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dc.contributor.authorMelo, Rodrigo Morel Vieira de-
dc.contributor.authorOikawa, Fernando Teiichi Costa-
dc.contributor.authorHueb, Whady-
dc.contributor.authorNomura, Cesar Higa-
dc.contributor.authorHueb, Alexandre Ciappina-
dc.contributor.authorVilla, Alexandre Volney-
dc.contributor.authorCosta, Leandro Menezes Alves da-
dc.contributor.authorRezende, Paulo Cury-
dc.contributor.authorSegre, Carlos Alexandre Wainrober-
dc.contributor.authorGarzillo, Cibele Larrosa-
dc.contributor.authorLima, Eduardo Gomes-
dc.contributor.authorRamires, Jose Antonio Franchini-
dc.contributor.authorKalil Filho, Roberto-
dc.date.accessioned2019-06-28T13:32:00Z-
dc.date.available2019-06-28T13:32:00Z-
dc.date.issued2017-
dc.identifier.issn1749-8090-
dc.identifier.numberVolume12 Nº122pt_BR
dc.identifier.urihttp://www7.bahiana.edu.br//jspui/handle/bahiana/2982-
dc.description.localpubSão Paulopt_BR
dc.description.abstractMyocardial necrosis biomarkers are frequently elevated after cardiac revascularization procedures. However, the diagnosis of acute myocardial infarction (MI) after a revascularization procedure is still a controversial issue. This inability to diagnose MI makes it more difficult to establish a specific therapeutic strategy. With the appearance of high-sensitivity troponins, a myriad of false-positive diagnoses for myocardial infarction have emerged. In 2000 and 2007 in an attempt to standardize the criteria for diagnosing MI, the European Society of Cardiology, the American College of Cardiology, the American Heart Association, and the World Heart Federation formed a joint task force to address this issue, but the task force was unable to make a satisfactory decision. Therefore, the problem still remained. To reduce diagnostic mistakes, in 2012, this same group arbitrarily raised the cutoff point to 10 times the 99th percentile, but with no solid scientific basis for doing so [1]. Troponin (cTnI) and the creatine kinase isoform (CK-MB) do not reflect, alone, the occurrence of MI related to occlusion of the graft or native artery or varying degrees of myocardial injury. Release of myocardial necrosis markers may be related to incomplete myocardial protection; reperfusion injury; a systemic inflammatory state, including inevitable postsurgical trauma; the handling of intramyocardial vessels; and cardiac defibrillator use [2, 3]. Cardiac troponin may also be increased when nonsurgical damage is present, such as sepsis and thromboembolic phenomena [1]. cTnIs have also been found elevated in athletes after marathons [4]. This makes the identification of small areas of injury very difficult to assess in clinical practice [5]. Parallel to the increased sensitivity of troponin assays, imaging methods have achieved better accuracy for exclusion of the diagnosis of myocardial infarction. Thus, due to the limitations on the interpretation of biomarkers after coronary artery bypass grafting (CABG) and the difficulty of excluding MI, cardiac magnetic resonance imaging (CMR) has enabled a more detailed evaluation of the myocardium. Therefore, in this study, we aimed to examine the release of biomarkers after CABG in patients with no evidence of late enhancement on CMR.pt_BR
dc.language.isoenpt_BR
dc.sourcehttps://cardiothoracicsurgery.biomedcentral.com/pt_BR
dc.subjectMyocardial infarction; Biomarkers; Coronary bypass surgery; Periprocedural; Troponinpt_BR
dc.titleAbnormal elevation of myocardial necrosis biomarkers after coronary artery bypass grafting without established myocardial infarction assessed by cardiac magnetic resonancept_BR
dc.title.alternativeJournal of Cardiothoracic Surgerypt_BR
dc.typeProdução bibliográfica: Artigos completos publicados em periódicospt_BR
Aparece nas coleções:Artigos Completos Publicados em Periódicos

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