Читать книгу Interventional Cardiology - Группа авторов - Страница 47

1 1 Herrington W, Lacey B, Sherliker P, et al. Epidemiology of Atherosclerosis and the Potential to Reduce the Global Burden of Atherothrombotic Disease. Circ Res. 2016; 118:535–46.

2 2 Pahwa R and Jialal I. Atherosclerosis StatPearls Treasure Island (FL); 2020.

3 3 Wu MY, Li CJ, Hou MF and Chu PY. New Insights into the Role of Inflammation in the Pathogenesis of Atherosclerosis. Int J Mol Sci. 2017; 18.

4 4 Insull W, Jr. The pathology of atherosclerosis: plaque development and plaque responses to medical treatment. Am J Med. 2009; 122:S3–S14.

5 5 Forstermann U, Xia N, Li H. Roles of Vascular Oxidative Stress and Nitric Oxide in the Pathogenesis of Atherosclerosis. Circ Res. 2017; 120:713–735.

6 6 Libby P, Ridker PM, Hansson GK, Leducq Transatlantic Network on A. Inflammation in atherosclerosis: from pathophysiology to practice. J Am Coll Cardiol. 2009; 54:2129–38.

7 7 Libby P, Buring JE, Badimon L, Atherosclerosis. Nat Rev Dis Primers. 2019; 5:56.

8 8 Gimbrone MA, Jr., Garcia‐Cardena G. Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis. Circ Res. 2016; 118:620–36.

9 9 Ghattas A, Griffiths HR, Devitt A, Monocytes in coronary artery disease and atherosclerosis: where are we now? J Am Coll Cardiol. 2013; 62:1541–51.

10 10 Gimbrone MA, Jr., Garcia‐Cardena G. Vascular endothelium, hemodynamics, and the pathobiology of atherosclerosis. Cardiovasc Pathol. 2013; 22:9–15.

11 11 Davies PF. Flow‐mediated endothelial mechanotransduction. Physiol Rev. 1995; 75:519–60.

12 12 Gimbrone MA, Jr., Topper JN, Nagel T, Anderson KR and Garcia‐Cardena G. Endothelial dysfunction, hemodynamic forces, and atherogenesis. Ann N Y Acad Sci. 2000; 902:230–9; discussion 239–40.

13 13 Pober JS, Cotran RS. The role of endothelial cells in inflammation. Transplantation. 1990; 50:537–44.

14 14 Egan K, FitzGerald GA. Eicosanoids and the vascular endothelium. Handb Exp Pharmacol. 2006:189–211.

15 15 Pober JS, Sessa WC. Evolving functions of endothelial cells in inflammation. Nat Rev Immunol. 2007; 7:803–15.

16 16 Stevens T, Garcia JG, Shasby DM, Bhattacharya J and Malik AB. Mechanisms regulating endothelial cell barrier function. Am J Physiol Lung Cell Mol Physiol. 2000; 279:L419–22.

17 17 De Caterina R, Libby P, Peng HB, et al. Nitric oxide decreases cytokine‐induced endothelial activation. Nitric oxide selectively reduces endothelial expression of adhesion molecules and proinflammatory cytokines. J Clin Invest. 1995; 96:60–8.

18 18 Frangogiannis NG. Targeting the inflammatory response in healing myocardial infarcts. Curr Med Chem. 2006; 13:1877–93.

19 19 Gainetdinov RR, Premont RT, Bohn LM, et al. Desensitization of G protein‐coupled receptors and neuronal functions. Annu Rev Neurosci. 2004; 27:107–44.

20 20 Pober JS. Effects of tumour necrosis factor and related cytokines on vascular endothelial cells. Ciba Found Symp. 1987; 131:170–84.

21 21 Petrache I, Birukova A, Ramirez SI, et al. The role of the microtubules in tumor necrosis factor‐alpha‐induced endothelial cell permeability. Am J Respir Cell Mol Biol. 2003; 28:574–81.

22 22 Cybulsky MI, Gimbrone MA, Jr. Endothelial expression of a mononuclear leukocyte adhesion molecule during atherogenesis. Science. 1991; 251:788–91.

23 23 Osborn L, Hession C, Tizard R, et al. Direct expression cloning of vascular cell adhesion molecule 1, a cytokine‐induced endothelial protein that binds to lymphocytes. Cell. 1989; 59:1203–11.

24 24 Lambert JM, Lopez EF, Lindsey ML. Macrophage roles following myocardial infarction. Int J Cardiol. 2008; 130:147–58.

25 25 Frangogiannis NG, Mendoza LH, Ren G, et al. MCSF expression is induced in healing myocardial infarcts and may regulate monocyte and endothelial cell phenotype. Am J Physiol Heart Circ Physiol. 2003; 285:H483–92.

26 26 Hansson GK, Libby P. The immune response in atherosclerosis: a double‐edged sword. Nat Rev Immunol. 2006; 6:508–19.

27 27 Hansson GK, Libby P, Schonbeck U, Yan ZQ. Innate and adaptive immunity in the pathogenesis of atherosclerosis. Circ Res. 2002; 91:281–91.

28 28 Verma S, Devaraj S, Jialal I. Is C‐reactive protein an innocent bystander or proatherogenic culprit? C‐reactive protein promotes atherothrombosis. Circulation. 2006; 113:2135–50; discussion 2150.

