Imaging Plaque Inflammation in Higher-Risk Patients: What Do We Know and What Are We Looking For?

被引：0
作者：
Ishai A. [1 ]
Tawakol A. [1 ,2 ]
机构：
[1] Cardiac MR PET CT Program, Department of Imaging, Massachusetts General Hospital and Harvard Medical School Boston, 165 Cambridge Street, Suite 400, Boston, 02114-2750, MA
[2] Cardiology Division, Massachusetts General Hospital and Harvard Medical School Boston, 165 Cambridge Street, Suite 400, Boston, 02114-2750, MA
来源：
Current Cardiovascular Risk Reports | 2015年 / 9卷 / 6期
关键词：
Atherosclerosis; FDG-PET; Inflammation;
D O I：
10.1007/s12170-015-0459-0
中图分类号：
学科分类号：
摘要：
Atherosclerosis is a chronic inflammatory condition complicating cholesterol accumulation within the artery wall. Inflammation is believed to play an important role in the formation, progression, and ultimately the rupture of atherosclerotic plaques (the principle event leading to most myocardial infarctions and strokes). An enhanced understanding of the inflammatory process within the atheroma may therefore facilitate risk stratification and treatment strategies. Molecular imaging techniques such as PET/CT have the ability to quantify arterial inflammation and assess the high-risk features of atheromas thus may be useful for identifying patients who are at higher risk for an atherothrombotic event. In this review, we focus on the potential of FDG-PET/CT as a tool to measure arterial inflammation, enhance risk stratification, and to evaluate novel therapies directed against atherosclerotic disease. Additionally, this review will provide a discussion on current challenges as well as future directions. © 2015, Springer Science+Business Media New York.
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页码：1 / 8
页数：7
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共 65 条
  • [1] Lozano R., Naghavi M., Foreman K., Lim S., Shibuya K., Aboyans V., Et al., Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010, Lancet, 380, 9859, pp. 2095-2128, (2012)
  • [2] Sanz J., Fayad Z.A., Imaging of atherosclerotic cardiovascular disease, Nature, 451, 7181, pp. 953-957, (2008)
  • [3] Libby P., Inflammation in atherosclerosis, Nature, 420, 6917, pp. 868-874, (2002)
  • [4] Moore K.J., Tabas I., Macrophages in the pathogenesis of atherosclerosis, Cell, 145, 3, pp. 341-355, (2011)
  • [5] Cai J., Hatsukami T.S., Ferguson M.S., Kerwin W.S., Saam T., Chu B., Et al., In vivo quantitative measurement of intact fibrous cap and lipid-rich necrotic core size in atherosclerotic carotid plaque: comparison of high-resolution, contrast-enhanced magnetic resonance imaging and histology, Circulation, 112, 22, pp. 3437-3444, (2005)
  • [6] Motoyama S., Sarai M., Harigaya H., Anno H., Inoue K., Hara T., Et al., Computed tomographic angiography characteristics of atherosclerotic plaques subsequently resulting in acute coronary syndrome, J Am Coll Cardiol, 54, 1, pp. 49-57, (2009)
  • [7] Obaid D.R., Calvert P.A., Gopalan D., Parker R.A., Hoole S.P., West N.E., Et al., Atherosclerotic plaque composition and classification identified by coronary computed tomography: assessment of computed tomography-generated plaque maps compared with virtual histology intravascular ultrasound and histology, Circ Cardiovasc Imaging, 6, 5, pp. 655-664, (2013)
  • [8] Falk E., Shah P.K., Fuster V., Coronary plaque disruption, Circulation, 92, 3, pp. 657-671, (1995)
  • [9] Maddox T.M., Stanislawski M.A., Grunwald G.K., Bradley S.M., Ho P.M., Tsai T.T., Et al., Nonobstructive coronary artery disease and risk of myocardial infarction, Jama, 312, 17, pp. 1754-1763, (2014)
  • [10] Li H., Cybulsky M.I., Gimbrone M.A., Libby P., An atherogenic diet rapidly induces VCAM-1, a cytokine-regulatable mononuclear leukocyte adhesion molecule, in rabbit aortic endothelium, Arterioscler Thromb J Vasc Biol Am Heart Assoc, 13, 2, pp. 197-204, (1993)
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