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Prognostic Value of Troponins in Patients With or Without Coronary Heart Disease: Is it Dependent on Structure and Biology?
Lippi, G, Cervellin, G, Sanchis-Gomar, F
Heart, lung & circulation. 2020;(3):324-330
Abstract
Convincing evidence has emerged that cardiac troponins (cTns) T and I are the biochemical gold standard for diagnosing cardiac injury, and may also be used as efficient screening and risk stratification tools, especially when measured with the new high-sensitivity (hs-) immunoassays. In this narrative review, we aim to explore and critically discuss the results of recent epidemiological studies that have attempted to characterise the prognostic value of cTns in patients with or without cardiovascular disease, and then interpret this information according to cTn biology. Overall, all recent studies agree that higher blood levels of cTns reflect the larger risk of cardiovascular events and/or death, both in the general population and in patients with cardiovascular disease. Additional evidence has shown that the clinical information provided by assessment of both cTns molecules is greater compared to that of either protein alone, and this is mostly due to differential metabolism and clearance of cTnI and cTnT after release in the bloodstream. Although it seems likely that the prognostic value of these biomarkers may be higher than that of other conventional cardiovascular risk factors such as cholesterol or C reactive protein, large and reliable cost-effectiveness investigations are needed to define whether cTns-based population screening may be biologically plausible, clinically effective and economically sustainable.
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Utility of traditional circulating and imaging-based cardiac biomarkers in patients with predialysis CKD.
Colbert, G, Jain, N, de Lemos, JA, Hedayati, SS
Clinical journal of the American Society of Nephrology : CJASN. 2015;(3):515-29
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Abstract
Cardiac biomarkers, such as cardiac troponin T (cTnT), brain natriuretic peptide (BNP), and N-terminal-pro-BNP (NT-pro-BNP), are commonly used to diagnose acute coronary syndrome and congestive heart failure exacerbation in symptomatic patients. Levels of these biomarkers are frequently chronically elevated in asymptomatic patients with ESRD who are receiving maintenance dialysis. Other imaging biomarkers commonly encountered in nephrologists' clinical practice, such as coronary artery calcium measured by computed tomography, left ventricular hypertrophy, and carotid intima-media thickness, are also frequently abnormal in asymptomatic patients with ESRD. This article critically reviews the limited observational data on associations between cTnT, BNP, NT-pro-BNP, coronary artery calcium, left ventricular hypertrophy, and carotid intima-media thickness with cardiovascular events and death in non-dialysis-dependent patients with CKD. Although sufficient evidence suggests that these biomarkers may be used for prognostication, the diagnostic utility of cTnT, BNP, and NT-pro-BNP remain challenging in patients with CKD. Decreased renal clearance may affect the plasma levels of these biomarkers, and upper reference limits were originally derived in patients without CKD. Until better data are available, higher cutoffs, or a rise in level compared with previous values, have been proposed to help distinguish acute myocardial infarction from chronic elevations of cTnT in symptomatic patients with CKD. Additionally, it is not known whether these biomarkers are modifiable and amenable to interventions that could change hard clinical outcomes in patients with CKD not yet undergoing long-term dialysis.
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Current trends in diagnostic biomarkers of acute coronary syndrome.
Moe, KT, Wong, P
Annals of the Academy of Medicine, Singapore. 2010;(3):210-5
Abstract
The diagnosis and management of patients with acute coronary syndrome (ACS) have evolved dramatically over the past decade. Biomarkers play an important role in the diagnosis of ACS, especially in unstable angina and non-ST-segment elevation myocardial infarction. Among these, cardiac troponin and creatine kinase appear to be the most sensitive and specific markers of myocardial injury. Recent studies have revealed several novel biomarkers. Elevated levels of C-reactive protein and interleukin-6 are strong independent markers of increased mortality among patients with ACS. However, the ideal biomarkers that offer early detection, risk stratification, selection of therapy, monitoring disease progression, and treatment efficacy remain to be elucidated. This review assesses limitations and contemporary needs for biomarkers in the context of diagnosis of ACS. It also discusses the newly developing technologies for novel biomarkers or novel biomarker protein signatures discovery, and importance of point-of-care testing for future management.
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[The use of cardiac troponins (T or I) measurement in cardiology and various clinical settings].