29 29 Rader DJ, Daugherty A. Translating molecular discoveries into new therapies for atherosclerosis. Nature. 2008; 451:904–13.

30 30 Herder M, Arntzen KA, Johnsen SH, et al. Long‐term use of lipid‐lowering drugs slows progression of carotid atherosclerosis: the Tromso study 1994 to 2008. Arterioscler Thromb Vasc Biol. 2013; 33:858–62.

31 31 Puri R, Nissen SE, Shao M, et al. Antiatherosclerotic effects of long‐term maximally intensive statin therapy after acute coronary syndrome: insights from Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin Versus Atorvastatin. Arterioscler Thromb Vasc Biol. 2014; 34:2465–72.

32 32 Berneis KK, Krauss RM. Metabolic origins and clinical significance of LDL heterogeneity. J Lipid Res. 2002; 43:1363–79.

33 33 Rader DJ, Hovingh GK. HDL and cardiovascular disease. The Lancet. 2014; 384:618–625.

34 34 Barter PJ, Caulfield M, Eriksson M, et al. Effects of torcetrapib in patients at high risk for coronary events. N Engl J Med. 2007; 357:2109–22.

35 35 Toth PP, Barter PJ, Rosenson RS, et al. High‐density lipoproteins: a consensus statement from the National Lipid Association. J Clin Lipidol. 2013; 7:484–525.

36 36 Degoma EM, Rader DJ. Novel HDL‐directed pharmacotherapeutic strategies. Nat Rev Cardiol. 2011; 8:266–77.

37 37 Kratzer A, Giral H, Landmesser U. High‐density lipoproteins as modulators of endothelial cell functions: alterations in patients with coronary artery disease. Cardiovasc Res. 2014; 103:350–61.

38 38 Boren J, Williams KJ. The central role of arterial retention of cholesterol‐rich apolipoprotein‐B‐containing lipoproteins in the pathogenesis of atherosclerosis: a triumph of simplicity. Curr Opin Lipidol. 2016; 27:473–83.

39 39 Miller YI, Choi SH, Wiesner P et al. Oxidation‐specific epitopes are danger‐associated molecular patterns recognized by pattern recognition receptors of innate immunity. Circ Res. 2011; 108:235–48.

40 40 Navab M, Ananthramaiah GM, Reddy ST, et al. The oxidation hypothesis of atherogenesis: the role of oxidized phospholipids and HDL. J Lipid Res. 2004; 45:993–1007.

41 41 Linton MRF, Yancey PG, Davies SS, et al. The Role of Lipids and Lipoproteins in Atherosclerosis. In: KR Feingold, B Anawalt, A Boyce, et al. eds. Endotext South Dartmouth (MA); 2000.

42 42 Gistera A, Hansson GK. The immunology of atherosclerosis. Nat Rev Nephrol. 2017; 13:368–380.

43 43 Witztum JL, Steinberg D. The oxidative modification hypothesis of atherosclerosis: does it hold for humans? Trends Cardiovasc Med. 2001; 11:93–102.

44 44 Stocker R, Keaney JF, Jr. Role of oxidative modifications in atherosclerosis. Physiol Rev. 2004; 84:1381–478.

45 45 Quinn MT, Gauss KA. Structure and regulation of the neutrophil respiratory burst oxidase: comparison with nonphagocyte oxidases. J Leukoc Biol. 2004; 76:760–81.

46 46 Lambeth JD. NOX enzymes and the biology of reactive oxygen. Nat Rev Immunol. 2004; 4:181–9.

47 47 Octavia Y, Brunner‐La Rocca HP, Moens AL. NADPH oxidase‐dependent oxidative stress in the failing heart: From pathogenic roles to therapeutic approach. Free Radic Biol Med. 2012; 52:291–7.

48 48 Opitz N, Drummond GR, Selemidis S, et al. The 'A's and 'O's of NADPH oxidase regulation: a commentary on “Subcellular localization and function of alternatively spliced Noxo1 isoforms”. Free Radic Biol Med. 2007; 42:175–9.

49 49 Lyle AN, Griendling KK. Modulation of vascular smooth muscle signaling by reactive oxygen species. Physiology (Bethesda). 2006; 21:269–80.

50 50 Briones AM, Tabet F, Callera GE, et al. Differential regulation of Nox1, Nox2 and Nox4 in vascular smooth muscle cells from WKY and SHR. J Am Soc Hypertens. 2011; 5:137–53.

51 51 Akki A, Zhang M, Murdoch C, et al. NADPH oxidase signaling and cardiac myocyte function. J Mol Cell Cardiol. 2009; 47:15–22.

52 52 Kattoor AJ, Pothineni NVK, Palagiri D, Mehta JL. Oxidative Stress in Atherosclerosis. Curr Atheroscler Rep. 2017; 19:42.

53 53 Vendrov AE, Hakim ZS, Madamanchi NR, et al. Atherosclerosis is attenuated by limiting superoxide generation in both macrophages and vessel wall cells. Arterioscler Thromb Vasc Biol. 2007; 27:2714–21.

54 54 Forstermann U, Sessa WC. Nitric oxide synthases: regulation and function. Eur Heart J. 2012; 33:829–37, 837a–837d.

55 55 Khan BV, Harrison DG, Olbrych MT, et al. Nitric oxide regulates vascular cell adhesion molecule 1 gene expression and redox‐sensitive transcriptional events in human vascular endothelial cells. Proc Natl Acad Sci U S A. 1996; 93:9114–9.

