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Erschienen in: Journal of Nuclear Cardiology 5/2021

24.04.2020 | Editorial

18F-FDG PET imaging of myocardial inflammation and viability following experimental infarction and anti-inflammatory treatment with compound MCC950

verfasst von: Jeremy Jong, BS, René R. Sevag Packard, MD, PhD

Erschienen in: Journal of Nuclear Cardiology | Ausgabe 5/2021

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Excerpt

In this issue of the Journal of Nuclear Cardiology, Li and Yang et al. explore the role of 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging to assess myocardial inflammation and viability in the context of treatment with the anti-inflammatory molecule sulfonylurea MCC950 following acute myocardial infarction (AMI).1 The effect of MCC950, a NOD [nucleotide-binding and oligomerization domain]-like receptor pyrin domain-containing protein-3 (NLRP-3) inflammasome inhibitor, was assessed using various FDG PET protocols to image the myocardium following experimental ligation of the left main coronary artery and ensuing AMI in C57BL/6 adult male mice.2 MCC950 was administered immediately after surgery and daily for 7 days. Following surgery, FDG PET imaging was conducted to (i) quantify myocardial inflammation at days 3 and 5, and (ii) determine myocardial viability at days 7 and 28. Histology, immunohistochemistry, and Western blotting were used as reference standards and cardiac mechanical parameters were obtained by echocardiography. …
Literatur
2.
Zurück zum Zitat Gao E, Lei YH, Shang X, Huang ZM, Zuo L, Boucher M, Fan Q, Chuprun JK, Ma XL, Koch WJ. A novel and efficient model of coronary artery ligation and myocardial infarction in the mouse. Circ Res 2010;107:1445-53.CrossRef Gao E, Lei YH, Shang X, Huang ZM, Zuo L, Boucher M, Fan Q, Chuprun JK, Ma XL, Koch WJ. A novel and efficient model of coronary artery ligation and myocardial infarction in the mouse. Circ Res 2010;107:1445-53.CrossRef
3.
Zurück zum Zitat Yan X, Anzai A, Katsumata Y, Matsuhashi T, Ito K, Endo J, Yamamoto T, Takeshima A, Shinmura K, Shen W, Fukuda K, Sano M. Temporal dynamics of cardiac immune cell accumulation following acute myocardial infarction. J Mol Cell Cardiol 2013;62:24-35.CrossRef Yan X, Anzai A, Katsumata Y, Matsuhashi T, Ito K, Endo J, Yamamoto T, Takeshima A, Shinmura K, Shen W, Fukuda K, Sano M. Temporal dynamics of cardiac immune cell accumulation following acute myocardial infarction. J Mol Cell Cardiol 2013;62:24-35.CrossRef
4.
Zurück zum Zitat Fang L, Moore XL, Dart AM, Wang LM. Systemic inflammatory response following acute myocardial infarction. J Geriatr Cardiol 2015;12:305-12.PubMedPubMedCentral Fang L, Moore XL, Dart AM, Wang LM. Systemic inflammatory response following acute myocardial infarction. J Geriatr Cardiol 2015;12:305-12.PubMedPubMedCentral
5.
Zurück zum Zitat Frangogiannis NG. The immune system and the remodeling infarcted heart: Cell biological insights and therapeutic opportunities. J Cardiovasc Pharmacol 2014;63:185-95.CrossRef Frangogiannis NG. The immune system and the remodeling infarcted heart: Cell biological insights and therapeutic opportunities. J Cardiovasc Pharmacol 2014;63:185-95.CrossRef
6.
Zurück zum Zitat Westman PC, Lipinski MJ, Luger D, Waksman R, Bonow RO, Wu E, Epstein SE. Inflammation as a driver of adverse left ventricular remodeling after acute myocardial infarction. J Am Coll Cardiol 2016;67:2050-60.CrossRef Westman PC, Lipinski MJ, Luger D, Waksman R, Bonow RO, Wu E, Epstein SE. Inflammation as a driver of adverse left ventricular remodeling after acute myocardial infarction. J Am Coll Cardiol 2016;67:2050-60.CrossRef