Berroëta, C, Provenchère, S, Mongredien, A, Lasocki, S, Benessiano, J, Dehoux, M, Philip, I
Annales francaises d'anesthesie et de reanimation. 2006;(10):1053-63
Abstract
Measurement of cardiac troponin I or T in serum (highly specific for the myocardium) have replaced classical markers, such as creatine kinase MB. Cardiac troponins are preferred markers because of their high specificity and sensitivity. This had led to modifications of the original World Health Organization criteria for acute myocardial infarction. Furthermore, the place of the troponins as superior markers of subsequent cardiac risk in acute coronary syndrome has now become firmly established, for both diagnostic and risk stratification purposes. The use of C-reactive protein and/or other inflammatory biomarkers may add independent information in this context. After non cardiac surgery, the total cardiospecificity of cardiac troponins explains why other biomarkers of necrosis should no longer be used. Recent studies suggest that any elevation of troponin in the postoperative period is indicative of increased risk of long-term cardiac complications. This prognostic value has been previously demonstrated in other clinical settings such as invasive coronary intervention (surgical myocardial revascularization and percutaneous coronary intervention) and after heart valve surgery. Increases of troponin indicate cardiac damage, whatever the mechanism (ischemic or not). Other causes of cardiac injury include: pulmonary embolism, myocarditis, pericarditis, congestive heart failure, septic shock, myocardial contusion. In most cases, elevation of troponins has been shown to be associated with a bad outcome.
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Myocardial regulatory proteins and heart failure.
Adamcová, M, Stĕrba, M, Simůnek, T, Potácová, A, Popelová, O, Gersl, V
European journal of heart failure. 2006;(4):333-42
Abstract
Cardiac troponin T (cTnT) and cardiac troponin I (cTnI) are considered to be the most specific and sensitive biochemical markers of myocardial damage. Troponins have been studied in a wide range of clinical settings, including heart failure; however, there are few data on the role of regulatory proteins in the pathogenesis of heart failure, although a few interesting hypotheses have been proposed. A considerable body of evidence favours the view that alteration of the myocardial thin filament is the primary event leading to defective contractility of the failing myocardium, while the changes in Ca(2+) handling are a compensatory response. A better understanding of the role of regulatory proteins under different physiological and pathological conditions could lead to new therapeutic approaches in heart failure. Recently, calcium sensitisation has been proposed as a novel method by which cardiac performance may be enhanced via an increase in the affinity of troponin C for calcium but without affecting intracellular calcium concentration. To date, the only calcium sensitizer used in clinical practice is levosimendan.
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The miscommunicative cardiac cell: when good proteins go bad.
Gomes, AV, Venkatraman, G, Potter, JD
Annals of the New York Academy of Sciences. 2005;:30-7
Abstract
Troponin (Tn) is made up of three subunits, troponin T (TnT), troponin I (TnI), and troponin C (TnC). In cardiac muscle, TnI can exist as two isoforms, slow skeletal TnI (ssTnI) or cardiac TnI (cTnI), whereas TnT occurs as multiple isoforms. The predominant form of TnI in fetal cardiac muscle is ssTnI, which is derived from a different gene than cTnI. However, the predominant form of cardiac TnT (cTnT) in fetal muscle is cTnT1, which is derived from the same gene that produces the adult cTnT isoform (cTnT3). Fetal cardiac muscle is more sensitive to Ca(2+) than adult muscle and this may be due in part to the fetal cTnT1 and ssTnI isoforms. cTnT1 and/or ssTnI by themselves cause a significant increase in Ca(2+) sensitivity when compared to cTnT3 and/or cTnI. Mutations in the gene for cTnT can cause hypertrophic cardiomyopathy or dilated cardiomyopathy (DCM). Investigation of DCM mutations in the fetal cTnT1 isoform showed that the cTnT isoform is an important determinant of the effect of the mutation. The TnI isoform also affects the physiological function of the cardiac muscle. The presence of both the fetal TnT isoform, containing a DCM mutation, and ssTnI results in larger changes in Ca(2+) sensitivity than the same DCM mutant in the adult TnT isoform and in the presence of cTnI (when compared to their respective wild-type TnT controls). These recent results suggest that some mutations may have different severities in fetal and adult hearts.
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7.
