PET imaging of atherosclerosis

Future Cardiology

Volumn 11, Issue 1, 2015, Pages 115-131

  Tarkin, Jason M ^a   Joshi, Francis R ^a   Rajani, Nikil K ^a   Rudd, James Hf ^a  

^a UNIVERSITY OF CAMBRIDGE   (United Kingdom)

Author keywords

18F fluorodeoxyglucose; atherosclerosis; inflammation; molecular imaging; positron emission tomography; vulnerable plaque

Indexed keywords

FLUORODEOXYGLUCOSE F 18; HYDROXYMETHYLGLUTARYL COENZYME A REDUCTASE INHIBITOR; RADIOPHARMACEUTICAL AGENT;

ANGIOGENESIS; ATHEROSCLEROSIS; ATHEROSCLEROTIC PLAQUE; BLOOD VESSEL CALCIFICATION; CARDIOVASCULAR INFLAMMATION; CARDIOVASCULAR RISK; HUMAN; HYPOXIA; INFLAMMATION; MOLECULAR IMAGING; POSITRON EMISSION TOMOGRAPHY; PRIORITY JOURNAL; REVIEW; RISK ASSESSMENT; ANOXIA; CALCINOSIS; COMPUTER ASSISTED TOMOGRAPHY; DIAGNOSTIC USE; MULTIMODALITY CANCER THERAPY; NEOVASCULARIZATION (PATHOLOGY); RADIOGRAPHY; SCINTISCANNING; STROKE;

ANOXIA; ATHEROSCLEROSIS; CALCINOSIS; COMBINED MODALITY THERAPY; FLUORODEOXYGLUCOSE F18; HUMANS; HYDROXYMETHYLGLUTARYL-COA REDUCTASE INHIBITORS; INFLAMMATION; NEOVASCULARIZATION, PATHOLOGIC; PLAQUE, ATHEROSCLEROTIC; POSITRON-EMISSION TOMOGRAPHY; RADIOPHARMACEUTICALS; RISK ASSESSMENT; STROKE; TOMOGRAPHY, X-RAY COMPUTED;

EID: 84921685175     PISSN: 14796678     EISSN: 17448298     Source Type: Journal    
DOI: 10.2217/fca.14.55     Document Type: Review

References (138)

1. Falk E. Pathogenesis of atherosclerosis. J. Am. Coll. Cardiol. 47(8), C7-C12 (2006).
2. Libby P, Theroux P. Pathophysiology of coronary artery disease. Circulation 111(25), 3481-3488 (2005).
3. Wentzel JJ, Chatzizisis YS, Gijsen FJH, Giannoglou GD, Feldman CL, Stone PH. Endothelial shear stress in the evolution of coronary atherosclerotic plaque and vascular remodelling: current understanding and remaining questions. Cardiovasc. Res. 96(2), 234-243 (2012).
4. 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 126(2), 172-181 (2012).
5. Stary HC, Chandler AB, Glagov S et al. A definition of initial, fatty streak, and intermediate lesions of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation 89(5), 2462-2478 (1994).
6. Stary HC, Chandler AB, Dinsmore RE et al. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation 92(5), 1355-1374 (1995).
7. Davies MJ, Thomas A. Thrombosis and acute coronary-artery lesions in sudden cardiac ischemic death. N. Engl. J. Med. 310(18), 1137-1140 (1984).
8. Virmani R, Kolodgie FD, Burke AP, Farb A, Schwartz SM. Lessons from sudden coronary death : a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler. Thromb. Vasc. Biol. 20(5), 1262-1275 (2000).
9. Lozano R, Naghavi M, Foreman K 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), 2095-2128 (2013).
10. Global Atlas on Cardiovascular Disease Prevention and Control. Mendis S, Puska P, Norrving B, Mendis S, Puska P, Norrving B (Eds). WHO, Switzerland (2011).
11. Nichols M, Townsend N, Luengo-Fernandez R et al. European Cardiovascular Disease Statistics 2012. Løgstrup S, O'Kelly S (Eds). European Heart Network, Belgium, and European Society of Cardiology, France (2012).
12. Go AS, Mozaffarian D, Roger VL et al. Heart disease and stroke statistics-2014 update: a report from the American Heart Association. Circulation 129(3), e28-e292 (2014).
