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High-Risk Atherosclerotic Plaques Mechanisms, Imaging, by Levon Michael Khachigian

By Levon Michael Khachigian

Susceptible plaque improvement is the results of a fancy sequence of molecular and mobile occasions related to irritation, apoptosis, rupture, and thrombosis. an in depth figuring out of the mechanisms underlying the improvement of high-risk plaques, in addition to the power to imagine and diagnose those susceptible lesions, will bring about the potent administration of acute coronary syndromes.
High-Risk Atherosclerotic Plaques: Mechanisms, Imaging, versions, and remedy brings jointly well timed, in-depth reports by way of popular foreign cardiologists and scientists. Chapters hide the definition, constitution, and mobile and molecular mechanisms of excessive hazard plaque improvement, in addition to animal versions of weak plaque, plaque imaging, and present and destiny treatments. health workers speak about intravascular ultrasound, optimum coherence tomography, magnetic resonance imaging, and coronary thermography. the ultimate bankruptcy studies either present and destiny neighborhood and systematic thoughts for the healing administration of susceptible plaque.
Exploring all elements of this first explanation for acute coronary syndromes, this informative ebook updates our wisdom at the detection and remedy of susceptible plaques. it's a precious source which can vastly boost the growth in remedy and prevention.

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Circulation 2000, 101: 841–843. 9. Kolodgie FD, Narula J, Burke AP, Haider N, Farb A, Hui-Liang Y, Smialek J, and Virmani R. Localization of apoptotic macrophages at the site of plaque rupture in sudden coronary death. Am J Pathol 2000, 157: 1259–1268. 10. Tricot O, Mallat Z, Heymes C, Belmin J, Leseche G, and Tedgui A. Relation between endothelial cell apoptosis and blood flow direction in human atherosclerotic plaques. Circulation 2000, 101: 2450–2453. 11. Libby P. Inflammation in atherosclerosis.

Fas, the prototypic member of the tumor necrosis factor death receptor family, binds to its cognate ligand. Recruitment of the adapter molecule FADD and procaspase-8 results in activation of the latter. Caspase-8 activation directly activates downstream caspases (-3, -6, and -7) and results in DNA fragmentation and cleavage of cellular proteins. This pathway is thought to occur in type I cells and does not involve mitochondrial pathways. 2). 5 APOPTOSIS OF VSMCs VSMCs in normal vessel walls demonstrate little if any basal cell proliferation or apoptosis.

Arterioscler Thromb Vasc Biol 2001, 21: 955–960. 55. Martinet W, Knaapen MW, De Meyer GR, Herman AG, and Kockx MM. Oxidative DNA damage and repair in experimental atherosclerosis are reversed by dietary lipid lowering. Circ Res 2001, 88: 733–739. 56. Berceli SA, Davies MG, Kenagy RD, and Clowes AW. Flow-induced neointimal regression in baboon polytetrafluoroethylene grafts is associated with decreased cell proliferation and increased apoptosis. J Vasc Surg 2002, 36: 1248–1255. 57. Kraemer R. Reduced apoptosis and increased lesion development in the flowrestricted carotid artery of p75(NTR)-null mutant mice.

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