Endothelial, platelet, and macrophage microparticle levels do not change acutely following transcatheter aortic valve replacement

Imagem de Miniatura
Arquivos
art_MARCHINI_Endothelial_platelet_and_macrophage_microparticle_levels_do_not_2016.PDF (854.5 KB)
Citações na Scopus
7
Tipo de produção
article
Data de publicação
2016
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
BIOMED CENTRAL LTD
Autores
CROCE, Kevin
Citação
JOURNAL OF NEGATIVE RESULTS IN BIOMEDICINE, v.15, article ID 7, 5p, 2016
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background: Patients with severe aortic stenosis have increased levels of prothrombotic and proinflammatory microparticles (MP), and MPs actively regulate pathological processes that lead to atherothrombotic cardiovascular events. Shear stress is a validated stimulus of MP production, and abnormal shear stress in aortic stenosis increases MP release in ex-vivo studies. We hypothesized that in patients with severe aortic stenosis, percutaneous replacement of the aortic valve (TAVR) would reduce abnormal shear stress and would decrease levels of circulating MPs. Findings: The experimental protocol utilized flow cytometry (FC) and nanoparticle tracking analysis (NTA) to quantify circulating plasma MP levels in aortic stenosis patients at baseline and 5 days after TAVR. The baseline and 5 day MP counts measured by FC were 6.10.10(5) +/- 1.21.10(5) MP/mu L and 5.74.10(5) +/- 9.54.10(4) MP/mu L, respectively (p = 0.91). The baseline and 5 day MP counts measured by NTA were 9.29.10(13) +/- 1.66.10(13) MP/mu L and 3.95.10(14) +/- 3.11.10(14) MP/mu L, respectively (p = 0.91). When MPs were stratified by cell source, there was no difference in pre/post TAVR endothelial, platelet, or leukocyte MP levels. Conclusion: Levels of circulating MPs do not change acutely following TAVR therapy for aortic stenosis. Trial registered at clinicaltrials. gov NCT02193035 on July 11, 2014.
Palavras-chave
Severe aortic stenosis, Microparticles, Nanoparticle-tracking analysis, Flow cytometry
URI
https://observatorio.fm.usp.br/handle/OPI/17030
Referências
  1. Boulanger CM, 2001, CIRCULATION, V104, P2649, DOI 10.1161/hc4701.100516
  2. Diehl P, 2008, THROMB HAEMOSTASIS, V99, P711, DOI 10.1160/TH07-05-0334
  3. Dragovic RA, 2011, NANOMED-NANOTECHNOL, V7, P780, DOI 10.1016/j.nano.2011.04.003
  4. Gardiner C., 2013, J EXTRACELL VESICLES, V2, DOI [10.3402/jev.v2i0.19671, DOI 10.3402/JEV.V2I0.19671]
  5. Horn P, 2015, EUROINTERVENTION, V10, P1456, DOI 10.4244/EIJY14M10_02
  6. Hron G, 2007, THROMB HAEMOSTASIS, V97, P119, DOI 10.1160/TH06-03-0141
  7. Huber J, 2002, ARTERIOSCL THROM VAS, V22, P101, DOI 10.1161/hq0102.101525
  8. Jimenez JJ, 2003, BRIT J HAEMATOL, V123, P896, DOI 10.1046/j.1365-2141.2003.04716.x
  9. Jy W, 2004, J THROMB HAEMOST, V2, P1842, DOI 10.1111/j.1538-7836.2004.00936.x
  10. McCabe JM, 2014, CATHETER CARDIO INTE, V83, P633, DOI 10.1002/ccd.25206
  11. Mesri M, 1999, J BIOL CHEM, V274, P23111, DOI 10.1074/jbc.274.33.23111
  12. Nomura S, 2001, ATHEROSCLEROSIS, V158, P277, DOI 10.1016/S0021-9150(01)00433-6
  13. Petrov G, 2010, CIRCULATION, V122, pS23, DOI 10.1161/CIRCULATIONAHA.109.927764
  14. Pfister SL, 2004, HYPERTENSION, V43, P428, DOI 10.1161/01.HYP.0000110906.77479.91
  15. Toti F, 1996, BLOOD, V87, P1409
  16. van der Pol E, 2014, J THROMB HAEMOST, V12, P1182, DOI 10.1111/jth.12602
  17. van der Pol E, 2010, J THROMB HAEMOST, V8, P2596, DOI 10.1111/j.1538-7836.2010.04074.x
  18. Viera AJ, 2012, J AM SOC HYPERTENS, V6, P243, DOI 10.1016/j.jash.2012.06.003

Coleções
Artigos e Materiais de Revistas Científicas - FM/MCP
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - HC/InCor
Artigos e Materiais de Revistas Científicas - LIM/11
Artigos e Materiais de Revistas Científicas - LIM/13