13. Glagov S, Weisenberg E, Zarins CK, Stankunavicius R, Kolettis GJ. Compensatory enlargement of human atherosclerotic coronary arteries. N. Engl. J. Med. 316(22), 1371-1375 (1987).
14. Varnava AM, Mills PG, Davies MJ. Relationship between coronary artery remodeling and plaque vulnerability. Circulation 105(8), 939-943 (2002).
15. Smits PC, Pasterkamp G, van Ufford MAQ et al. Coronary artery disease: arterial remodelling and clinical presentation. Heart 82(4), 461-464 (1999).
16. Mintz GS, Painter JA, Pichard AD et al. Atherosclerosis in angiographically 'normal' coronary artery reference segments: an intravascular ultrasound study with clinical correlations. J. Am. Coll. Cardiol. 25(7), 1479-1485 (1995).
17. Hackett DD, Davies GG, Maseri AA. Pre-existing coronary stenoses in patients with first myocardial infarction are not necessarily severe. Eur. Heart J. 9(12), 1317-1323 (1988).
18. Ambrose JAJ, Tannenbaum MAM, Alexopoulos DD et al. Angiographic progression of coronary artery disease and the development of myocardial infarction. J. Am. Coll. Cardiol. 12(1), 56-62 (1988).
19. Little WC, Constantinescu M, Applegate RJ et al. Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild-to-moderate coronary artery disease? Circulation 78(5), 1157-1166 (1988).
20. Narula J, Nakano M, Virmani R et al. Histopathologic characteristics of atherosclerotic coronary disease and implications of the findings for the invasive and noninvasive detection of vulnerable plaques. J. Am. Coll. Cardiol. 61(10), 1041-1051 (2013).
21. Tian J, Ren X, Vergallo R et al. Distinct morphological features of ruptured culprit plaque for acute coronary events compared to those with silent rupture and thin-cap fibroatheroma: a combined optical coherence tomography and intravascular ultrasound study. J. Am. Coll. Cardiol. 63(21), 2209-2216 (2014).
22. Arbab-Zadeh A, Nakano M, Virmani R, Fuster V. Acute coronary events. Circulation 125(9), 1147-1156 (2012).
23. Zaman T, Agarwal S, Anabtawi AG et al. Angiographic lesion severity and subsequent myocardial infarction. Am. J. Cardiol. 110(2), 167-172 (2012).
24. Ojio S, Takatsu H, Tanaka T et al. Considerable time from the onset of plaque rupture and/or thrombi until the onset of acute myocardial infarction in humans coronary angiographic findings within 1 week before the onset of infarction. Circulation 102(17), 2063-2069 (2000).
25. Puri R, Nicholls SJ, Ellis SG, Tuzcu EM, Kapadia SR. High-risk coronary atheroma: the interplay between ischemia, plaque burden, and disease progression. J. Am. Coll. Cardiol. 63(12), 1134-1140 (2014).
26. Bentzon JF, Otsuka F, Virmani R, Falk E. Mechanisms of plaque formation and rupture. Circ. Res. 114(12), 1852-1866 (2014).
27. Falk E, Nakano M, Bentzon JF, Finn AV, Virmani R. Update on acute coronary syndromes: the pathologists' view. Eur. Heart J. 34(10), 719-728 (2013).
28. Prati F, Albertucci M. Searching between the plaques layers to understand the past and predict the future. J. Am. Coll. Cardiol. 63(21), 2217-2219 (2014).
29. Epstein FH, Ross R. Atherosclerosis-an inflammatory disease. N. Engl. J. Med. 340(2), 115-126 (1999).
30. Libby P. Inflammation in atherosclerosis. Arterioscler. Thromb. Vasc. Biol. 32(9), 2045-2051 (2012).
31. Dutta P, Courties G, Wei Y et al. Myocardial infarction accelerates atherosclerosis. Nature 487(7407), 325-329 (2012).
32. Virmani R, Burke AP, Farb A, Kolodgie FD. Pathology of the vulnerable plaque. J. Am. Coll. Cardiol. 47(8), C13-C18 (2006).
33. Stone GW, Maehara A, Lansky AJ et al. A prospective natural-history study of coronary atherosclerosis. N. Engl. J. Med. 364(3), 226-235 (2011).
34. 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 4(8), 894-901 (2011).