56 56 Kubes P, Suzuki M, Granger DN. Nitric oxide: an endogenous modulator of leukocyte adhesion. Proc Natl Acad Sci U S A. 1991; 88:4651–5.

57 57 Zeiher AM, Fisslthaler B, Schray‐Utz B, Busse R. Nitric oxide modulates the expression of monocyte chemoattractant protein 1 in cultured human endothelial cells. Circ Res. 1995; 76:980–6.

58 58 Teplyakov AI. Endothelin‐1 involved in systemic cytokine network inflammatory response at atherosclerosis. Journal of cardiovascular pharmacology. 2004; 44 Suppl 1:S274–5.

59 59 Lerman A, Edwards BS, Hallett JW, et al. Circulating and tissue endothelin immunoreactivity in advanced atherosclerosis. N Engl J Med. 1991; 325:997–1001.

60 60 Dang A, Wang B, Li W, et al. Plasma endothelin‐1 levels and circulating endothelial cells in patients with aortoarteritis. Hypertension research: official journal of the Japanese Society of Hypertension. 2000; 23:541–4.

61 61 McCarron RM, Wang L, Stanimirovic DB, Spatz M. Endothelin induction of adhesion molecule expression on human brain microvascular endothelial cells. Neuroscience letters. 1993; 156:31–4.

62 62 Halim A, Kanayama N, el Maradny E, et al. Coagulation in vivo microcirculation and in vitro caused by endothelin‐1. Thrombosis research. 1993; 72:203–9.

63 63 Li H, Forstermann U. Uncoupling of endothelial NO synthase in atherosclerosis and vascular disease. Curr Opin Pharmacol. 2013; 13:161–7.

64 64 Antoniades C, Shirodaria C, Crabtree M, et al. Altered plasma versus vascular biopterins in human atherosclerosis reveal relationships between endothelial nitric oxide synthase coupling, endothelial function, and inflammation. Circulation. 2007; 116:2851–9.

65 65 Porkert M, Sher S, Reddy U, et al. Tetrahydrobiopterin: a novel antihypertensive therapy. J Hum Hypertens. 2008; 22:401–7.

66 66 Stroes E, Kastelein J, Cosentino F, et al. Tetrahydrobiopterin restores endothelial function in hypercholesterolemia. J Clin Invest. 1997; 99:41–6.

67 67 Thum T, Fraccarollo D, Schultheiss M, et al. Endothelial nitric oxide synthase uncoupling impairs endothelial progenitor cell mobilization and function in diabetes. Diabetes. 2007; 56:666–74.

68 68 Ueda S, Matsuoka H, Miyazaki H, et al. Tetrahydrobiopterin restores endothelial function in long‐term smokers. J Am Coll Cardiol. 2000; 35:71–5.

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

70 70 Nishino T, Okamoto K, Eger BT, et al. Mammalian xanthine oxidoreductase – mechanism of transition from xanthine dehydrogenase to xanthine oxidase. FEBS J. 2008; 275:3278–89.

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.

73 73 Kragel AH, Reddy SG, Wittes JT, Roberts WC. Morphometric analysis of the composition of atherosclerotic plaques in the four major epicardial coronary arteries in acute myocardial infarction and in sudden coronary death. Circulation. 1989; 80:1747–56.

74 74 Clinton SK, Underwood R, Hayes L, et al. Macrophage colony‐stimulating factor gene expression in vascular cells and in experimental and human atherosclerosis. The American Journal of Pathology. 1992; 140:301–16.

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.

79 79 Falk E, Nakano M, Bentzon JF, et al. Update on acute coronary syndromes: the pathologists' view. Eur Heart J. 2013; 34:719–28.

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.

82 82 Fuster V, Badimon L, Badimon JJ, Chesebro JH. The pathogenesis of coronary artery disease and the acute coronary syndromes (1). N Engl J Med. 1992; 326:242–50.

83 83 Davies MJ. Stability and instability: two faces of coronary atherosclerosis. The Paul Dudley White Lecture 1995. Circulation. 1996; 94:2013–20.

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 Ultrasound and No‐Reflow After Stenting in Acute Myocardial Infarction. The HORIZONS‐AMI (Harmonizing Outcomes With Revascularization and Stents in Acute Myocardial Infarction) Trial. 2011; 4:495–502.

108 108 Yamagishi M, Terashima M, Awano K, et al. Morphology of vulnerable coronary plaque: insights from follow‐up of patients examined by intravascular ultrasound before an acute coronary syndrome. J Am Coll Cardiol. 2000; 35:106–111.

109 109 Ehara S, Kobayashi Y, Yoshiyama M, et al. Spotty calcification typifies the culprit plaque in patients with acute myocardial infarction: an intravascular ultrasound study. Circulation. 2004; 110:3424–3429.

110 110 Lee T, Kakuta T, Yonetsu T, et al. Assessment of echo‐attenuated plaque by optical coherence tomography and its impact on post‐procedural creatine kinase‐myocardial band elevation in elective stent implantation. JACC: Cardiovascular Interventions. 2011; 4:483–491.

111 111 Kataoka Y, Wolski K, Uno K, et al. Spotty calcification as a marker of accelerated progression of coronary atherosclerosis: insights from serial intravascular ultrasound. J Am Coll Cardiol. 2012; 59:1592–1597.