7.
Zurück zum Zitat Ong SB, Hernandez-Resendiz S, Crespo-Avilan GE, Mukhametshina RT, Kwek XY, Cabrera-Fuentes HA, Hausenloy DJ. Inflammation following acute myocardial infarction: Multiple players, dynamic roles, and novel therapeutic opportunities. Pharmacol Ther 2018;186:73-87.CrossRef Ong SB, Hernandez-Resendiz S, Crespo-Avilan GE, Mukhametshina RT, Kwek XY, Cabrera-Fuentes HA, Hausenloy DJ. Inflammation following acute myocardial infarction: Multiple players, dynamic roles, and novel therapeutic opportunities. Pharmacol Ther 2018;186:73-87.CrossRef
8.
Zurück zum Zitat Shimamoto A, Chong AJ, Yada M, Shomura S, Takayama H, Fleisig AJ, Agnew ML, Hampton CR, Rothnie CL, Spring DJ, Pohlman TH, Shimpo H, Verrier ED. Inhibition of Toll-like receptor 4 with eritoran attenuates myocardial ischemia-reperfusion injury. Circulation 2006;114:I270-4.CrossRef Shimamoto A, Chong AJ, Yada M, Shomura S, Takayama H, Fleisig AJ, Agnew ML, Hampton CR, Rothnie CL, Spring DJ, Pohlman TH, Shimpo H, Verrier ED. Inhibition of Toll-like receptor 4 with eritoran attenuates myocardial ischemia-reperfusion injury. Circulation 2006;114:I270-4.CrossRef
9.
Zurück zum Zitat Shishido T, Nozaki N, Yamaguchi S, Shibata Y, Nitobe J, Miyamoto T, Takahashi H, Arimoto T, Maeda K, Yamakawa M, Takeuchi O, Akira S, Takeishi Y, Kubota I. Toll-like receptor-2 modulates ventricular remodeling after myocardial infarction. Circulation 2003;108:2905-10.CrossRef Shishido T, Nozaki N, Yamaguchi S, Shibata Y, Nitobe J, Miyamoto T, Takahashi H, Arimoto T, Maeda K, Yamakawa M, Takeuchi O, Akira S, Takeishi Y, Kubota I. Toll-like receptor-2 modulates ventricular remodeling after myocardial infarction. Circulation 2003;108:2905-10.CrossRef
10.
Zurück zum Zitat Toldo S, Abbate A. The NLRP3 inflammasome in acute myocardial infarction. Nat Rev Cardiol 2018;15:203-14.CrossRef Toldo S, Abbate A. The NLRP3 inflammasome in acute myocardial infarction. Nat Rev Cardiol 2018;15:203-14.CrossRef
11.
Zurück zum Zitat Ruparelia N, Chai JT, Fisher EA, Choudhury RP. Inflammatory processes in cardiovascular disease: A route to targeted therapies. Nat Rev Cardiol 2017;14:133-44.CrossRef Ruparelia N, Chai JT, Fisher EA, Choudhury RP. Inflammatory processes in cardiovascular disease: A route to targeted therapies. Nat Rev Cardiol 2017;14:133-44.CrossRef
12.
Zurück zum Zitat Coll RC, Robertson AA, Chae JJ, Higgins SC, Munoz-Planillo R, Inserra MC, Vetter I, Dungan LS, Monks BG, Stutz A, Croker DE, Butler MS, Haneklaus M, Sutton CE, Nunez G, Latz E, Kastner DL, Mills KH, Masters SL, Schroder K, Cooper MA, O’Neill LA. A small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases. Nat Med 2015;21:248-55.CrossRef Coll RC, Robertson AA, Chae JJ, Higgins SC, Munoz-Planillo R, Inserra MC, Vetter I, Dungan LS, Monks BG, Stutz A, Croker DE, Butler MS, Haneklaus M, Sutton CE, Nunez G, Latz E, Kastner DL, Mills KH, Masters SL, Schroder K, Cooper MA, O’Neill LA. A small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases. Nat Med 2015;21:248-55.CrossRef
13.
Zurück zum Zitat Coll RC, Hill JR, Day CJ, Zamoshnikova A, Boucher D, Massey NL, Chitty JL, Fraser JA, Jennings MP, Robertson AAB, Schroder K. MCC950 directly targets the NLRP3 ATP-hydrolysis motif for inflammasome inhibition. Nat Chem Biol 2019;15:556-9.CrossRef Coll RC, Hill JR, Day CJ, Zamoshnikova A, Boucher D, Massey NL, Chitty JL, Fraser JA, Jennings MP, Robertson AAB, Schroder K. MCC950 directly targets the NLRP3 ATP-hydrolysis motif for inflammasome inhibition. Nat Chem Biol 2019;15:556-9.CrossRef