35. Falk E, Shah PK, Fuster V. Coronary plaque disruption. Circulation 92(3), 657-671 (1995).
36. Noguchi T, Kawasaki T, Tanaka A et al. High-intensity signals in coronary plaques on noncontrast T1-weighted magnetic resonance imaging as a novel determinant of coronary events. J. Am. Coll. Cardiol. 63(10), 989-999 (2014).
37. Libby P. Molecular bases of the acute coronary syndromes. Circulation 91(11), 2844-2850 (1995).
38. 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. 94(6), 2493-2503 (1994).
39. Sluimer JC, Gasc J-M, van Wanroij JL et al. Hypoxia, hypoxia-inducible transcription factor, and macrophages in human atherosclerotic plaques are correlated with intraplaque angiogenesis. J. Am. Coll. Cardiol. 51(13), 1258-1265 (2008).
40. Sluimer JC, Daemen MJ. Novel concepts in atherogenesis: angiogenesis and hypoxia in atherosclerosis. 218(1), 7-29 (2009).
41. Virmani R. Atherosclerotic plaque progression and vulnerability to rupture: angiogenesis as a source of intraplaque hemorrhage. Arterioscler. Thromb. Vasc. Biol. 25(10), 2054-2061 (2005).
42. Marsch E, Sluimer JC, Daemen MJAP. Hypoxia in atherosclerosis and inflammation. Curr. Opin Lipidol. 24(5), 393-400 (2013).
43. Boström P, Magnusson B, Svensson P-A et al. Hypoxia converts human macrophages into triglyceride-loaded foam cells. Arterioscler. Thromb. Vasc. Biol. 26(8), 1871-1876 (2006).
44. Aikawa E, Nahrendorf M, Figueiredo J-L et al. Osteogenesis associates with inflammation in early-stage atherosclerosis evaluated by molecular imaging in vivo. Circulation 116(24), 2841-2850 (2007).
45. Menini S, Iacobini C, Ricci C et al. The galectin-3/RAGE dyad modulates vascular osteogenesis in atherosclerosis. Cardiovasc. Res. 100(3), 472-480 (2013).
46. New SEP, Goettsch C, Aikawa M et al. Macrophage-derived matrix vesicles: an alternative novel mechanism for microcalcification in atherosclerotic plaques. Circ. Res. 113(1), 72-77 (2013).
47. 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. 59(18), 1592-1597 (2012).
48. 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. USA 103(40), 14678-14683 (2006).
49. Abedin M, Tintut Y, Demer LL. Vascular calcification: mechanisms and clinical ramifications. Arterioscler. Thromb. Vasc. Biol. 24(7), 1161-1170 (2004).
50. Mochizuki T, Tsukamoto E, Kuge Y et al. FDG uptake and glucose transporter subtype expressions in experimental tumor and inflammation models. J. Nucl. Med. 42(10), 1551-1555 (2001).
51. Zanzonico P. Positron emission tomography: a review of basic principles, scanner design and performance, and current systems. Semin. Nucl. Med. 34(2), 87-111 (2004).
52. Bucerius J, Mani V, Moncrieff C et al. Optimizing 18F-FDG PET/CT imaging of vessel wall inflammation: the impact of 18F-FDG circulation time, injected dose, uptake parameters, and fasting blood glucose levels. Eur. J. Nucl. Med. Mol. Imaging 41(2), 369-383 (2013).
53. Vallabhajosula S, Machac J, Knesaurek K et al. Imaging atherosclerotic macrophage density by positron emission tomography using F-18-fluorodeoxyglucose (FDG). J. Nucl. Med. 5, (38), 144 (1996).
54. Helft G, Worthley SG, Zhang ZY et al. Non-invasive in vivo imaging of atherosclerotic lesions using fluorine-18 deoxyglucose (18-FDG) pet correlates with macrophage content in a rabbit model. Circulation 100 (18 Suppl.), I1-I928 (1999).
55. Lederman RJ, Raylman RR, Fisher SJ et al. Detection of atherosclerosis using a novel positron-sensitive probe and 18-fluorodeoxyglucose (FDG). Nucl. Med. Commun. 22(7), 747-753 (2001).
56. Yun M, Yeh D, Araujo LI, Jang S, Newberg A, Alavi A. F-18 FDG uptake in the large arteries: a new observation. Clin. Nucl. Med. 26(4), 314-319 (2001).
