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 knowing of the mechanisms underlying the advance of high-risk plaques, besides the power to imagine and diagnose those weak lesions, will result in the potent administration of acute coronary syndromes.
High-Risk Atherosclerotic Plaques: Mechanisms, Imaging, versions, and remedy brings jointly well timed, in-depth studies by way of popular overseas cardiologists and scientists. Chapters hide the definition, constitution, and mobile and molecular mechanisms of excessive danger plaque improvement, in addition to animal versions of susceptible plaque, plaque imaging, and present and destiny remedies. health workers speak about intravascular ultrasound, optimum coherence tomography, magnetic resonance imaging, and coronary thermography. the ultimate bankruptcy experiences either present and destiny neighborhood and systematic suggestions for the healing administration of weak plaque.
Exploring all features of this first explanation for acute coronary syndromes, this informative booklet updates our wisdom at the detection and therapy of susceptible plaques. it's a helpful source which may vastly strengthen the growth in remedy and prevention.
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Additional resources for High-Risk Atherosclerotic Plaques Mechanisms, Imaging, Models, and Therapy
Sample text
1 Plaque rupture or erosion may lead to coronary artery occlusion resulting in myocardial infarction or, if repaired successfully, plaque growth. 5). The fibrous cap overlying the lipid-rich core is rich in VSMCs and loss of these cells at the plaque shoulders may contribute to rupture via loss of mechanical integrity. 7,8 These particles are increased in patients with unstable coronary disease, and account for the vast proportion of the pro-coagulant activity of the plaque. However, the majority of apoptotic cells at the site of rupture are macrophages,9 implicating macrophage apoptosis in plaque rupture.
Von der Thusen JH, van Vlijmen BJ, Hoeben RC, Kockx MM, Havekes LM, van Berkel TJ, and Biessen EA. Induction of atherosclerotic plaque rupture in apolipoprotein E–/– mice after adenovirus-mediated transfer of p53. Circulation 2002, 105: 2064–2070. fm Page 33 Wednesday, September 29, 2004 1:15 PM Apoptosis and Plaque Vulnerability 33 65. Majesky MW. Mouse model for atherosclerotic plaque rupture. Circulation 2002, 105: 2010–2011. 66. Davis BB, Dong Y, and Weiss RH. Overexpression of p73 causes apoptosis in vascular smooth muscle cells.
Inhibition of neointimal cell bcl-x expression induces apoptosis and regression of vascular disease. Nat Med 1998, 4: 222–227. 25. Pollman MJ, Hall JL, and Gibbons GH. Determinants of vascular smooth muscle cell apoptosis after balloon angioplasty injury: influence of redox state and cell phenotype. Circ Res 1999, 84: 113–121. 26. Malik N, Francis SE, Holt CM, Gunn J, Thomas GL, Shepherd L, Chamberlain J, Newman CMH, Cumberland DC, and Crossman DC. Apoptosis and cell proliferation after porcine coronary angioplasty.