Interventional Cardiology. Группа авторов

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      69 69 Madamanchi NR and Runge MS. Mitochondrial dysfunction in atherosclerosis. Circ Res. 2007; 100:460–73.

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      71 71 Patetsios P, Song M, Shutze WP, et al. Identification of uric acid and xanthine oxidase in atherosclerotic plaque. Am J Cardiol. 2001; 88:188–91, A6.

      72 72 Bentzon JF, Otsuka F, Virmani R, Falk E. Mechanisms of plaque formation and rupture. Circ Res. 2014; 114:1852–66.

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      75 75 Saigusa R, Winkels H, Ley K. T cell subsets and functions in atherosclerosis. Nat Rev Cardiol. 2020; 17:387–401.

      76 76 Fernandez DM, Rahman AH, Fernandez NF, et al. Single‐cell immune landscape of human atherosclerotic plaques. Nat Med. 2019; 25:1576–1588.

      77 77 Galis ZS, Sukhova GK, Lark MW, Libby P. Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques. J Clin Invest. 1994; 94:2493–503.

      78 78 Schwartz RS, Topol EJ, Serruys PW, et al. Artery size, neointima, and remodeling: time for some standards. J Am Coll Cardiol. 1998; 32:2087–94.

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      80 80 Burke AP, Farb A, Malcom GT, et al. Coronary risk factors and plaque morphology in men with coronary disease who died suddenly. The N Engl J Med. 1997; 336:1276–82.

      81 81 Wang JC, Normand SL, Mauri L, Kuntz RE. Coronary artery spatial distribution of acute myocardial infarction occlusions. Circulation. 2004; 110:278–84.

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      84 84 Mauriello A, Sangiorgi G, Fratoni S, et al. Diffuse and active inflammation occurs in both vulnerable and stable plaques of the entire coronary tree: a histopathologic study of patients dying of acute myocardial infarction. J Am Coll Cardiol. 2005; 45:1585–93.

      85 85 Spagnoli LG, Bonanno E, Mauriello A, et al. Multicentric inflammation in epicardial coronary arteries of patients dying of acute myocardial infarction. J Am Coll Cardiol. 2002; 40:1579–88.

      86 86 Buffon A, Biasucci LM, Liuzzo G, et al. Widespread coronary inflammation in unstable angina. N Engl J Med. 2002; 347:5–12.

      87 87 Goldstein JA, Demetriou D, Grines CL, et al. Multiple complex coronary plaques in patients with acute myocardial infarction. N Engl J Med. 2000; 343:915–22.

      88 88 Kolodgie FD, Burke AP, Farb A, et al. The thin‐cap fibroatheroma: a type of vulnerable plaque: the major precursor lesion to acute coronary syndromes. Curr Opin Cardiol. 2001; 16:285–92.

      89 89 Kolodgie FD, Gold HK, Burke AP, et al. Intraplaque hemorrhage and progression of coronary atheroma. N Engl J Med. 2003; 349:2316–25.

      90 90 van der Wal AC, Becker AE, van der Loos CM, Das PK. Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology. Circulation. 1994; 89:36–44.

      91 91 Mittleman MA, Mostofsky E. Physical, psychological and chemical triggers of acute cardiovascular events: preventive strategies. Circulation. 2011; 124:346–54.

      92 92 Widlansky ME, Gokce N, Keaney JF, Jr., Vita JA. The clinical implications of endothelial dysfunction. J Am Coll Cardiol. 2003; 42:1149–60.

      93 93 Benagiano M, D'Elios MM, Amedei A, et al. Human 60‐kDa heat shock protein is a target autoantigen of T cells derived from atherosclerotic plaques. Journal of Immunology. 2005; 174:6509–17.

      94 94 Ludwig A, Berkhout T, Moores K, et al. Fractalkine is expressed by smooth muscle cells in response to IFN‐gamma and TNF‐alpha and is modulated by metalloproteinase activity. Journal of Immunology. 2002; 168:604–12.

      95 95 Fong AM, Robinson LA, Steeber DA, et al. Fractalkine and CX3CR1 mediate a novel mechanism of leukocyte capture, firm adhesion, and activation under physiologic flow. The Journal of Experimental Medicine. 1998; 188:1413–9.

      96 96 Pasterkamp G, den Ruijter HM, Libby P. Temporal shifts in clinical presentation and underlying mechanisms of atherosclerotic disease. Nat Rev Cardiol. 2017; 14:21–29.

      97 97 Quillard T, Franck G, Mawson T, et al. Mechanisms of erosion of atherosclerotic plaques. Curr Opin Lipidol. 2017; 28:434–441.

      98 98 Hao H, Gabbiani G, Camenzind E, Bacchetta M, et al. Phenotypic modulation of intima and media smooth muscle cells in fatal cases of coronary artery lesion. Arterioscler Thromb Vasc Biol. 2006; 26:326–32.

      99 99 Finn AV, Otsuka F. Neoatherosclerosis: a culprit in very late stent thrombosis. Circ Cardiovasc Interv. 2012; 5:6–9.

      100 100 Nakazawa G, Otsuka F, Nakano M, et al. The pathology of neoatherosclerosis in human coronary implants bare‐metal and drug‐eluting stents. J Am Coll Cardiol. 2011; 57:1314–22.

      101 101 Park SJ, Kang SJ, Virmani R, et al. In‐stent neoatherosclerosis: a final common pathway of late stent failure. J Am Coll Cardiol. 2012; 59:2051–7.

      102 102 Inoue K, Abe K, Ando K, et al. Pathological analyses of long‐term intracoronary Palmaz‐Schatz stenting; Is its efficacy permanent? Cardiovasc Pathol. 2004; 13:109–15.

      103 103 Nakazawa G, Vorpahl M, Finn AV, et al. One step forward and two steps back with drug‐eluting‐stents: from preventing restenosis to causing late thrombosis and nouveau atherosclerosis. JACC Cardiovasc Imaging. 2009; 2:625–8.

      104 104 Kang SJ, Lee CW, Song H, et al. OCT analysis in patients with very late stent thrombosis. JACC Cardiovasc Imaging. 2013; 6:695–703.

      105 105 Virmani R, Burke AP, Kolodgie FD, Farb A. Vulnerable plaque: the pathology of unstable coronary lesions. J Interv Cardiol. 2002; 15:439–46.

      106 106 Shishikura D, Kataoka Y, Di Giovanni G, et al. Progression of ultrasound plaque attenuation and low echogenicity associates with major adverse cardiovascular events. Eur Heart J. 2020.

      107 107 Wu X, Mintz GS, Xu K, et al. The Relationship Between Attenuated Plaque Identified by Intravascular