14.
Zurück zum Zitat Laliberte RE, Perregaux DG, Hoth LR, Rosner PJ, Jordan CK, Peese KM, Eggler JF, Dombroski MA, Geoghegan KF, Gabel CA. Glutathione S-transferase omega 1-1 is a target of cytokine release inhibitory drugs and may be responsible for their effect on interleukin-1 beta posttranslational processing. J Biol Chem 2003;278:16567-78.CrossRef Laliberte RE, Perregaux DG, Hoth LR, Rosner PJ, Jordan CK, Peese KM, Eggler JF, Dombroski MA, Geoghegan KF, Gabel CA. Glutathione S-transferase omega 1-1 is a target of cytokine release inhibitory drugs and may be responsible for their effect on interleukin-1 beta posttranslational processing. J Biol Chem 2003;278:16567-78.CrossRef
15.
Zurück zum Zitat Tapia-Abellan A, Angosto-Bazarra D, Martinez-Banaclocha H, de Torre-Minguela C, Ceron-Carrasco JP, Perez-Sanchez H, Arostegui JI, Pelegrin P. MCC950 closes the active conformation of NLRP3 to an inactive state. Nat Chem Biol 2019;15:560-4.CrossRef Tapia-Abellan A, Angosto-Bazarra D, Martinez-Banaclocha H, de Torre-Minguela C, Ceron-Carrasco JP, Perez-Sanchez H, Arostegui JI, Pelegrin P. MCC950 closes the active conformation of NLRP3 to an inactive state. Nat Chem Biol 2019;15:560-4.CrossRef
16.
Zurück zum Zitat Gao R, Shi H, Chang S, Gao Y, Li X, Lv C, Yang H, Xiang H, Yang J, Xu L, Tang Y. The selective NLRP3-inflammasome inhibitor MCC950 reduces myocardial fibrosis and improves cardiac remodeling in a mouse model of myocardial infarction. Int Immunopharmacol 2019;74:105575.CrossRef Gao R, Shi H, Chang S, Gao Y, Li X, Lv C, Yang H, Xiang H, Yang J, Xu L, Tang Y. The selective NLRP3-inflammasome inhibitor MCC950 reduces myocardial fibrosis and improves cardiac remodeling in a mouse model of myocardial infarction. Int Immunopharmacol 2019;74:105575.CrossRef
17.
Zurück zum Zitat van Hout GP, Bosch L, Ellenbroek GH, de Haan JJ, van Solinge WW, Cooper MA, Arslan F, de Jager SC, Robertson AA, Pasterkamp G, Hoefer IE. The selective NLRP3-inflammasome inhibitor MCC950 reduces infarct size and preserves cardiac function in a pig model of myocardial infarction. Eur Heart J 2017;38:828-36.PubMed van Hout GP, Bosch L, Ellenbroek GH, de Haan JJ, van Solinge WW, Cooper MA, Arslan F, de Jager SC, Robertson AA, Pasterkamp G, Hoefer IE. The selective NLRP3-inflammasome inhibitor MCC950 reduces infarct size and preserves cardiac function in a pig model of myocardial infarction. Eur Heart J 2017;38:828-36.PubMed
18.
Zurück zum Zitat Frantz S, Nahrendorf M. Cardiac macrophages and their role in ischaemic heart disease. Cardiovasc Res 2014;102:240-8.CrossRef Frantz S, Nahrendorf M. Cardiac macrophages and their role in ischaemic heart disease. Cardiovasc Res 2014;102:240-8.CrossRef
19.
Zurück zum Zitat Nahrendorf M, Swirski FK. Abandoning M1/M2 for a network model of macrophage function. Circ Res 2016;119:414-7.CrossRef Nahrendorf M, Swirski FK. Abandoning M1/M2 for a network model of macrophage function. Circ Res 2016;119:414-7.CrossRef
20.
Zurück zum Zitat Osborne MT, Hulten EA, Murthy VL, Skali H, Taqueti VR, Dorbala S, DiCarli MF, Blankstein R. Patient preparation for cardiac fluorine-18 fluorodeoxyglucose positron emission tomography imaging of inflammation. J Nucl Cardiol 2017;24:86-99.CrossRef Osborne MT, Hulten EA, Murthy VL, Skali H, Taqueti VR, Dorbala S, DiCarli MF, Blankstein R. Patient preparation for cardiac fluorine-18 fluorodeoxyglucose positron emission tomography imaging of inflammation. J Nucl Cardiol 2017;24:86-99.CrossRef
21.