57. Rudd JH, Warburton EA, Fryer TD et al. Imaging atherosclerotic plaque inflammation with [18F]-fluorodeoxyglucose positron emission tomography. Circulation 105(23), 2708-2711 (2002).
58. Tawakol A, Migrino RQ, Bashian GG et al. In vivo18F-fluorodeoxyglucose positron emission tomography imaging provides a noninvasive measure of carotid plaque inflammation in patients. J. Am. Coll. Cardiol. 48(9), 1818-1824 (2006).
59. Niccoli Asabella A, Ciccone MM, Cortese F et al. Higher reliability of 18F-FDG target background ratio compared to standardized uptake value in vulnerable carotid plaque detection: a pilot study. Ann. Nucl. Med. 28(6), 571-579 (2014).
60. Bural GG, Torigian DA, Chamroonrat W et al. FDG-PET is an effective imaging modality to detect and quantify age-related atherosclerosis in large arteries. Eur. J. Nucl. Med. Mol. Imaging 35(3), 562-569 (2008).
61. Rudd JHF, Myers KS, Bansilal S et al. Relationships among regional arterial inflammation, calcification, risk factors, and biomarkers: a prospective fluorodeoxyglucose positron-emission tomography/computed tomography imaging study. Circ. Cardiovasc. Imaging 2(2), 107-115 (2009).
62. Wassélius JA, Larsson SA, Jacobsson H. FDG-accumulating atherosclerotic plaques identified with 18F-FDG-PET/CT in 141 patients. Mol. Imaging Biol. 11(6), 455-459 (2009).
63. Noh TS, Moon S-H, Cho YS et al. Relation of carotid artery 18F-FDG uptake to C-reactive protein and Framingham risk score in a large cohort of asymptomatic adults. J. Nucl. Med. 54(12), 2070-2076 (2013).
64. Yoo HJ, Kim S, Park MS et al. Vascular inflammation stratified by C-reactive protein and low-density lipoprotein cholesterol levels: analysis with 18F-FDG PET. J. Nucl. Med. 52(1), 10-17 (2011).
65. Græbe M, Pedersen SF, Højgaard L, Kjær A, Sillesen H. 18FDG PET and ultrasound echolucency in carotid artery plaques. JACC Cardiovasc. Imaging 3(3), 289-295 (2010).
66. Silvera SS, Aidi HE, Rudd JHF et al. Multimodality imaging of atherosclerotic plaque activity and composition using FDG-PET/CT and MRI in carotid and femoral arteries. Atherosclerosis 207(1), 139-143 (2009).
67. Figueroa AL, Subramanian SS, Cury RC et al. Distribution of inflammation within carotid atherosclerotic plaques with high-risk morphological features: a comparison between positron emission tomography activity, plaque morphology, and histopathology. Circ. Cardiovasc. Imaging 5(1), 69-77 (2012). • Demonstrates that carotid artery 18F-fluorodeoxyglucose (FDG) uptake correlates with high-risk plaque features on computed tomography and histology.
68. Rudd JHF, Myers KS, Bansilal S et al. 18Fluorodeoxyglucose positron emission tomography imaging of atherosclerotic plaque inflammation is highly reproducible: implications for atherosclerosis therapy trials. J. Am. Coll. Cardiol. 50(9), 892-896 (2007).
69. Rudd JHF, Myers KS, Bansilal S et al. Atherosclerosis inflammation imaging with 18F-FDG PET: carotid, iliac, and femoral uptake reproducibility, quantification methods, and recommendations. J. Nucl. Med. 49(6), 871-878 (2008).
70. Font MA, Fernandez A, Carvajal A et al. Imaging of early inflammation in low-tomoderate carotid stenosis by 18-FDG-PET. Front. Biosci. (Landmark Ed.) 14, 3352-3360 (2009).
71. Pedersen SF, Græbe M, Fisker Hag AM, Højgaard L, Sillesen H, Kjær A. Gene expression and 18FDG uptake in atherosclerotic carotid plaques. Nucl. Med. Commun. 31(5), 423-429 (2010).
72. Græbe M, Pedersen SF, Borgwardt L, Højgaard L, Sillesen H, Kjaer A. Molecular pathology in vulnerable carotid plaques: correlation with [18]-fluorodeoxyglucose positron emission tomography (FDG-PET). Eur. J. Vasc. Endovasc. Surg. 37(6), 714-721 (2009).