112 112 Pu J, Mintz GS, Biro S, et al. Insights into echo‐attenuated plaques, echolucent plaques, and plaques with spotty calcification: novel findings from comparisons among intravascular ultrasound, near‐infrared spectroscopy, and pathological histology in 2,294 human coronary artery segments. J Am Coll Cardiol. 2014; 63:2220–2233.

113 113 Nair A, Kuban BD, Tuzcu EM, et al. Coronary plaque classification with intravascular ultrasound radiofrequency data analysis. Circulation. 2002; 106:2200–6.

114 114 Farb A, Burke AP, Tang AL, et al. Coronary plaque erosion without rupture into a lipid core. A frequent cause of coronary thrombosis in sudden coronary death. Circulation. 1996; 93:1354–63.

115 115 Virmani R, Kolodgie FD, Burke AP, et al. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol. 2000; 20:1262–75.

116 116 Hong MK, Mintz GS, Lee CW, et al. A three‐vessel virtual histology intravascular ultrasound analysis of frequency and distribution of thin‐cap fibroatheromas in patients with acute coronary syndrome or stable angina pectoris. Am J Cardiol. 2008; 101:568–72.

117 117 Stone GW, Maehara A, Lansky AJ, et al. A prospective natural‐history study of coronary atherosclerosis. N Engl J Med. 2011; 364:226–35.

118 118 Calvert PA, Obaid DR, O'Sullivan M, et al. Association between IVUS findings and adverse outcomes in patients with coronary artery disease: the VIVA (VH‐IVUS in Vulnerable Atherosclerosis) Study. JACC Cardiovasc Imaging. 2011; 4:894–901.

119 119 Cheng JM, Garcia‐Garcia HM, de Boer SP, et al. in vivo detection of high‐risk coronary plaques by radiofrequency intravascular ultrasound and cardiovascular outcome: results of the ATHEROREMO‐IVUS study. Eur Heart J. 2014; 35:639–47.

120 120 Virmani R, Burke AP, Farb A, Kolodgie FD. Pathology of the vulnerable plaque. J Am Coll Cardiol. 2006; 47:C13–8.

121 121 Stone PH, Saito S, Takahashi S, et al. Prediction of progression of coronary artery disease and clinical outcomes using vascular profiling of endothelial shear stress and arterial plaque characteristics: the PREDICTION Study. Circulation. 2012; 126:172–181.

122 122 Ino Y, Kubo T, Tanaka A, et al. Difference of culprit lesion morphologies between ST‐segment elevation myocardial infarction and non‐ST‐segment elevation acute coronary syndrome: an optical coherence tomography study. JACC Cardiovasc Interv. 2011; 4:76–82.

123 123 Vergallo R, Ren X, Yonetsu T, et al. Pancoronary plaque vulnerability in patients with acute coronary syndrome and ruptured culprit plaque: a 3‐vessel optical coherence tomography study. Am Heart J. 2014; 167:59–67.

124 124 Virmani R, Kolodgie FD, Burke AP et al., Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arteriosclerosis, thrombosis, and vascular biology. 2000; 20:1262–1275.

125 125 Soeda T, Higuma T, Abe N, et al. Morphological predictors for no reflow phenomenon after primary percutaneous coronary intervention in patients with ST‐segment elevation myocardial infarction caused by plaque rupture. European Heart Journal‐Cardiovascular Imaging. 2017; 18:103–110.

126 126 Satogami K, Ino Y, Kubo T, et al. Impact of plaque rupture detected by optical coherence tomography on transmural extent of infarction after successful stenting in ST‐segment elevation acute myocardial infarction. JACC: Cardiovascular Interventions. 2017; 10:1025–1033.

127 127 Burke AP, Farb A, Malcom GT, et al. Effect of risk factors on the mechanism of acute thrombosis and sudden coronary death in women. Circulation. 1998; 97:2110–6.

128 128 Tearney GJ, Regar E, Akasaka T, et al. Consensus standards for acquisition, measurement, and reporting of intravascular optical coherence tomography studies: a report from the International Working Group for Intravascular Optical Coherence Tomography Standardization and Validation. J Am Coll Cardiol. 2012; 59:1058–72.

129 129 Campbell IC, Suever JD, Timmins LH, et al. Biomechanics and inflammation in atherosclerotic plaque erosion and plaque rupture: implications for cardiovascular events in women. PLoS One. 2014; 9:e111785.

130 130 Chandran S, Watkins J, Abdul‐Aziz A, et al. Inflammatory Differences in Plaque Erosion and Rupture in Patients With ST‐Segment Elevation Myocardial Infarction. J Am Heart Assoc. 2017; 6.

131 131 Kramer MC, Rittersma SZ, de Winter RJ, et al. Relationship of thrombus healing to underlying plaque morphology in sudden coronary death. J Am Coll Cardiol. 2010; 55:122–32.

132 132 Jia H, Abtahian F, Aguirre AD, et al. in vivo diagnosis of plaque erosion and calcified nodule in patients with acute coronary syndrome by intravascular optical coherence tomography. J Am Coll Cardiol. 2013; 62:1748–58.

133 133 Prati F, Uemura S, Souteyrand G, et al. OCT‐based diagnosis and management of STEMI associated with intact fibrous cap. JACC Cardiovasc Imaging. 2013; 6:283–7.

