Regional Myocardial Perfusion Disturbance in Experimental Chronic Chagas Cardiomyopathy

Imagem de Miniatura
Arquivos
art_OLIVEIRA_Regional_Myocardial_Perfusion_Disturbance_in_Experimental_Chronic_Chagas_2018.PDF (2.11 MB)
Citações na Scopus
11
Tipo de produção
article
Data de publicação
2018
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
SOC NUCLEAR MEDICINE INC
Autores
OLIVEIRA, Luciano Fonseca Lemos de
THACKERAY, James T.
MARIN NETO, Jose Antonio
ROMANO, Minna Moreira Dias
CARVALHO, Eduardo Elias Vieira de
MEJIA, Jorge
TANAKA, Denise Mayumi
SILVA, Grace Kelly da
ABDALLA, Douglas Reis
MALAMUT, Carlos
Citação
JOURNAL OF NUCLEAR MEDICINE, v.59, n.9, p.1430-1436, 2018
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Altered myocardial perfusion is a common finding in chronic Chagas cardiomyopathy (CCC), but its underlying histologic changes have not been elucidated. We investigated the occurrence of myocardial perfusion defects (MPDs) and the correlated regional changes to histology in an experimental model of CCC in hamsters. Methods: Female Syrian hamsters (n = 34) were infected with 3.5 x 10(4) to 10(5) trypomastigote forms of Trypanosoma cruzi, Y strain, and 6-10 mo afterward underwent in vivo imaging including resting Tc-99m-sestamibi SPECT, segmental and global left ventricular function assessment using 2-dimensional echocardiography, and F-18-FDG PET for evaluation of myocardial viability. Histologic analysis included quantification of fibrosis, inflammatory infiltration, and the diameter and density of myocardial microcirculation. Results: MPDs were present in 17 (50%) of the infected animals. Histologic analysis revealed no transmural scar in segments with an MPD, and normal or mildly reduced F-18-FDG uptake, indicating viable myocardium. Infected animals with an MPD, in comparison to infected animals without an MPD and control animals, showed a lower left ventricular ejection fraction (P = 0.012), a higher wall motion score index (P = 0.004), and a higher extent of inflammatory infiltration (P = 0.018) but a similar extent of fibrosis (P = 0.15) and similar microvascular diameter and density (P > 0.05). Segments with an MPD (n = 65), as compared with normally perfused regions in the same animal (n = 156), showed a higher wall motion score index (P = 0.005) but a similar extent of inflammatory infiltration, a similar extent of fibrosis, and a similar microvascular diameter and density. Conclusion: Resting MPDs are frequent in experimental CCC and are associated with myocardial inflammation but do not designate scar tissue, corresponding to regions with metabolically viable myocardium.
Palavras-chave
chronic Chagas cardiomyopathy, myocardial perfusion, myocardial inflammation
URI
https://observatorio.fm.usp.br/handle/OPI/29343
Referências
  1. Ashton AW, 2007, J EXP MED, V204, P929, DOI 10.1084/jem.20062432
  2. Bilate AMB, 2003, MICROBES INFECT, V5, P1116, DOI 10.1016/j.micinf.2003.07.001