73. Folco EJ, Sheikine Y, Rocha VZ et al. Hypoxia but not inflammation augments glucose uptake in human macrophages. J. Am. Coll. Cardiol. 58(6), 603-614 (2011). • In vitro study showing that hypoxia augments glucose uptake in macrophages.
74. Pedersen SF, Græbe M, Hag AMF, Højgaard L, Sillesen H, Kjær A. 18F-FDG imaging of human atherosclerotic carotid plaques reflects gene expression of the key hypoxia marker HIF-1α. Am. J. Nucl. Med. Mol. Imaging 3(5), 384-392 (2013).
75. Pedersen SF, Græbe M, Hag AMF, Hoejgaard L, Sillesen H, Kjær A. Microvessel density but not neoangiogenesis is associated with 18F-FDG uptake in human atherosclerotic carotid plaques. Mol. Imaging Biol. 14(3), 384-392 (2011).
76. Ogawa M, Nakamura S, Saito Y, Kosugi M, Magata Y. What can be seen by 18F-FDG PET in atherosclerosis imaging? The effect of foam cell formation on 18F-FDG uptake to macrophages in vitro. J. Nucl. Med. 53(1), 55-58 (2012).
77. Satomi T, Ogawa M, Mori I et al. Comparison of contrast agents for atherosclerosis imaging using cultured macrophages: FDG versus ultrasmall superparamagnetic iron oxide. J. Nucl. Med. 54(6), 999-1004 (2013).
78. Dunphy MPS, Freiman A, Larson SM, Strauss HW. Association of vascular 18F-FDG uptake with vascular calcification. J. Nucl. Med. 46(8), 1278-1284 (2005).
79. Menezes LJ, Kotze CW, Agu O et al. Investigating vulnerable atheroma using combined 18F-FDG PET/CT angiography of carotid plaque with immunohistochemical validation. J. Nucl. Med. 52(11), 1698-1703 (2011).
80. Ben-Haim S, Kupzov E, Tamir A, Frenkel A, Israel O. Changing patterns of abnormal vascular wall F-18 fluorodeoxyglucose uptake on follow-up PET/CT studies. J. Nucl. Cardiol. 13(6), 791-800 (2006).
81. Elkhawad M, Rudd JHF, Sarov-Blat L et al. Effects of p38 mitogen-activated protein kinase inhibition on vascular and systemic inflammation in patients with atherosclerosis. JACC Cardiovasc. Imaging 5(9), 911-922 (2012).
82. Fayad ZA, Mani V, Woodward M et al. Safety and efficacy of dalcetrapib on atherosclerotic disease using novel non-invasive multimodality imaging (dal-PLAQUE): a randomised clinical trial. Lancet 378(9802), 1547-1559 (2011).
83. Ryu Y, Yoshida K, Suzuki Y et al. Long-term changes of aortic 18F-FDG uptake and calcification in health-screening subjects. Ann. Nucl. Med. 27(3), 239-246 (2012).
84. Alexopoulos N, Katritsis D, Raggi P. Visceral adipose tissue as a source of inflammation and promoter of atherosclerosis. Atherosclerosis 233(1), 104-112 (2014).
85. Grundy SM. Obesity, metabolic syndrome, and coronary atherosclerosis. Circulation 105(23), 2696-2698 (2002).
86. Apovian CM, Bigornia S, Mott M et al. Adipose macrophage infiltration is associated with insulin resistance and vascular endothelial dysfunction in obese subjects. Arterioscler. Thromb. Vasc. Biol. 28(9), 1654-1659 (2008).
87. Bucerius J, Mani V, Wong S et al. Arterial and fat tissue inflammation are highly correlated: a prospective 18F-FDG PET/CT study. Eur. J. Nucl. Med. Mol. Imaging 41(5), 934-945 (2014).
88. Kang S, Kyung C, Park JS et al. Subclinical vascular inflammation in subjects with normal weight obesity and its association with body fat: an 18 F-FDG-PET/CT study. Cardiovasc. Diabetol. 13(1), 70 (2014).