134 134 Jia H, Dai J, Hou J, et al. Effective anti‐thrombotic therapy without stenting: intravascular optical coherence tomography‐based management in plaque erosion (the EROSION study). Eur Heart J. 2017; 38:792–800.

135 135 Greenland P, Bonow RO, Brundage BH, et al. American College of Cardiology Foundation Clinical Expert Consensus Task F, Society of Atherosclerosis I, Prevention and Society of Cardiovascular Computed T. ACCF/AHA 2007 clinical expert consensus document on coronary artery calcium scoring by computed tomography in global cardiovascular risk assessment and in evaluation of patients with chest pain: a report of the American College of Cardiology Foundation Clinical Expert Consensus Task Force (ACCF/AHA Writing Committee to Update the 2000 Expert Consensus Document on Electron Beam Computed Tomography) developed in collaboration with the Society of Atherosclerosis Imaging and Prevention and the Society of Cardiovascular Computed Tomography. J Am Coll Cardiol. 2007; 49:378–402.

136 136 Vengrenyuk Y, Carlier S, Xanthos S, et al. A hypothesis for vulnerable plaque rupture due to stress‐induced debonding around cellular microcalcifications in thin fibrous caps. Proc Natl Acad Sci U S A. 2006; 103:14678–83.

137 137 Kume T, Okura H, Kawamoto T, et al. Assessment of the coronary calcification by optical coherence tomography. EuroIntervention. 2011; 6:768–72.

138 138 Yabushita H, Bouma BE, Houser SL, et al. Characterization of human atherosclerosis by optical coherence tomography. Circulation. 2002; 106:1640–5.

139 139 Hao H, Fujii K, Shibuya M, et al. Different findings in a calcified nodule between histology and intravascular imaging such as intravascular ultrasound, optical coherence tomography, and coronary angioscopy. JACC Cardiovasc Interv. 2014; 7:937–8.

140 140 Alfonso F, Cuesta J, Bastante T, et al. Calcified nodule mimicking red thrombus on optical coherence tomography. JACC Cardiovasc Interv. 2015; 8:120–1.

141 141 Alfonso F, Gonzalo N, Nunez‐Gil I, Banuelos C. Coronary thrombosis from large, nonprotruding, superficial calcified coronary plaques. J Am Coll Cardiol. 2013; 62:2254.

142 142 Kume T, Akasaka T, Kawamoto T, et al. Measurement of the thickness of the fibrous cap by optical coherence tomography. Am Heart J. 2006; 152:755 e1–4.

143 143 Kubo T, Imanishi T, Kashiwagi M, et al. Multiple coronary lesion instability in patients with acute myocardial infarction as determined by optical coherence tomography. Am J Cardiol. 2010; 105:318–22.

144 144 Fujii K, Kawasaki D, Masutani M, et al. OCT assessment of thin‐cap fibroatheroma distribution in native coronary arteries. JACC Cardiovasc Imaging. 2010; 3:168–75.

145 145 Uemura S, Ishigami K, Soeda T,et al. Thin‐cap fibroatheroma and microchannel findings in optical coherence tomography correlate with subsequent progression of coronary atheromatous plaques. Eur Heart J. 2012; 33:78–85.

146 146 Takarada S, Imanishi T, Kubo T, et al. Effect of statin therapy on coronary fibrous‐cap thickness in patients with acute coronary syndrome: assessment by optical coherence tomography study. Atherosclerosis. 2009; 202:491–7.

147 147 Komukai K, Kubo T, Kitabata H, et al. Effect of atorvastatin therapy on fibrous cap thickness in coronary atherosclerotic plaque as assessed by optical coherence tomography: the EASY‐FIT study. J Am Coll Cardiol. 2014; 64:2207–17.

148 148 Fuster V. Lewis A. Conner Memorial Lecture. Mechanisms leading to myocardial infarction: insights from studies of vascular biology. Circulation. 1994; 90:2126–46.

149 149 Lendon CL, Davies MJ, Born GV, Richardson PD. Atherosclerotic plaque caps are locally weakened when macrophages density is increased. Atherosclerosis. 1991; 87:87–90.

150 150 Moreno PR, Falk E, Palacios IF, et al. Macrophage infiltration in acute coronary syndromes. Implications for plaque rupture. Circulation. 1994; 90:775–8.

151 151 Tearney GJ, Yabushita H, Houser SL, et al. Quantification of macrophage content in atherosclerotic plaques by optical coherence tomography. Circulation. 2003; 107:113–9.

152 152 Raffel OC, Tearney GJ, Gauthier DD, et al. Relationship between a systemic inflammatory marker, plaque inflammation, and plaque characteristics determined by intravascular optical coherence tomography. Arterioscler Thromb Vasc Biol. 2007; 27:1820–7.

153 153 Duewell P, Kono H, Rayner KJ, et al. NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals. Nature. 2010; 464:1357–61.

154 154 Abela GS, Aziz K, Vedre A, et al. Effect of cholesterol crystals on plaques and intima in arteries of patients with acute coronary and cerebrovascular syndromes. Am J Cardiol. 2009; 103:959–68.

155 155 Abela GS, Aziz K. Cholesterol crystals cause mechanical damage to biological membranes: a proposed mechanism of plaque rupture and erosion leading to arterial thrombosis. Clin Cardiol. 2005; 28:413–20.

156 156 Kataoka Y, Puri R, Hammadah M, et al. Cholesterol crystals associate with coronary plaque vulnerability in vivo. J Am Coll Cardiol. 2015; 65:630–2.

