic kidney disease have been found to be associated with IAC. The severity of IAC can be assessed using different visual grading scales or various quantitative methods (by measuring volume or intensity). An objective method for assessing IAC using consistent criteria is urgently required to facilitate comparisons between multiple studies involving diverse populations. There is accumulating evidence from clinical studies that IAC could be utilized as an indicator of intracranial atherosclerosis. However, the pathophysiology underlying the potential correlation between IAC and ischemic stroke—through direct arterial stenosis or plaque stability—remains to be determined. More well-designed clinical studies are needed to explore the predictive values of IAC in vascular events and the underlying pathophysiological mechanisms.

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          Most cited references54

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          Atherosclerosis: Basic Mechanisms

          Circulation, 91(9), 2488-2496
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            Differential expression of bone matrix regulatory proteins in human atherosclerotic plaques.

            In the present study, we examined the expression of regulators of bone formation and osteoclastogenesis in human atherosclerosis because accumulating evidence suggests that atherosclerotic calcification shares features with bone calcification. The most striking finding of this study was the constitutive immunoreactivity of matrix Gla protein, osteocalcin, and bone sialoprotein in nondiseased aortas and the absence of bone morphogenetic protein (BMP)-2, BMP-4, osteopontin, and osteonectin in nondiseased aortas and early atherosclerotic lesions. When atherosclerotic plaques demonstrated calcification or bone formation, BMP-2, BMP-4, osteopontin, and osteonectin were upregulated. Interestingly, this upregulation was associated with a sustained immunoreactivity of matrix Gla protein, osteocalcin, and bone sialoprotein. The 2 modulators of osteoclastogenesis (osteoprotegerin [OPG] and its ligand, OPGL) were present in the nondiseased vessel wall and in early atherosclerotic lesions. In advanced calcified lesions, OPG was present in bone structures, whereas OPGL was only present in the extracellular matrix surrounding calcium deposits. The observed expression patterns suggest a tight regulation of the expression of bone matrix regulatory proteins during human atherogenesis. The expression pattern of both OPG and OPGL during atherogenesis might suggest a regulatory role of these proteins not only in osteoclastogenesis but also in atherosclerotic calcification.
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              The impact of calcification on the biomechanical stability of atherosclerotic plaques.

              Increased biomechanical stresses in the fibrous cap of atherosclerotic plaques contribute to plaque rupture and, consequently, to thrombosis and myocardial infarction. Thin fibrous caps and large lipid pools are important determinants of increased plaque stresses. Although coronary calcification is associated with worse cardiovascular prognosis, the relationship between atheroma calcification and stresses is incompletely described. To test the hypothesis that calcification impacts biomechanical stresses in human atherosclerotic lesions, we studied 20 human coronary lesions with techniques that have previously been shown to predict plaque rupture locations accurately. Ten ruptured and 10 stable lesions derived from post mortem coronary arteries were studied using large-strain finite element analysis. Maximum stress was not correlated with percentage of calcification, but it was positively correlated with the percentage of lipid (P:=0.024). When calcification was eliminated and replaced with fibrous plaque, stress changed insignificantly; the median increase in stress for all specimens was 0.1% (range, 0% to 8%; P:=0.85). In contrast, stress decreased by a median of 26% (range, 1% to 78%; P:=0.02) when lipid was replaced with fibrous plaque. Calcification does not increase fibrous cap stress in typical ruptured or stable human coronary atherosclerotic lesions. In contrast to lipid pools, which dramatically increase stresses, calcification does not seem to decrease the mechanical stability of the coronary atheroma.
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                Author and article information

                Journal
                J Clin Neurol
                J Clin Neurol
                JCN
                Journal of Clinical Neurology (Seoul, Korea)
                Korean Neurological Association
                1738-6586
                2005-5013
                July 2016
                04 May 2016
                : 12
                : 3
                : 253-261
                Affiliations
                [a ]Department of Medicine and Therapeutics, Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.
                [b ]Department of Neurology, The First Hospital of Jilin University, Jilin, China.
                Author notes
                Correspondence: Xiang-Yan Chen, MD. Department of Medicine and Therapeutics, Prince of Wales Hospital, 30-32 Ngan Shing Street, Shatin, New Territories, Hong Kong SAR. Tel +852 26352130, Fax +852 26493761, fionachen@ 123456cuhk.edu.hk
                Article
                10.3988/jcn.2016.12.3.253
                4960208
                27165425
                75fc1a5e-7b75-482d-89c8-e383a24f8186
                Copyright © 2016 Korean Neurological Association

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 02 November 2015
                : 20 December 2015
                : 21 December 2015
                Funding
                Funded by: Health and Medical Research Fund, CrossRef http://dx.doi.org/10.13039/501100005847;
                Award ID: 11120161
                Funded by: Shenzhen Science and Technology Innovation Committee;
                Award ID: JC20140606164105360
                Funded by: National Natural Science Foundation of China, CrossRef http://dx.doi.org/10.13039/501100001809;
                Award ID: 81371297
                Categories
                Review

                Neurology
                intracranial arterial calcification,ischemic stroke,computed tomography,risk factor,vascular stenosis

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