89. Kim TN, Kim S, Yang SJ et al. Vascular inflammation in patients with impaired glucose tolerance and Type 2 diabetes: analysis with 18F-fluorodeoxyglucose positron emission tomography. Circ. Cardiovasc. Imaging 3(2), 142-148 (2010).
90. Tahara N, Kai H, Yamagishi S-I et al. Vascular inflammation evaluated by [18F]-fluorodeoxyglucose positron emission tomography is associated with the metabolic syndrome. J. Am. Coll. Cardiol. 49(14), 1533-1539 (2007).
91. Kim EJ, Kim S, Seo HS, Kang DO. The metabolic activity of the spleen and bone marrow in patients with acute myocardial infarction evaluated by 18F-FDG PET imaging. Circ. Cardiovasc. Imaging 7(3), 454-460 (2014). • Highlights the systemic inflammatory response that occurs in patients with atherosclerosis.
92. Davies JR, Rudd JHF, Fryer TD et al. Identification of culprit lesions after transient ischemic attack by combined 18F fluorodeoxyglucose positron-emission tomography and high-resolution magnetic resonance imaging. Stroke 36(12), 2642-2647 (2005).
93. Moustafa RR, Izquierdo-Garcia D, Fryer TD et al. Carotid plaque inflammation is associated with cerebral microembolism in patients with recent transient ischemic attack or stroke: a pilot study. Circ. Cardiovasc. Imaging 3(5), 536-541 (2010).
94. Marnane M, Merwick A, Sheehan OC et al. Carotid plaque inflammation on 18F-fluorodeoxyglucose positron emission tomography predicts early stroke recurrence. Ann. Neurol. 71(5), 709-718 (2012).
95. Chroínín DN, Marnane M, Akijian L et al. Serum lipids associated with inflammationrelated PET-FDG uptake in symptomatic carotid plaque. Neurology 82(19), 1693-1699 (2014).
96. Paulmier B, Duet M, Khayat R et al. Arterial wall uptake of fluorodeoxyglucose on PET imaging in stable cancer disease patients indicates higher risk for cardiovascular events. J. Nucl. Cardiol. 15(2), 209-217 (2008).
97. Rominger A, Saam T, Wolpers S et al. 18F-FDG PET/CT identifies patients at risk for future vascular events in an otherwise asymptomatic cohort with neoplastic disease. J. Nucl. Med. 50(10), 1611-1620 (2009).
98. Figueroa AL, Abdelbaky A, Truong QA et al. Measurement of arterial activity on routine FDG PET/CT images improves prediction of risk of future CV events. JACC Cardiovasc. Imaging 6(12), 1250-1259 (2013).
99. Muntendam P, McCall C, Sanz J, Falk E, Fuster V; High-Risk Plaque Initiative. The BioImage Study: novel approaches to risk assessment in the primary prevention of atherosclerotic cardiovascular disease-study design and objectives. Am. Heart J. 160(1), 49-57.e1 (2010).
100. Fernández-Ortiz A, Jiménez-Borreguero LJ, Penãlvo JL et al. The Progression and Early Detection of Subclinical Atherosclerosis (PESA) study: rationale and design. Am. Heart J. 166(6), 990-998 (2013).
101. Tahara N, Kai H, Ishibashi M et al. Simvastatin attenuates plaque inflammation. J. Am. Coll. Cardiol. 48(9), 1825-1831 (2006).
102. Ishii H, Nishio M, Takahashi H et al. Comparison of atorvastatin 5 and 20 mg/d for reducing F-18 fluorodeoxyglucose uptake in atherosclerotic plaques on positron emission tomography/computed tomography: a randomized, investigator-blinded, open-label, 6-month study in Japanese adults scheduled for percutaneous coronary intervention. Clin. Ther. 32(14), 2337-2347 (2010).
103. Wu Y-W, Kao H-L, Huang C-L et al. The effects of 3-month atorvastatin therapy on arterial inflammation, calcification, abdominal adipose tissue and circulating biomarkers. Eur. J. Nucl. Med. Mol. Imaging 39(3), 399-407 (2011).
104. Tawakol A, Fayad ZA, Mogg R et al. Intensification of statin therapy results in a rapid reduction in atherosclerotic inflammation: results of a multicenter fluorodeoxyglucose-positron emission tomography/computed tomography feasibility study. J. Am. Coll. Cardiol. 62(10), 909-917 (2013). • Demonstrates how 18F-FDG PET can be used as a surrogate end point in clinical drug trials.
