Serum levels of cardiac troponin I and troponin T in estimating myocardial infarct size soon after reperfusion

Tanaka, Hiromitsu; Abe, Satoshi; Yamashita, T; Arima, Shinichi; Saigo, Masahiko; Nakao, Shoichiro; Toda, Hitoshi; Nomoto, Kunihiro; Tahara, Masaki

doi:10.1097/00019501-199707000-00005

Cited by 42 publications

(20 citation statements)

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“…The data are stronger for this approach with cTnT than with cTnI (27,28). For cTnI, peak levels work better (29,30), but the data vary depending on whether or not there has been acute reperfusion (29). High-risk patients with ACS.…”

Section: Abbreviations and Acronymsmentioning

confidence: 99%

Biomarkers in Acute Cardiac Disease

Jaffe

Babuin

Apple

2006

Journal of the American College of Cardiology

553

311

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The use of biomarkers to aid diagnosis and treatment is increasing rapidly as genomics and proteomics help us expand the number of markers we can use and as an improved understanding of the pathophysiology of cardiac disease guides their use. However, as with all rapidly expanding fields, there is the risk of excessive enthusiasm unless we are circumspect about the data that guide the clinical use of these new tools. This review focuses first on how to use troponin, which at present is the best validated of the new markers, and will hopefully provide insight into how to use this biomarker more productively by distinguishing subsets of patients and by providing an understanding of the meaning of elevations in various clinical situations. The review then discusses the use as well as the knowledge gaps associated with emerging biomarkers such as B-type natriuretic peptide and C-reactive protein, which are increasingly moving toward more productive clinical use. Finally, it reflects on some of the large number of markers that are still in development.

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Section: Abbreviations and Acronymsmentioning

confidence: 99%

Biomarkers in Acute Cardiac Disease

Jaffe

Babuin

Apple

2006

Journal of the American College of Cardiology

553

311

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“…27,28 Elevated troponin levels then persist in the blood owing to the slow release and degradation of the structural pool, 23,29 since the half-life of troponin and its complex is about 2 hours. 30 The prolonged window during which troponin levels are elevated allows for increased clinical detection of cardiac events and thus, functionally, greater clinical sensitivity.…”

Section: Characteristics Of Troponin Assaysmentioning

confidence: 99%

“…The data are stronger for this approach with cTnT than with cTnI, 102,103 which suggest that the cTnT level measured at 72 hours is a good estimate of scintigraphic infarct size whether patients were reperfused or not. 103 For cTnI, peak levels work better, 28,104 but the data vary depending on whether or not there has been acute reperfusion. 104 The estimates of infarct size are superior to those provided by CK or CK-MB.…”

Section: Troponin and Infarct Sizementioning

confidence: 99%

Troponin: the biomarker of choice for the detection of cardiac injury

Babuin¹

2005

Canadian Medical Association Journal

550

390

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T roponin is the biomarker of choice for the detection of cardiac injury. To use it properly, one must understand how sensitive the specific assay being used is for detecting cardiac injury, the fact that elevated troponin levels are highly specific for cardiac injury and some critical issues related to the basic science of the protein and its measurement. In this article, we review the biology of troponin, characteristics of assays that measure serum troponin levels and how to apply these measurements to patients who present with possible cardiovascular disease. We also discuss other clinical situations in which troponin levels may be elevated. The biology of troponinThe 3-unit troponin complex (troponin I, T and C) along with tropomyosin is located on the actin filament and is essential for the calcium-mediated regulation of skeletal and cardiac muscle contraction. 1 There are tissue-specific isoforms of troponin I, T and C. 2,3 Because the cardiac isoform of troponin C is shared by slow-twitch skeletal muscles, troponin C does not have cardiac specificity and thus is not used in assays for the diagnosis of cardiac injury. 4 There is one cardiac troponin I (cTnI) isoform in myocardial tissue. 5 This isoform has a post-translational tail of 32 amino acids on the N-terminus. 6,7 This sequence and the 42% and 45% dissimilarity with sequences of the other isoforms 8 have made possible the generation of highly specific monoclonal antibodies without cross-reactivity with other noncardiac forms. 9 Three genes control cardiac troponin T (cTnT). 10 These genes and alternative mRNA splicing produce a series of isoforms 10,11 with variable sequences close to the regions of the N-terminus and C-terminus. 10,12 Human cardiac muscle contains 4 troponin T isoforms, but only one is characteristic of the normal adult heart. 13,14 Highly specific antibodies have been made to the N-terminus-specific sequence of this cTnT isoform. 15 The skeletal isoforms present in the fetal heart are replaced by cTnI and cTnT late during fetal development. 16,17 cTnI is not expressed in skeletal muscle or other tissues during development 17 or in response to degenerative or regenerative muscle disease processes. 18 Thus, it is unlikely to be reexpressed in damaged tissues. The situation is more complex for cTnT. Re-expression of fetal forms occurs in cardiac tissue 12 and in diseased skeletal muscle. 19 With the firstgeneration cTnT assay, this problem was compounded by a nonspecific tag antibody that cross-reacted with troponin T in skeletal muscle. 20 Once this antibody was replaced by one with high specificity, false-positive elevations from skeletal muscle were eliminated. 15 Studies using immunohistochemistry and polymerase chain reaction have confirmed that these fetal isoforms are not detected by the assay used today. 21,22 Thus, the assay used to measure cTnT levels has cardiac specificity equivalent to that of assays for cTnI. Characteristics of troponin assaysMost troponin is found in the 3-unit complex (troponin I, T and C) of the c...

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“…Troponin I must be validated separately, both experimentally and clinically, given the heterogenicity among troponin assays and potentially different clearance. Initial data are promising (24).…”

Section: Reperfusionmentioning

confidence: 99%

The quantification of infarct size

Gibbons

Valeti

Araoz

et al. 2004

Journal of the American College of Cardiology

320

224

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We sought to summarize the published evidence regarding the measurement of infarct size by serum markers, technetium-99m sestamibi single-photon emission computed tomography (SPECT) myocardial perfusion imaging, and magnetic resonance imaging. The measurement of infarct size is an attractive surrogate end point for the early assessment of new therapies for acute myocardial infarction. For each of these three approaches, we reviewed reports published in English providing the clinical validation for the measurement of infarct size and the relevant clinical trial experience. The measurement of infarct size by serum markers has multiple theoretical and practical limitations. The measurement of troponin is promising, but the available data validating this marker are limited. Sestamibi SPECT imaging has five separate lines of published evidence supporting its validity and has received extensive study in multicenter trials. Magnetic resonance imaging has great promise but has less clinical validation and no multicenter trial experience. Therefore, SPECT sestamibi imaging is currently the best available technique for the quantitation of infarct size to assess the incremental treatment benefit of new therapies in multicenter trials of acute myocardial infarction.

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Serum levels of cardiac troponin I and troponin T in estimating myocardial infarct size soon after reperfusion

Cited by 42 publications

References 0 publications

Biomarkers in Acute Cardiac Disease

Biomarkers in Acute Cardiac Disease

Troponin: the biomarker of choice for the detection of cardiac injury

The quantification of infarct size

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