Preprocedural statin therapy, inflammation, and myocardial injury in low-risk stable coronary artery disease patients submitted to coronary stent implantation

Imagem de Miniatura
Arquivos
art_GREQUE_Preprocedural_statin_therapy_inflammation_and_myocardial_injury_in_2016.PDF (114.86 KB)
Citações na Scopus
5
Tipo de produção
article
Data de publicação
2016
Editora
WILEY-BLACKWELL
DOI
Indexadores
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Autores
GREQUE, Gilmar V.
SANTOS, Marcio
PIVATELI, Flavio
JACOB, Jose Luis B.
PESARO, Antonio Eduardo P.
Autor de Grupo de pesquisa
Editores
Coordenadores
Organizadores
Citação
CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, v.87, n.2, p.222-229, 2016
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
ObjectiveEvaluate if statin therapy prior to elective coronary stent implantation (CSI) reduces the plasma levels of markers of inflammation and of myocardial necrosis in low-risk stable coronary artery disease patients (CAD). BackgroundThe elevation of markers of inflammation and of myocardial necrosis after percutaneous coronary intervention may interfere with clinical outcome. Among acute coronary syndrome patients, statins improve clinical outcomes when used before CSImostly due to reduction of CSI-related myocardial infarction. However, little is known concerning preprocedural statin therapy on the reduction of these markers in stable patients at low-risk. MethodsIn this prospective, observational study, 100 patients (n = 50 on statin therapy vs. n = 50 not on statin) with stable coronary artery disease underwent elective CSI. Inflammatory (C-reactive protein [CRP], interleukin [IL]-6, tumor necrosis factor- and matrix metalloproteinase-9) and myocardial necrosis markers (troponin I and CK-MB) were determined before and 24 hr after CSI. ResultsAll patients presented a significant increase of CRP and IL-6 after CSI. However, this increase was attenuated in patients on statin therapy prior to CSI than those without statin therapy: 75% vs. 150% (P < 0.001) and 192% vs. 300% (P < 0.01). The other pro-inflammatory markers were similar for both sets of patients. Troponin I and CK-MB did not change after CSI regardless of previous statin therapy or not. ConclusionsPretreatment with statin attenuates procedural inflammation, denoted by markedly lower increases of CRP and IL-6 levels, in elective CSI within low-risk stable CAD patients. Periprocedural myocardial injury was irrelevant and was not affected by preprocedural statin therapy in this population. (c) 2015 Wiley Periodicals, Inc.
Palavras-chave
stable coronary artery disease, coronary stent implantation, inflammatory markers, myocardial damage, statin
URI
https://observatorio.fm.usp.br/handle/OPI/13889
Referências
  1. Iliodromitis EK, 2006, HEART, V92, P1821, DOI 10.1136/hrt.2006.089060
  2. Stumpf C, 2009, CLIN SCI, V116, P45, DOI 10.1042/CS20080042
  3. Nallamothu BK, 2003, J AM COLL CARDIOL, V42, P1412, DOI 10.1016/S0735-1097(03)01037-4