  3. Cucunuba ZM, 2016, PARASITE VECTOR, V9, DOI 10.1186/s13071-016-1315-x
  4. de Almeida OC, 2002, J AM SOC ECHOCARDIOG, V15, P610, DOI 10.1067/mje.2002.117845
  5. FACTOR SM, 1985, AM J TROP MED HYG, V34, P246, DOI 10.4269/ajtmh.1985.34.246
  6. FERREIRA C S, 1980, Arquivos Brasileiros de Cardiologia, V34, P81
  7. Garcia MN, 2015, AM J CARDIOL, V115, P113, DOI 10.1016/j.amjcard.2014.09.050
  8. HAGAR JM, 1991, NEW ENGL J MED, V325, P763, DOI 10.1056/NEJM199109123251103
  9. Hayashi D, 2013, J AM COLL CARDIOL, V61, P2007, DOI 10.1016/j.jacc.2013.01.074
  10. Hiss FC, 2009, JACC-CARDIOVASC IMAG, V2, P164, DOI 10.1016/j.jcmg.2008.09.012
  11. Lagana B, 1999, ANGIOLOGY, V50, P143, DOI 10.1177/000331979905000208
  12. LARANJA FS, 1956, CIRCULATION, V14, P1035, DOI 10.1161/01.CIR.14.6.1035
  13. de Oliveira LFL, 2013, ARQ BRAS CARDIOL, V101, P59, DOI 10.5935/abc.20130110
  14. Marin JA, 2007, CIRCULATION, V115, P1109, DOI 10.1161/CIRCULATIONAHA.106.624296
  15. Marin-Neto JA, 2013, REV SOC BRAS MED TRO, V46, P536, DOI 10.1590/0037-8682-0028-2013
  16. MARINNETO JA, 1992, AM J CARDIOL, V69, P780, DOI 10.1016/0002-9149(92)90505-S
  17. Masuda A, 2016, EJNMMI RES, V6, DOI 10.1186/s13550-016-0196-5
  18. Oliveira LFL, 2016, J AM HEART ASSOC, V5
  19. Nunes MCP, 2013, J AM COLL CARDIOL, V62, P767, DOI 10.1016/j.jacc.2013.05.046
  20. Petkova SB, 2001, INT J PARASITOL, V31, P499, DOI 10.1016/S0020-7519(01)00168-0
  21. Ferreira LRP, 2014, WORLD J CARDIOL, V6, P782, DOI 10.4330/wjc.v6.i8.782
  22. Prado CM, 2009, AM J TROP MED HYG, V81, P900, DOI 10.4269/ajtmh.2009.09-0338
  23. Punukollu G, 2007, INT J CARDIOL, V115, P279, DOI 10.1016/j.ijcard.2006.03.004
  24. ROSSI MA, 1984, AM J PATHOL, V114, P209
  25. Rossi MA, 2010, PLOS NEGLECT TROP D, V4, DOI 10.1371/journal.pntd.0000674
  26. Salimy MS, 2017, CLIN NUCL MED, V42, pE265, DOI 10.1097/RLU.0000000000001622
  27. Schwartz RG, 2009, JACC-CARDIOVASC IMAG, V2, P173, DOI 10.1016/j.jcmg.2008.12.002
  28. Simoes M V, 1993, Arq Bras Cardiol, V60, P315
  29. Simoes MV, 2000, AM J CARDIOL, V86, P975, DOI 10.1016/S0002-9149(00)01133-4
  30. Sun Y, 2003, NUCL MED COMMUN, V24, P779, DOI 10.1097/01.ninm.0000080254.50447.5a
  31. Tanowitz HB, 1996, J PARASITOL, V82, P124, DOI 10.2307/3284127
  32. Monteiro JAT, 2014, J VASC SURG, V59, P1393, DOI 10.1016/j.jvs.2013.04.064
  33. Thackeray JT, 2015, EUR J NUCL MED MOL I, V42, P771, DOI 10.1007/s00259-014-2956-7
  34. TORRES C M, 1958, Hospital (Rio J), V54, P597
  35. TORRES C M, 1960, Mem Inst Oswaldo Cruz, V58, P161
  36. TORRES FW, 1995, AM HEART J, V129, P995, DOI 10.1016/0002-8703(95)90122-1
  37. Umezawa ES, 1996, J CLIN MICROBIOL, V34, P2143
  38. de Morais SDV, 2015, STEM CELLS DEV, V24, P2181, DOI 10.1089/scd.2014.0573

Coleções
Artigos e Materiais de Revistas Científicas - FM/MCM
Artigos e Materiais de Revistas Científicas - HC/InCor
Artigos e Materiais de Revistas Científicas - LIM/19
Artigos e Materiais de Revistas Científicas - ODS/03