157 157 Dai J, Tian J, Hou J, et al. Association between cholesterol crystals and culprit lesion vulnerability in patients with acute coronary syndrome: An optical coherence tomography study. Atherosclerosis. 2016; 247:111–7.

158 158 Barger AC, Beeuwkes R, 3rd. Rupture of coronary vasa vasorum as a trigger of acute myocardial infarction. Am J Cardiol. 1990; 66:41G–43G.

159 159 Tenaglia AN, Peters KG, Sketch MH, Jr. Annex BH. Neovascularization in atherectomy specimens from patients with unstable angina: implications for pathogenesis of unstable angina. Am Heart J. 1998; 135:10–4.

160 160 Kitabata H, Tanaka A, Kubo T, et al. Relation of microchannel structure identified by optical coherence tomography to plaque vulnerability in patients with coronary artery disease. Am J Cardiol. 2010; 105:1673–8.

161 161 Caplan JD, Waxman S, Nesto RW, Muller JE. Near‐infrared spectroscopy for the detection of vulnerable coronary artery plaques. J Am Coll Cardiol. 2006; 47:C92–6.

162 162 Moreno PR, Lodder RA, Purushothaman KR, et al. Detection of lipid pool, thin fibrous cap, and inflammatory cells in human aortic atherosclerotic plaques by near‐infrared spectroscopy. Circulation. 2002; 105:923–7.

163 163 Puri R, Madder RD, Madden SP, et al. Near‐Infrared Spectroscopy Enhances Intravascular Ultrasound Assessment of Vulnerable Coronary Plaque: A Combined Pathological and in vivo Study. Arterioscler Thromb Vasc Biol. 2015; 35:2423–31.

164 164 Madder RD, Smith JL, Dixon SR, Goldstein JA. Composition of target lesions by near‐infrared spectroscopy in patients with acute coronary syndrome versus stable angina. Circ Cardiovasc Interv. 2012; 5:55–61.

165 165 Madder RD, Goldstein JA, Madden SP, et al. Detection by near‐infrared spectroscopy of large lipid core plaques at culprit sites in patients with acute ST‐segment elevation myocardial infarction. JACC Cardiovasc Interv. 2013; 6:838–46.

166 166 Madder RD, Husaini M, Davis AT, et al. Detection by near‐infrared spectroscopy of large lipid cores at culprit sites in patients with non‐ST‐segment elevation myocardial infarction and unstable angina. Catheter Cardiovasc Interv. 2015; 86:1014–21.

167 167 Kini AS, Baber U, Kovacic JC, et al. Changes in plaque lipid content after short‐term intensive versus standard statin therapy: the YELLOW trial (reduction in yellow plaque by aggressive lipid‐lowering therapy). J Am Coll Cardiol. 2013; 62:21–29.

168 168 Oemrawsingh RM, Cheng JM, Garcia‐Garcia HM, et al. Near‐infrared spectroscopy predicts cardiovascular outcome in patients with coronary artery disease. J Am Coll Cardiol. 2014; 64:2510–8.

169 169 Kini AS, Baber U, Kovacic JC, et al. Changes in plaque lipid content after short‐term intensive versus standard statin therapy: the YELLOW trial (reduction in yellow plaque by aggressive lipid‐lowering therapy). J Am Coll Cardiol. 2013; 62:21–9.

170 170 Oemrawsingh RM, Garcia‐Garcia HM, van Geuns RJ, et al. Integrated Biomarker and Imaging Study 3 (IBIS‐3) to assess the ability of rosuvastatin to decrease necrotic core in coronary arteries. EuroIntervention. 2016; 12:734–9.

171 171. Naghavi M, Libby P, Falk E, et al. From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part II. Circulation. 2003; 108:1772–8.

172 172 Ross R. Atherosclerosis‐‐an inflammatory disease. N Engl J Med. 1999; 340:115–26.

173 173 Vasan RS. Biomarkers of cardiovascular disease: molecular basis and practical considerations. Circulation. 2006; 113:2335–62.

174 174 Creemers EE, Tijsen AJ, Pinto YM. Circulating microRNAs: novel biomarkers and extracellular communicators in cardiovascular disease? Circulation research. 2012; 110:483–495.

175 175 Fuster V, Fayad ZA, Moreno PR, et al. Atherothrombosis and high‐risk plaque: Part II: approaches by noninvasive computed tomographic/magnetic resonance imaging. J Am Coll Cardiol. 2005; 46:1209–18.

176 176 Fuster V, Moreno PR, Fayad ZA, et al. Atherothrombosis and high‐risk plaque: part I: evolving concepts. J Am Coll Cardiol. 2005; 46:937–54.

177 177 Tsimikas S, Willerson JT and Ridker PM. C‐reactive protein and other emerging blood biomarkers to optimize risk stratification of vulnerable patients. J Am Coll Cardiol. 2006; 47:C19–31.

178 178 Wang G‐K, Zhu J‐Q, Zhang J‐T, et al. Circulating microRNA: a novel potential biomarker for early diagnosis of acute myocardial infarction in humans. Eur Heart J. 2010; 31:659–666.

179 179 D'Alessandra Y, Devanna P, Limana F, et al. Circulating microRNAs are new and sensitive biomarkers of myocardial infarction. Eur Heart J. 2010; 31:2765–2773.