  4. Serrano CV, 1997, J AM COLL CARDIOL, V29, P1276
  5. Mills EJ, 2011, QJM-INT J MED, V104, P109, DOI 10.1093/qjmed/hcq165
  6. Chang SM, 2004, CATHETER CARDIO INTE, V62, P193, DOI 10.1002/ccd.20078
  7. Chan AW, 2003, CIRCULATION, V107, P1750, DOI 10.1161/01.CIR.0000060541.18923.E9
  8. Caixeta AM, 2007, CATHETER CARDIO INTE, V69, P500, DOI 10.1002/ccd.21007
  9. Paiva MSM, 2008, J INTERV CARDIOL, V21, P403, DOI 10.1111/j.1540-8183.2008.00385.x
  10. Loppnow H, 2011, J CELL MOL MED, V15, P994, DOI 10.1111/j.1582-4934.2010.01036.x
  11. Li JJ, 2010, TEX HEART I J, V37, P49
  12. Veselka J, 2009, AM J CARDIOL, V104, P630, DOI 10.1016/j.amjcard.2009.04.048
  13. Blake GJ, 2001, CIRC RES, V89, P763, DOI 10.1161/hh2101.099270
  14. Jensen LO, 2007, J AM COLL CARDIOL, V50, P463, DOI 10.1016/j.jacc.2007.06.002
  15. Phipps RP, 2009, ARTERIOSCL THROM VAS, V29, P620, DOI 10.1161/ATVBAHA.109.184648
  16. Packard RRS, 2008, CLIN CHEM, V54, P24, DOI 10.1373/clinchem.2007.097360
  17. Antoniades C, 2009, J AM COLL CARDIOL, V54, P669, DOI 10.1016/j.jacc.2009.03.076
  18. Patti G, 2006, J AM COLL CARDIOL, V48, P1560, DOI 10.1016/j.jacc.2006.06.061
  19. Hong SJ, 2006, HEART, V92, P1119, DOI 10.1136/hrt.2005.075960
  20. Huang W, 2009, CORONARY ARTERY DIS, V20, P245, DOI 10.1097/MCA.0b013e32832a1950
  21. Winchester DE, 2010, J AM COLL CARDIOL, V56, P1099, DOI 10.1016/j.jacc.2010.04.023
  22. Crisby M, 2001, CIRCULATION, V103, P926
  23. Antonopoulos AS, 2012, CURR PHARM DESIGN, V18, P1519
  24. Pesaro AEP, 2012, INT J CARDIOL, V158, P400, DOI 10.1016/j.ijcard.2011.01.062
  25. Kaesemeyer W, 2009, ATHEROSCLEROSIS, V207, P343, DOI 10.1016/j.atherosclerosis.2009.05.026
  26. Wenaweser P, 2007, AM J CARDIOL, V99, P353, DOI 10.1016/j.amjcard.2006.08.036
  27. Cipollone F, 2003, CIRCULATION, V107, P1479, DOI 10.1161/01.CIR.0000056530.03783.81
  28. Briguori C, 2009, J AM COLL CARDIOL, V54, P2157, DOI 10.1016/j.jacc.2009.07.005
  29. Ascer E, 2004, ATHEROSCLEROSIS, V177, P161, DOI 10.1016/j.atherosclerosis.2004.07.003
  30. Patti G, 2007, J AM COLL CARDIOL, V49, P1272, DOI 10.1016/j.jacc.2007.02.025
  31. Cesar LAM, 2004, ARQ BRAS CARDIOL S2, V83, P1
  32. Delhaye Cédric, 2009, Cardiovasc Revasc Med, V10, P144, DOI 10.1016/j.carrev.2009.01.005
  33. Devaraj Sridevi, 2007, Curr Atheroscler Rep, V9, P33, DOI 10.1007/BF02693938
  34. Feldman TE, ACC AHA SCAI 2005 GU
  35. Ferrante Giuseppe, 2008, Cardiovasc Revasc Med, V9, P156, DOI 10.1016/j.carrev.2008.01.003
  36. Melfi Rosetta, 2010, Curr Cardiol Rep, V12, P295, DOI 10.1007/s11886-010-0110-0
  37. Saad Jamil Abdalla, 2004, Arq. Bras. Cardiol., V82, P1, DOI 10.1590/S0066-782X2004000700001
  38. SAS Institute Inc, 1985, SAS PROC GUID PERS C
  39. Wassmann S, 2003, CIRC RES, V93, pE98, DOI 10.1161/01.RES.0000099503.13312.7B

Coleções
Artigos e Materiais de Revistas Científicas - FM/MCP
Artigos e Materiais de Revistas Científicas - HC/InCor
Artigos e Materiais de Revistas Científicas - LIM/11
Artigos e Materiais de Revistas Científicas - ODS/03