Antigenic Definition of Cardiac Troponin I

Larue, Catherine; Ferrières, Gaëlle; Laprade, Michel; Calzolari, Charles; Granier, Claude

doi:10.1515/cclm.1998.061

Cited by 13 publications

(4 citation statements)

References 30 publications

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“…The free form is present in a minor quantity (~5%) (Katrukha et al, 1997;Apple et al, 2012). On the other hand, the cTnI molecule presents highly antigenic regions that correspond to the amino and carboxyl-terminal extremes and internal antigenic sequences (Ferrieres et al, 1998). Figure 3 shows the epitopic map of cTnI that contains the external and internal epitopes reported so far (Filatov et al, 1998;HyTest, 2022).…”

Section: Severe Pulmonary Hypertensionmentioning

confidence: 93%

“…The three isoforms are highly homologous: the sequence identity of cTnI with ssTnI is approximately 52% and with fsTnI is 46% ( HyTest, 2022 ). Despite of this, the cTnI isoform is well-differentiated from the skeletal isoforms because it presents an N-terminal region between amino acid residues 1-32, considered the cardiospecific region ( Al-Hillawi et al, 1995 ; Keane et al, 1997 ; Larue et al, 1998 ). Once a cardiac event occurs, the great majority >95% of the blood cTnI has been found in the detectable dominant forms such as the non-covalent ternary cTnI-TC complex (TIC complex), the binary cTnI-C complex (IC complex), and the cTnI-T binary complex (IT complex).…”

Section: Ctni Biochemistrymentioning

confidence: 99%

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A review of cardiac troponin I detection by surface enhanced Raman spectroscopy: Under the spotlight of point-of-care testing

Saviñon-Flores

Trejo

et al. 2022

Front. Chem.

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Cardiac troponin I (cTnI) is a biomarker widely related to acute myocardial infarction (AMI), one of the leading causes of death around the world. Point-of-care testing (POCT) of cTnI not only demands a short turnaround time for its detection but the highest accuracy levels to set expeditious and adequate clinical decisions. The analytical technique Surface-enhanced Raman spectroscopy (SERS) possesses several properties that tailor to the POCT format, such as its flexibility to couple with rapid assay platforms like microfluidics and paper-based immunoassays. Here, we analyze the strategies used for the detection of cTnI by SERS considering POCT requirements. From the detection ranges reported in the reviewed literature, we suggest the diseases other than AMI that could be diagnosed with this technique. For this, a section with information about cardiac and non-cardiac diseases with cTnI release, including their release kinetics or cut-off values are presented. Likewise, POCT features, the use of SERS as a POCT technique, and the biochemistry of cTnI are discussed. The information provided in this review allowed the identification of strengths and lacks of the available SERS-based point-of-care tests for cTnI and the disclosing of requirements for future assays design.

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Section: Severe Pulmonary Hypertensionmentioning

confidence: 93%

Section: Ctni Biochemistrymentioning

confidence: 99%

A review of cardiac troponin I detection by surface enhanced Raman spectroscopy: Under the spotlight of point-of-care testing

Saviñon-Flores

Trejo

et al. 2022

Front. Chem.

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“…Genetic differences in cardiac and skeletal muscle tissue have allowed development of monoclonal antibodies that are specific for release of cardiac troponins T and I during myocardial injury [5,6]. Sporadic reports [7,8] confirmed the ability of troponins to identify micronecrotic pathology, despite exclusion of MI on conventional grounds.…”