105. Subramanian S, Emami H, Vucic E et al. High-dose atorvastatin reduces periodontal inflammation: a novel pleiotropic effect of statins. J. Am. Coll. Cardiol. 62(25), 2382-2391 (2013).
106. Tawakol A, Singh P, Rudd JHF et al. Effect of treatment for 12 weeks with rilapladib, a lipoprotein-associated phospholipase A2 inhibitor, on arterial inflammation as assessed with 18F-fluorodeoxyglucose-positron emission tomography imaging. J. Am. Coll. Cardiol. 63(1), 86-88 (2014).
107. Burg S, Dupas A, Stute S et al. Partial volume effect estimation and correction in the aortic vascular wall in PET imaging. Phys. Med. Biol. 58(21), 7527-7542 (2013).
108. Izquierdo-Garcia D, Davies JR, Graves MJ et al. Comparison of methods for magnetic resonance-guided [18-F]fluorodeoxyglucose positron emission tomography in human carotid arteries: reproducibility, partial volume correction, and correlation between methods. Stroke 40(1), 86-93 (2009).
109. Buther F, Dawood M, Stegger L et al. List mode-driven cardiac and respiratory gating in PET. J. Nucl. Med. 50(5), 674-681 (2009).
110. Saam T, Rominger A, Wolpers S et al. Association of inflammation of the left anterior descending coronary artery with cardiovascular risk factors, plaque burden and pericardial fat volume: a PET/CT study. Eur. J. Nucl. Med. Mol. Imaging 37(6), 1203-1212 (2010).
111. Wykrzykowska J, Lehman S, Williams G et al. Imaging of inflamed and vulnerable plaque in coronary arteries with 18F-FDG PET/CT in patients with suppression of myocardial uptake using a low-carbohydrate, high-fat preparation. J. Nucl. Med. 50(4), 563-568 (2009).
112. Williams G, Kolodny GM. Suppression of myocardial 18F-FDG uptake by preparing patients with a high-fat, low-carbohydrate diet. AJR Am. J. Roentgenol. 190(2), W151-W156 (2008).
113. Rogers IS, Nasir K, Figueroa AL et al. Feasibility of FDG imaging of the coronary arteries. JACC Cardiovasc. Imaging 3(4), 388-397 (2010).
114. Laitinen IEK, Luoto P, Nagren K et al. Uptake of 11C-choline in mouse atherosclerotic plaques. J. Nucl. Med. 51(5), 798-802 (2010).
115. Matter CM. 18F-choline images murine atherosclerotic plaques ex vivo. Arterioscler. Thromb. Vasc. Biol. 26(3), 584-589 (2005).
116. Kato K, Schober O, Ikeda M et al. Evaluation and comparison of 11C-choline uptake and calcification in aortic and common carotid arterial walls with combined PET/CT. Eur. J. Nucl. Med. Mol. Imaging 36(10), 1622-1628 (2009).
117. Bucerius J, Schmaljohann J, Böhm I et al. Feasibility of 18F-fluoromethylcholine PET/CT for imaging of vessel wall alterations in humans-first results. Eur. J. Nucl. Med. Mol. Imaging 35(4), 815-820 (2008). 118 18F-choline PET-CT and MRI of Carotid Plaques (ParisK). www.clinicaltrials.gov
118. Boy C, Heusner TA, Poeppel TD et al. 68Ga-DOTATOC PET/CT and somatostatin receptor (sst1-sst5) expression in normal human tissue: correlation of sst2 mRNA and SUVmax. Eur. J. Nucl. Med. Mol. Imaging 38(7), 1224-1236 (2011).
119. Armani C, Catalani E, Balbarini A, Bagnoli P, Cervia D. Expression, pharmacology, and functional role of somatostatin receptor subtypes 1 and 2 in human macrophages. J. Leukoc. Biol. 81(3), 845-855 (2006).
120. Adams RL, Adams IP, Lindow SW, Zhong W, Atkin SL. Somatostatin receptors 2 and 5 are preferentially expressed in proliferating endothelium. Br. J. Cancer 92(8), 1493-1498 (2005).
