Elevated High-Sensitivity Troponin I in the Stabilized Phase after an Acute Coronary Syndrome Predicts All-Cause and Cardiovascular Mortality in a Highly Admixed Population: A 7-Year Cohort

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Citações na Scopus
7
Tipo de produção
article
Data de publicação
2019
Título da Revista
ISSN da Revista
Título do Volume
Editora
ARQUIVOS BRASILEIROS CARDIOLOGIA
Citação
ARQUIVOS BRASILEIROS DE CARDIOLOGIA, v.112, n.3, p.230-237, 2019
Projetos de Pesquisa
Unidades Organizacionais
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Resumo
Background: High-sensitivity cardiac troponin I (hs-cTnl) has played an important role in the risk stratification of patients during the in-hospital phase of acute coronary syndrome (ACS), but few studies have determined its role as a long-term prognostic marker in the outpatient setting. Obiective : To investigate the association between levels of hs-cTnl measured in the subacute phase after an ACS event and long-term prognosis in a highly admixed population. Methods: We measured levels of hs-cTnl in 525 patients 25 to 90 days after admission for an ACS event; these patients were then divided into tertiles according to hs-cTnl levels and followed for up to 7 years. We compared all-cause and cardiovascular mortality using Cox proportional hazards models and adopting a significance level of 5%. Results: After a median follow-up of 51 months, patients in the highest tertile had a greater hazard ratio (HR) for all-cause mortality after adjustment for age, sex, known cardiovascular risk factors, medication use, and demographic factors (HR: 3.84, 95% Cl: 1.92-8.12). These findings persisted after further adjustment for estimated glomerular filtration rate < 60 ml/min/1.73 m(2) and left ventricular ejection fraction < 0.40 (HR: 6.53, 95% CI: 2.12-20.14). Cardiovascular mortality was significantly higher in the highest tertile after adjustment for age and sex (HR: 5.65, 95% CI: 1.94-16.47) and both in the first (HR: 4.90, 95% CI: 1.35-17.82) and second models of multivariate adjustment (HR: 5.89, 95% CI: 1.08-32.27). Conclusions: Elevated hs-cTnl levels measured in the stabilized phase after an ACS event are independent predictors of all-cause and cardiovascular mortality in a highly admixed population.
Palavras-chave
Coronary Artery Disease / mortality, Troponin I, Prognosis, Metabolic Syndrome, Biological Variation, population, Risk Factors
Referências
  1. Amsterdam, 2014, CIRCULATION, V130, pE433, DOI 10.1161/CIR.0000000000000151
  2. Ang DSC, 2012, HEART, V98, P1160, DOI 10.1136/heartjnl-2012-301635
  3. Antman EM, 1996, NEW ENGL J MED, V335, P1342, DOI 10.1056/NEJM199610313351802
  4. Biener M, 2018, OPEN HEART, V5, DOI 10.1136/openhrt-2017-000710
  5. CAPASSO JM, 1992, CIRC RES, V70, P148, DOI 10.1161/01.RES.70.1.148
  6. De Lemos JA, 2011, JAMA-J AM MED ASSOC, V305, P1200, DOI 10.1001/jama.2011.349
  7. Eggers KM, 2007, CIRCULATION, V116, P1907, DOI 10.1161/CIRCULATIONAHA.107.708529
  8. Goodman SG, 2009, AM HEART J, V158, P193, DOI 10.1016/j.ahj.2009.06.003
  9. Goulart AC, 2013, CLINICS, V68, P431, DOI 10.6061/clinics/2013(03)RC02
  10. Grodin JL, 2015, AM J MED, V128, P276, DOI 10.1016/j.amjmed.2014.09.029
  11. HAMM CW, 1992, NEW ENGL J MED, V327, P146, DOI 10.1056/NEJM199207163270302
  12. Ibanez B, 2018, EUR HEART J, V39, P119, DOI 10.1093/eurheartj/ehx393
  13. James SK, 2003, J AM COLL CARDIOL, V41, P916, DOI 10.1016/S0735-1097(02)02969-8
  14. Koenig W, 2012, CLIN CHEM, V58, P1215, DOI 10.1373/clinchem.2012.183319
  15. Latini R, 2007, CIRCULATION, V116, P1242, DOI 10.1161/CIRCULATIONAHA.106.655076
  16. Lindahl B, 2000, NEW ENGL J MED, V343, P1139, DOI 10.1056/NEJM200010193431602
  17. Lindahl B, 2001, J AM COLL CARDIOL, V38, P979, DOI 10.1016/S0735-1097(01)01501-7
  18. McQueen MJ, 2013, CLIN BIOCHEM, V46, P5, DOI 10.1016/j.clinbiochem.2012.10.003
  19. Naghavi M, 2015, LANCET, V385, P117, DOI 10.1016/S0140-6736(14)61682-2
  20. Ndrepepa G, 2013, AM HEART J, V165, P1032
  21. Nicolau JC, 2012, ARQ BRAS CARDIOL, V98, P282, DOI 10.1590/S0066-782X2012000400001
  22. O'Gara PT, 2013, J AM COLL CARDIOL, V61, pE78, DOI 10.1016/j.jacc.2012.11.019
  23. Olivetti G, 1997, NEW ENGL J MED, V336, P1131, DOI 10.1056/NEJM199704173361603
  24. Omland T, 2014, J AM COLL CARDIOL, V63, P195, DOI 10.1016/j.jacc.2013.10.039
  25. Omland T, 2009, NEW ENGL J MED, V361, P2538, DOI 10.1056/NEJMoa0805299
  26. Roffi M, 2016, EUR HEART J, V37, P267, DOI 10.1093/eurheartj/ehv320
  27. Roger VL, 2010, CIRCULATION, V121, P863, DOI 10.1161/CIRCULATIONAHA.109.897249
  28. Rosjo H, 2011, AM J CARDIOL, V108, P88, DOI 10.1016/j.amjcard.2011.02.346
  29. Santos IS, 2015, ARQ BRAS CARDIOL, V105, P53, DOI 10.5935/abc.20150044
  30. Theroux P, 1998, CIRCULATION, V97, P1195, DOI 10.1161/01.CIR.97.12.1195
  31. Vashistha V, 2016, INT J CARDIOL, V223, P401, DOI 10.1016/j.ijcard.2016.07.175
  32. White HD, 2011, J AM COLL CARDIOL, V58, P2356, DOI 10.1016/j.jacc.2011.09.001
  33. White HD, 2014, J AM COLL CARDIOL, V63, P345, DOI 10.1016/j.jacc.2013.08.1643