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

dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorCASTRO, Leandro Teixeira de
dc.contributor.authorSANTOS, Itamar de Souza
dc.contributor.authorGOULART, Alessandra C.
dc.contributor.authorPEREIRA, Alexandre da Costa
dc.contributor.authorSTANIAK, Henrique Lane
dc.contributor.authorBITTENCOURT, Marcio Sommer
dc.contributor.authorLOTUFO, Paulo Andrade
dc.contributor.authorBENSENOR, Isabela Martins
dc.date.accessioned2019-05-30T13:19:56Z
dc.date.available2019-05-30T13:19:56Z
dc.date.issued2019
dc.description.abstractBackground: 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.eng
dc.description.indexMEDLINEeng
dc.identifier.citationARQUIVOS BRASILEIROS DE CARDIOLOGIA, v.112, n.3, p.230-237, 2019
dc.identifier.doi10.5935/abc.20180268
dc.identifier.issn0066-782X
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/31613
dc.language.isoeng
dc.publisherARQUIVOS BRASILEIROS CARDIOLOGIAeng
dc.relation.ispartofArquivos Brasileiros de Cardiologia
dc.rightsopenAccesseng
dc.rights.holderCopyright ARQUIVOS BRASILEIROS CARDIOLOGIAeng
dc.subjectCoronary Artery Disease / mortalityeng
dc.subjectTroponin Ieng
dc.subjectPrognosiseng
dc.subjectMetabolic Syndromeeng
dc.subjectBiological Variation, populationeng
dc.subjectRisk Factorseng
dc.subject.otherbase-line characteristicseng
dc.subject.othermyocardial-infarctioneng
dc.subject.otherprognostic valueeng
dc.subject.otherunstable anginaeng
dc.subject.othertask-forceeng
dc.subject.otherdiseaseeng
dc.subject.othermanagementeng
dc.subject.otherregistryeng
dc.subject.othereventseng
dc.subject.otherriskeng
dc.subject.wosCardiac & Cardiovascular Systemseng
dc.titleElevated 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 Cohorteng
dc.typearticleeng
dc.type.categoryoriginal articleeng
dc.type.versionpublishedVersioneng
dspace.entity.typePublication
hcfmusp.author.externalCASTRO, Leandro Teixeira de:Univ Sao Paulo, Ctr Pesquisa Clin & Epidemiol, Sao Paulo, SP, Brazil
hcfmusp.citation.scopus8
hcfmusp.contributor.author-fmusphcITAMAR DE SOUZA SANTOS
hcfmusp.contributor.author-fmusphcALESSANDRA CARVALHO GOULART
hcfmusp.contributor.author-fmusphcALEXANDRE DA COSTA PEREIRA
hcfmusp.contributor.author-fmusphcHENRIQUE LANE STANIAK
hcfmusp.contributor.author-fmusphcMARCIO SOMMER BITTENCOURT
hcfmusp.contributor.author-fmusphcPAULO ANDRADE LOTUFO
hcfmusp.contributor.author-fmusphcISABELA JUDITH MARTINS BENSEñOR
hcfmusp.description.beginpage230
hcfmusp.description.endpage237
hcfmusp.description.issue3
hcfmusp.description.volume112
hcfmusp.origemWOS
hcfmusp.origem.pubmed30916200
hcfmusp.origem.scieloSCIELO:S0066-782X2019000300230
hcfmusp.origem.scopus2-s2.0-85063961489
hcfmusp.origem.wosWOS:000461955200004
hcfmusp.publisher.cityRIO DE JANEIROeng
hcfmusp.publisher.countryBRAZILeng
hcfmusp.relation.referenceAmsterdam, 2014, CIRCULATION, V130, pE433, DOI 10.1161/CIR.0000000000000151eng
hcfmusp.relation.referenceAng DSC, 2012, HEART, V98, P1160, DOI 10.1136/heartjnl-2012-301635eng
hcfmusp.relation.referenceAntman EM, 1996, NEW ENGL J MED, V335, P1342, DOI 10.1056/NEJM199610313351802eng
hcfmusp.relation.referenceBiener M, 2018, OPEN HEART, V5, DOI 10.1136/openhrt-2017-000710eng
hcfmusp.relation.referenceCAPASSO JM, 1992, CIRC RES, V70, P148, DOI 10.1161/01.RES.70.1.148eng
hcfmusp.relation.referenceDe Lemos JA, 2011, JAMA-J AM MED ASSOC, V305, P1200, DOI 10.1001/jama.2011.349eng
hcfmusp.relation.referenceEggers KM, 2007, CIRCULATION, V116, P1907, DOI 10.1161/CIRCULATIONAHA.107.708529eng
hcfmusp.relation.referenceGoodman SG, 2009, AM HEART J, V158, P193, DOI 10.1016/j.ahj.2009.06.003eng