Zurück zum Zitat Alvi RM, Young BD, Shahab Z, Pan H, Winkler J, Herzog E, Miller EJ. Repeatability and optimization of FDG positron emission tomography for evaluation of cardiac sarcoidosis. JACC Cardiovasc Imaging 2019;12:1284-7.CrossRef Alvi RM, Young BD, Shahab Z, Pan H, Winkler J, Herzog E, Miller EJ. Repeatability and optimization of FDG positron emission tomography for evaluation of cardiac sarcoidosis. JACC Cardiovasc Imaging 2019;12:1284-7.CrossRef
22.
Zurück zum Zitat Abraham A, Nichol G, Williams KA, Guo A, deKemp RA, Garrard L, Davies RA, Duchesne L, Haddad H, Chow B, DaSilva J, Beanlands RS, Investigators P. 18F-FDG PET imaging of myocardial viability in an experienced center with access to 18F-FDG and integration with clinical management teams: The Ottawa-FIVE substudy of the PARR 2 trial. J Nucl Med 2010;51:567-74.CrossRef Abraham A, Nichol G, Williams KA, Guo A, deKemp RA, Garrard L, Davies RA, Duchesne L, Haddad H, Chow B, DaSilva J, Beanlands RS, Investigators P. 18F-FDG PET imaging of myocardial viability in an experienced center with access to 18F-FDG and integration with clinical management teams: The Ottawa-FIVE substudy of the PARR 2 trial. J Nucl Med 2010;51:567-74.CrossRef
23.
Zurück zum Zitat Henkel DM, Witt BJ, Gersh BJ, Jacobsen SJ, Weston SA, Meverden RA, Roger VL. Ventricular arrhythmias after acute myocardial infarction: A 20-year community study. Am Heart J 2006;151:806-12.CrossRef Henkel DM, Witt BJ, Gersh BJ, Jacobsen SJ, Weston SA, Meverden RA, Roger VL. Ventricular arrhythmias after acute myocardial infarction: A 20-year community study. Am Heart J 2006;151:806-12.CrossRef
24.
Zurück zum Zitat Gorenek B, Lundqvist CB, Terradellas JB, Camm AJ, Hindricks G, Huber K, Kirchhof P, Kuck KH, Kudaiberdieva G, Lin T, Raviele A, Santini M, Tilz RR, Valgimigli M, Vos MA, Vrints C, Zeymer U. Cardiac arrhythmias in acute coronary syndromes: Position paper from the joint EHRA, ACCA, and EAPCI task force. Eur Heart J Acute Cardiovasc Care 2015;4:386.CrossRef Gorenek B, Lundqvist CB, Terradellas JB, Camm AJ, Hindricks G, Huber K, Kirchhof P, Kuck KH, Kudaiberdieva G, Lin T, Raviele A, Santini M, Tilz RR, Valgimigli M, Vos MA, Vrints C, Zeymer U. Cardiac arrhythmias in acute coronary syndromes: Position paper from the joint EHRA, ACCA, and EAPCI task force. Eur Heart J Acute Cardiovasc Care 2015;4:386.CrossRef
25.
Zurück zum Zitat Prabhu SD, Frangogiannis NG. The biological basis for cardiac repair after myocardial infarction: From inflammation to fibrosis. Circ Res 2016;119:91-112.CrossRef Prabhu SD, Frangogiannis NG. The biological basis for cardiac repair after myocardial infarction: From inflammation to fibrosis. Circ Res 2016;119:91-112.CrossRef
26.
Zurück zum Zitat Frangogiannis NG. The extracellular matrix in ischemic and nonischemic heart failure. Circ Res 2019;125:117-46.CrossRef Frangogiannis NG. The extracellular matrix in ischemic and nonischemic heart failure. Circ Res 2019;125:117-46.CrossRef
27.
Zurück zum Zitat Frangogiannis NG. Can myocardial fibrosis be reversed? J Am Coll Cardiol 2019;73:2283-5.CrossRef Frangogiannis NG. Can myocardial fibrosis be reversed? J Am Coll Cardiol 2019;73:2283-5.CrossRef
Metadaten
Titel
18F-FDG PET imaging of myocardial inflammation and viability following experimental infarction and anti-inflammatory treatment with compound MCC950
verfasst von
Jeremy Jong, BS
René R. Sevag Packard, MD, PhD
Publikationsdatum
24.04.2020
Verlag
Springer International Publishing
Erschienen in
Journal of Nuclear Cardiology / Ausgabe 5/2021
Print ISSN: 1071-3581
Elektronische ISSN: 1532-6551
DOI
https://doi.org/10.1007/s12350-020-02104-5

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