180 180 Tijsen AJ, Creemers EE, Moerland PD, et al. MiR423‐5p as a circulating biomarker for heart failure. Circulation Research. 2010; 106:1035.

181 181 Fichtlscherer S, De Rosa S, Fox H, et al. Circulating microRNAs in patients with coronary artery disease. Circulation Research. 2010; 107:677–684.

182 182 Li S, Zhu J, Zhang W, et al. Signature microRNA expression profile of essential hypertension and its novel link to human cytomegalovirus infection. Circulation. 2011; 124:175–184.

183 183 Zampetaki A, Kiechl S, Drozdov I, et al. Plasma microRNA profiling reveals loss of endothelial miR‐126 and other microRNAs in type 2 diabetes. Circulation Research. 2010; 107:810–817.

184 184 Du Clos TW. Function of C‐reactive protein. Annals of Medicine. 2000; 32:274–8.

185 185 Calabro P, Willerson JT, Yeh ET. Inflammatory cytokines stimulated C‐reactive protein production by human coronary artery smooth muscle cells. Circulation. 2003; 108:1930–2.

186 186 Verma S, Wang CH, Li SH, et al. A self‐fulfilling prophecy: C‐reactive protein attenuates nitric oxide production and inhibits angiogenesis. Circulation. 2002; 106:913–9.

187 187 Ridker PM, Cushman M, Stampfer MJ, et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med. 1997; 336:973–9.

188 188 Haverkate F, Thompson SG, Pyke SD, et al. Production of C‐reactive protein and risk of coronary events in stable and unstable angina. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group. The Lancet. 1997; 349:462–6.

189 189 Ridker PM, Rifai N, Pfeffer MA, et al. Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events (CARE) Investigators. Circulation. 1998; 98:839–44.

190 190 Lindahl B, Toss H, Siegbahn A, et al. Markers of myocardial damage and inflammation in relation to long‐term mortality in unstable coronary artery disease. FRISC Study Group. Fragmin during Instability in Coronary Artery Disease. N Engl J Med. 2000; 343:1139–47.

191 191 Liuzzo G, Biasucci LM, Gallimore JR, et al. The prognostic value of C‐reactive protein and serum amyloid a protein in severe unstable angina. N Engl J Med. 1994; 331:417–24.

192 192 Ridker PM, Rifai N, Rose L, et al. Comparison of C‐reactive protein and low‐density lipoprotein cholesterol levels in the prediction of first cardiovascular events. N Engl J Med. 2002; 347:1557–65.

193 193 Ridker PM, Stampfer MJ, Rifai N. Novel risk factors for systemic atherosclerosis: A comparison of c‐reactive protein, fibrinogen, homocysteine, lipoprotein(a), and standard cholesterol screening as predictors of peripheral arterial disease. JAMA. 2001; 285:2481–2485.

194 194 Pai JK, Pischon T, Ma J, et al. Inflammatory markers and the risk of coronary heart disease in men and women. N Engl J Med. 2004; 351:2599–610.

195 195 Burke AP, Tracy RP, Kolodgie F, et al. Elevated C‐reactive protein values and atherosclerosis in sudden coronary death: association with different pathologies. Circulation. 2002; 105:2019–2023.

196 196 Ridker PM, Everett BM, Thuren T, et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease. N Engl J Med. 2017; 377:1119–1131.

197 197 Everett BM, Donath MY, Pradhan AD, et al. Anti‐inflammatory therapy with canakinumab for the prevention and management of diabetes. J Am Coll Cardiol. 2018; 71:2392–2401.

198 198 Ridker PM, MacFadyen JG, Thuren T, et al. Effect of interleukin‐1β inhibition with canakinumab on incident lung cancer in patients with atherosclerosis: exploratory results from a randomised, double‐blind, placebo‐controlled trial. The Lancet. 2017; 390:1833–1842.

199 199 Tardif J‐C, Kouz S, Waters DD, et al. Efficacy and safety of low‐dose colchicine after myocardial infarction. N Engl J Med. 2019; 381:2497–2505.

200 200 Ridker PM, Everett BM, Pradhan A, et al. Low‐dose methotrexate for the prevention of atherosclerotic events. N Engl J Med. 2019; 380:752–762.

201 201 Davies MJ, Gordon JL, Gearing AJ, et al. The expression of the adhesion molecules ICAM‐1, VCAM‐1, PECAM, and E‐selectin in human atherosclerosis. The Journal of pathology. 1993; 171:223–9.

202 202 Ridker PM, Rifai N, Stampfer MJ, Hennekens CH. Plasma concentration of interleukin‐6 and the risk of future myocardial infarction among apparently healthy men. Circulation. 2000; 101:1767–72.

203 203 Peter K, Nawroth P, Conradt C, et al. Circulating vascular cell adhesion molecule‐1 correlates with the extent of human atherosclerosis in contrast to circulating intercellular adhesion molecule‐1, E‐selectin, P‐selectin, and thrombomodulin. Arterioscler Thromb Vasc Biol. 1997; 17:505–12.

204 204 Libby P, Aikawa M. New insights into plaque stabilisation by lipid lowering. Drugs. 1998; 56 Suppl 1:9–13; discussion 33.

205 205 Urbich C, Dernbach E, Aicher A, et al. CD40 ligand inhibits endothelial cell migration by increasing production of endothelial reactive oxygen species. Circulation. 2002; 106:981–6.