Section: Introductionmentioning

confidence: 99%

Implications of troponin testing in clinical medicine

Goldmann

Christenson

Hamm

et al. 2001

Trials

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During the past decade considerable research has been conducted into the use of cardiac troponins, their diagnostic capability and their potential to allow risk stratification in patients with acute chest pain. Determination of risk in patients with suspected myocardial ischaemia is known to be as important as retrospective confirmation of a diagnosis of myocardial infarction (MI). Therefore, creatine kinase (CK)-MB -the former 'gold standard' in detecting myocardial necrosis -has been supplanted by new, more accurate biomarkers. Measurement of cardiac troponin levels constitute a substantial determinant in assessment of ischaemic heart disease, the presentations of which range from silent ischaemia to acute MI. Under these conditions, troponin release is regarded as surrogate marker of thrombus formation and peripheral embolization, and therefore new therapeutic strategies are focusing on potent antithrombotic regimens to improve long-term outcomes. Although elevated troponin levels are highly sensitive and specific indicators of myocardial damage, they are not always reflective of acute ischaemic coronary artery disease; other processes have been identified that cause elevations in these biomarkers. However, because prognosis appears to be related to the presence of troponins regardless of the mechanism of myocardial damage, clinicians increasingly rely on troponin assays when formulating individual therapeutic plans. have shown micronecrosis that was not reflected in routine enzyme measures [2,3]. In addition, myocardial biopsies taken during coronary artery bypass surgery in patients with unstable angina have shown the presence of platelet aggregates in small coronary vessels, with associated myocardial necrosis [4].New cardiac markers, such as troponins T, I and C, are subunits of the thin filament-associated troponintropomyosin complex, which is involved in regulating muscle contraction. Genetic differences in cardiac and skeletal muscle tissue have allowed development of monoclonal antibodies that are specific for release of cardiac troponins T and I during myocardial injury [5,6]. Sporadic reports [7,8] confirmed the ability of troponins to identify micronecrotic pathology, despite exclusion of MI on conventional grounds. Accordingly the new definition of MI reported in September 2000 [9] introduced cardiac troponins into daily routine clinical practice, allowing for highly accurate, sensitive and specific determination of myocardial injury (Table 2). Moreover troponin measurement is recommended in all patients with chest discomfort that is consistent with an acute coronary syndrome [10].The present review focuses on the potential of troponin measurement to identify myocardial damage of any origin, and the resulting diagnostic and therapeutic implications. Characteristics of troponin releaseBiochemical markers provide evidence of cell degradation, which forms the rationale for diagnosis of a disease using such markers; that is, detection of intracellular constituents that are released into the bl...

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“…The troponins (T, I, and C) are subunits of the thin filament-associated troponintropomyosin complex, which is involved in regulating striated muscle contraction. Monoclonal antibody-based assays have been developed that are specific for the cardiac isoforms of troponin (5,6). Using such assays, data are now available confirming that troponins can identify myocardial micronecrosis even when an MI diagnosis has been excluded according to the conventional definition (7,8).…”

mentioning

confidence: 99%

Troponin: an important prognostic marker and risk-stratification tool in non–ST-segment elevation acute coronary syndromes

Newby

Goldmann

Ohman

2003

Journal of the American College of Cardiology

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Over the past decade, there has been a progressive evolution of cardiac marker testing in patients with acute coronary syndromes (ACS). This has not only resulted in a dramatic shift in how we view the diagnosis of myocardial infarction (MI), but it has also extended the role of cardiac marker testing into risk stratification and guidance of treatment decisions. By the year 2000, the development of highly sensitive and cardiac-specific troponin assays had resulted in a consensus change in the definition of MI, placing increased emphasis on cardiac-marker testing with troponins as the new gold standard. Furthermore, and perhaps more importantly, the role of the troponins as superior markers of subsequent cardiac risk in ACS patients became firmly established. Most recently, the supportive role of these markers in identifying patients with ACS who may derive particular benefit from potent anti-thrombotic and anti-platelet therapy or early invasive treatment strategies has been demonstrated. This paper will review the evolution of these important roles of troponin testing for risk stratification in ACS.

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Antigenic Definition of Cardiac Troponin I

Cited by 13 publications

References 30 publications

A review of cardiac troponin I detection by surface enhanced Raman spectroscopy: Under the spotlight of point-of-care testing

A review of cardiac troponin I detection by surface enhanced Raman spectroscopy: Under the spotlight of point-of-care testing

Implications of troponin testing in clinical medicine

Troponin: an important prognostic marker and risk-stratification tool in non–ST-segment elevation acute coronary syndromes

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