121. Dalm VASH, van Hagen PM, van Koetsveld PM et al. Expression of somatostatin, cortistatin, and somatostatin receptors in human monocytes, macrophages, and dendritic cells. Am. J. Physiol. Endocrinol. Metab. 285(2), E344-E353 (2003).
122. Li X, Bauer W, Kreissl MC et al. Specific somatostatin receptor II expression in arterial plaque: 68Ga-DOTATATE autoradiographic, immunohistochemical and flow cytometric studies in apoE-deficient mice. Atherosclerosis 230(1), 33-39 (2013).
123. Rominger A, Saam T, Vogl E et al. In vivo imaging of macrophage activity in the coronary arteries using 68Ga-DOTATATE PET/CT: correlation with coronary calcium burden and risk factors. J. Nucl. Med. 51(2), 193-197 (2010).
124. Li X, Samnick S, Lapa C et al. 68Ga-DOTATATE PET/CT for the detection of inflammation of large arteries: correlation with 18F-FDG, calcium burden and risk factors. EJNMMI Res. 2(1), 52 (2012).
125. Vascular Inflammation Imaging Using Somatostatin Receptor Positron Emission Tomography (VISION). www.clinicaltrials.gov 127 Laitinen I
126. Laitinen I, Marjamäki P, Någren K et al. Uptake of inflammatory cell marker [11C] PK11195 into mouse atherosclerotic plaques. Eur. J. Nucl. Med. Mol. Imaging 36(1), 73-80 (2009).
127. Fujimura Y, Hwang PM, Trout Iii H et al. Increased peripheral benzodiazepine receptors in arterial plaque of patients with atherosclerosis: an autoradiographic study with [3H]PK 11195. Atherosclerosis 201(1), 108-111 (2008).
128. Bird JLE, Izquierdo-Garcia D, Davies JR et al. Evaluation of translocator protein quantification as a tool for characterising macrophage burden in human carotid atherosclerosis. Atherosclerosis 210(2), 388-391 (2010).
129. Gaemperli O, Shalhoub J, Owen DRJ et al. Imaging intraplaque inflammation in carotid atherosclerosis with 11C-PK11195 positron emission tomography/computed tomography. Eur. Heart J. 33(15), 1902-1910 (2012).
130. Shalhoub J, Oskrochi Y, Davies AH, Owen DRJ. Clinical assessment of carotid atherosclerosis inflammation by positron emission tomography. Curr. Mol. Med. 13(10), 1646-1652 (2013).
131. Lee ST, Scott AM. Hypoxia positron emission tomography imaging with 18F-fluoromisonidazole. Semin. Nucl. Med. 37(6), 451-461 (2007).
132. Markus R, Reutens DC, Kazui S et al. Topography and temporal evolution of hypoxic viable tissue identified by 18F-fluoromisonidazole positron emission tomography in humans after ischemic stroke. Stroke 34(11), 2646-2652 (2003).
133. Mateo J, Izquierdo-Garcia D, Badimon JJ, Fayad ZA, Fuster V. Noninvasive assessment of hypoxia in rabbit advanced atherosclerosis using 18F-fluoromisonidazole PET imaging. Circ. Cardiovasc. Imaging 7(2), 312-320 (2014).
134. Joshi FR, Manavak R, Fryer TD et al. Imaging of hypoxia and inflammation in carotid atherosclerosis with 18F-fluoromisonidazole and 18F-fluorodeoxyglucose positron emission tomography. Circulation 128, A14673 (2013).
135. Su H, Gorodny N, Gomez LF et al. Atherosclerotic plaque uptake of a novel integrin tracer 18F-Flotegatide in a mouse model of atherosclerosis. J. Nucl. Cardiol. 21(3), 553-562 (2014).
136. Beer AJ, Pelisek J, Heider P et al. PET/CT Imaging of integrin αvβ3 expression in human carotid atherosclerosis. JACC Cardiovasc. Imaging 7(2), 178-187 (2014).
137. Dweck MR, Jenkins WSA, Vesey AT et al. 18F-sodium fluoride uptake is a marker of active calcification and disease progression in patients with aortic stenosis. Circ. Cardiovasc. Imaging 7(2), 371-378 (2014).
138. Joshi NV, Vesey AT, Williams MC et al. 18F-fluoride positron emission tomography for identification of ruptured and high-risk coronary atherosclerotic plaques: a prospective clinical trial. Lancet 383(9918), 705-713 (2014)