206 206 Varo N, de Lemos JA, Libby P, et al. Soluble CD40L: risk prediction after acute coronary syndromes. Circulation. 2003; 108:1049–52.

207 207 Heeschen C, Dimmeler S, Hamm CW, et al. Soluble CD40 ligand in acute coronary syndromes. N Engl J Med. 2003; 348:1104–11.

208 208 Semb AG, van Wissen S, Ueland T, et al. et al. Raised serum levels of soluble CD40 ligand in patients with familial hypercholesterolemia: downregulatory effect of statin therapy. J Am Coll Cardiol. 2003; 41:275–9.

209 209 Mallat Z, Corbaz A, Scoazec A, et al. Expression of interleukin‐18 in human atherosclerotic plaques and relation to plaque instability. Circulation. 2001; 104:1598–603.

210 210 Bayes‐Genis A, Conover CA, Schwartz RS. The insulin‐like growth factor axis: A review of atherosclerosis and restenosis. Circ Res. 2000; 86:125–30.

211 211 Bayes‐Genis A, Conover CA, Overgaard MT, et al. Pregnancy‐associated plasma protein A as a marker of acute coronary syndromes. N Engl J Med. 2001; 345:1022–9.

212 212 Sangiorgi G, Mauriello A, Bonanno E, et al. Pregnancy‐associated plasma protein‐a is markedly expressed by monocyte‐macrophage cells in vulnerable and ruptured carotid atherosclerotic plaques: a link between inflammation and cerebrovascular events. J Am Coll Cardiol. 2006; 47:2201–11.

213 213 Jaffer FA, Libby P, Weissleder R. Molecular and cellular imaging of atherosclerosis: emerging applications. J Am Coll Cardiol. 2006; 47:1328–38.

214 214 Constantinides P. Cause of thrombosis in human atherosclerotic arteries. Am J Cardiol. 1990; 66:37g–40g.

215 215 Fayad ZA, Fuster V. Clinical imaging of the high‐risk or vulnerable atherosclerotic plaque. Circ Res. 2001; 89:305–16.

216 216 Stefanadis C, Toutouzas K, Tsiamis E, et al.Thermal heterogeneity in stable human coronary atherosclerotic plaques is underestimated in vivo: the “cooling effect” of blood flow. J Am Coll Cardiol. 2003; 41:403–8.

217 217 Ruehm SG, Corot C, Vogt P, et al. Magnetic resonance imaging of atherosclerotic plaque with ultrasmall superparamagnetic particles of iron oxide in hyperlipidemic rabbits. Circulation. 2001; 103:415–22.

218 218 Lederman RJ, Raylman RR, Fisher SJ, et al. Detection of atherosclerosis using a novel positron‐sensitive probe and 18‐fluorodeoxyglucose (FDG). Nuclear Medicine Communications. 2001; 22:747–53.

219 219 Ciavolella M, Tavolaro R, Taurino M, et al. Immunoscintigraphy of atherosclerotic uncomplicated lesions in vivo with a monoclonal antibody against D‐dimers of insoluble fibrin. Atherosclerosis. 1999; 143:171–5.

220 220 Schmitz SA, Coupland SE, Gust R, et al. Superparamagnetic iron oxide‐enhanced MRI of atherosclerotic plaques in Watanabe hereditable hyperlipidemic rabbits. Investigative Radiology. 2000; 35:460–71.

221 221 Schmitz SA, Taupitz M, Wagner S, et al. Iron‐oxide‐enhanced magnetic resonance imaging of atherosclerotic plaques: postmortem analysis of accuracy, inter‐observer agreement, and pitfalls. Investigative Radiology. 2002; 37:405–11.

222 222 Yuan C, Kerwin WS. MRI of atherosclerosis. Journal of Magnetic Resonance Imaging: JMRI. 2004; 19:710–9.

223 223 Yuan C, Kerwin WS, Ferguson MS, et al. Contrast‐enhanced high resolution MRI for atherosclerotic carotid artery tissue characterization. Journal of magnetic resonance imaging: JMRI. 2002; 15:62–7.

224 224 Asakura T, Karino T. Flow patterns and spatial distribution of atherosclerotic lesions in human coronary arteries. Circ Res. 1990; 66:1045–66.

225 225 Malek AM, Alper SL, Izumo S. Hemodynamic shear stress and its role in atherosclerosis. JAMA. 1999; 282:2035–42.

226 226 Chatzizisis YS, Coskun AU, Jonas M, et al. Role of endothelial shear stress in the natural history of coronary atherosclerosis and vascular remodeling: molecular, cellular, and vascular behavior. J Am Coll Cardiol. 2007; 49:2379–93.

227 227 Stone PH, Saito S, Takahashi S, et al. Prediction of progression of coronary artery disease and clinical outcomes using vascular profiling of endothelial shear stress and arterial plaque characteristics: the PREDICTION Study. Circulation. 2012; 126:172–81.

228 228 Samady H, Eshtehardi P, McDaniel MC, Coronary artery wall shear stress is associated with progression and transformation of atherosclerotic plaque and arterial remodeling in patients with coronary artery disease. Circulation. 2011; 124:779–88.

229 229 Gijsen FJ, Wentzel JJ, Thury A, et al. Strain distribution over plaques in human coronary arteries relates to shear stress. Am J Physiol Heart Circ Physiol. 2008; 295:H1608–14.