hcfmusp.relation.referenceGoulart AC, 2013, CLINICS, V68, P431, DOI 10.6061/clinics/2013(03)RC02eng
hcfmusp.relation.referenceGrodin JL, 2015, AM J MED, V128, P276, DOI 10.1016/j.amjmed.2014.09.029eng
hcfmusp.relation.referenceHAMM CW, 1992, NEW ENGL J MED, V327, P146, DOI 10.1056/NEJM199207163270302eng
hcfmusp.relation.referenceIbanez B, 2018, EUR HEART J, V39, P119, DOI 10.1093/eurheartj/ehx393eng
hcfmusp.relation.referenceJames SK, 2003, J AM COLL CARDIOL, V41, P916, DOI 10.1016/S0735-1097(02)02969-8eng
hcfmusp.relation.referenceKoenig W, 2012, CLIN CHEM, V58, P1215, DOI 10.1373/clinchem.2012.183319eng
hcfmusp.relation.referenceLatini R, 2007, CIRCULATION, V116, P1242, DOI 10.1161/CIRCULATIONAHA.106.655076eng
hcfmusp.relation.referenceLindahl B, 2000, NEW ENGL J MED, V343, P1139, DOI 10.1056/NEJM200010193431602eng
hcfmusp.relation.referenceLindahl B, 2001, J AM COLL CARDIOL, V38, P979, DOI 10.1016/S0735-1097(01)01501-7eng
hcfmusp.relation.referenceMcQueen MJ, 2013, CLIN BIOCHEM, V46, P5, DOI 10.1016/j.clinbiochem.2012.10.003eng
hcfmusp.relation.referenceNaghavi M, 2015, LANCET, V385, P117, DOI 10.1016/S0140-6736(14)61682-2eng
hcfmusp.relation.referenceNdrepepa G, 2013, AM HEART J, V165, P1032eng
hcfmusp.relation.referenceNicolau JC, 2012, ARQ BRAS CARDIOL, V98, P282, DOI 10.1590/S0066-782X2012000400001eng
hcfmusp.relation.referenceO'Gara PT, 2013, J AM COLL CARDIOL, V61, pE78, DOI 10.1016/j.jacc.2012.11.019eng
hcfmusp.relation.referenceOlivetti G, 1997, NEW ENGL J MED, V336, P1131, DOI 10.1056/NEJM199704173361603eng
hcfmusp.relation.referenceOmland T, 2014, J AM COLL CARDIOL, V63, P195, DOI 10.1016/j.jacc.2013.10.039eng
hcfmusp.relation.referenceOmland T, 2009, NEW ENGL J MED, V361, P2538, DOI 10.1056/NEJMoa0805299eng
hcfmusp.relation.referenceRoffi M, 2016, EUR HEART J, V37, P267, DOI 10.1093/eurheartj/ehv320eng
hcfmusp.relation.referenceRoger VL, 2010, CIRCULATION, V121, P863, DOI 10.1161/CIRCULATIONAHA.109.897249eng
hcfmusp.relation.referenceRosjo H, 2011, AM J CARDIOL, V108, P88, DOI 10.1016/j.amjcard.2011.02.346eng
hcfmusp.relation.referenceSantos IS, 2015, ARQ BRAS CARDIOL, V105, P53, DOI 10.5935/abc.20150044eng
hcfmusp.relation.referenceTheroux P, 1998, CIRCULATION, V97, P1195, DOI 10.1161/01.CIR.97.12.1195eng
hcfmusp.relation.referenceVashistha V, 2016, INT J CARDIOL, V223, P401, DOI 10.1016/j.ijcard.2016.07.175eng
hcfmusp.relation.referenceWhite HD, 2011, J AM COLL CARDIOL, V58, P2356, DOI 10.1016/j.jacc.2011.09.001eng
hcfmusp.relation.referenceWhite HD, 2014, J AM COLL CARDIOL, V63, P345, DOI 10.1016/j.jacc.2013.08.1643eng
hcfmusp.scopus.lastupdate2024-05-10
relation.isAuthorOfPublicatione566281f-a9d6-4882-b281-5031a0141a11
relation.isAuthorOfPublicationcd675f04-b4ad-47f1-8d3c-15f6cb73d8cf
relation.isAuthorOfPublication415ce7ca-65c1-4699-b6f4-19dae8b03849
relation.isAuthorOfPublication89157b04-1b82-4f40-8fcb-ed090079a864
relation.isAuthorOfPublicatione3193e19-6ede-49dd-bde8-98da34ff70d1
relation.isAuthorOfPublicationcb0c8dbb-6df5-4294-8d8e-e96645a3cec1
relation.isAuthorOfPublication6911f59e-7ec9-4ad2-b746-580bf8b3d64d
relation.isAuthorOfPublication.latestForDiscoverye566281f-a9d6-4882-b281-5031a0141a11
Arquivos
Pacote Original
Agora exibindo 1 - 2 de 2
Carregando...
Imagem de Miniatura
Nome:
art_CASTRO_Elevated_HighSensitivity_Troponin_I_in_the_Stabilized_Phase_2019_eng.PDF
Tamanho:
306.11 KB
Formato:
Adobe Portable Document Format
Descrição:
publishedVersion (English)
Carregando...
Imagem de Miniatura
Nome:
art_CASTRO_Elevated_HighSensitivity_Troponin_I_in_the_Stabilized_Phase_2019_por.PDF
Tamanho:
351.22 KB
Formato:
Adobe Portable Document Format
Descrição:
publishedVersion (Portuguese)