[Cardiac troponin I and T: specific biomarkers of cardiomyocyte].
Lavoinne, A, Cauliez, B
La Revue de medecine interne. 2004;(2):115-23
Abstract
PURPOSE Cardiac troponin I and troponin T have replaced creatine kinase MB (CK-MB) for the diagnosis of cardiomyocyte necrosis. Cardiac specificity of these new markers leads to a change in our practice. CURRENT KNOWLEDGE AND KEY POINTS Following necrosis, intracellular proteins are released into blood. This easy concept overlaps a biological complexity since troponins are released as complexes leading to various cut-off values depending on the assay used, as least for cardiac troponin I. The increase in both specificity and analytical sensitivity of these markers reached to propose a new definition of myocardial infarction. The diagnosis of acute coronary syndrome is a clinical based diagnosis, the use of troponin contributing to their classification. Finally, pathological processes leading to cardiac injury may induce an increase in the cardiac troponin level. FUTURE PROSPECTS AND PROJECTS Troponin standardization is a challenge for the near future leading to better follow-up of patients and comparison between cohorts.
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Role of cardiac troponin testing in percutaneous transluminal coronary angioplasty.
Davis, GK
Scandinavian journal of clinical and laboratory investigation. 2003;(3):167-74
Abstract
Percutaneous transluminal coronary angioplasty (PTCA) is a common invasive procedure for myocardial revascularization. This article reviews the role of monitoring cardiac troponins in identifying procedural myocardial damage as a result of PTCA, its associations with balloon inflation time, stenting, side-branch occlusion and the prognostic implications of elevated levels of cardiac troponins. A review of several studies demonstrates that cardiac troponins are more sensitive than creatine kinase MB, CK-MB (mass) in detecting minor myocardial damage during PTCA. Increases in post-procedural cardiac troponin T and cardiac troponin I are associated with a greater degree of morbidity and mortality. Increases are more common and more pronounced following a longer duration of balloon inflation time, stenting and side-branch occlusion. Elevated cardiac troponins pre-procedure are a poor prognostic indicator.
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Cardiac troponins in renal insufficiency: review and clinical implications.
Freda, BJ, Tang, WH, Van Lente, F, Peacock, WF, Francis, GS
Journal of the American College of Cardiology. 2002;(12):2065-71
Abstract
Patients with renal insufficiency may have increased serum troponins even in the absence of clinically suspected acute myocardial ischemia. While cardiovascular disease is the most common cause of death in patients with renal failure, we are just beginning to understand the clinical meaning of serum troponin elevations. Serum troponin T is increased more frequently than troponin I in patients with renal failure, leading clinicians to question its specificity for the diagnosis of myocardial infarction. Many large-scale trials demonstrating the utility of serum troponins in predicting adverse events and in guiding therapy and intervention in acute coronary syndromes have excluded patients with renal failure. Despite persistent uncertainty about the mechanism of elevated serum troponins in patients with reduced renal function, data from smaller groups of renal failure patients have suggested that troponin elevations are associated with added risk, including an increase in mortality. It is possible that increases in serum troponin from baseline in patients with renal insufficiency admitted to hospital with acute coronary syndrome may signify myocardial necrosis. Further studies are needed to clarify this hypothesis.
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10.
Accuracy of biomarkers to diagnose acute cardiac ischemia in the emergency department: a meta-analysis.
Balk, EM, Ioannidis, JP, Salem, D, Chew, PW, Lau, J
Annals of emergency medicine. 2001;(5):478-94
Abstract
STUDY OBJECTIVE We sought to evaluate quantitatively the evidence on the diagnostic performance of presentation and serial biochemical markers for emergency department diagnosis of acute cardiac ischemia (ACI), including acute myocardial infarction (AMI) and unstable angina. METHODS We conducted a systematic review and meta-analysis of the English-language literature published between 1966 and December 1998. We examined the diagnostic performance of creatine kinase, creatine kinase-MB, myoglobin, and troponin I and T testing. Diagnostic performance was assessed by using estimates of test sensitivity and specificity and was summarized by summary receiver-operating characteristic curves. RESULTS Only 4 studies were found that evaluated all patients with ACI; 73 were found that focused only on a diagnosis of AMI. To diagnose ACI, presentation biomarker tests had sensitivities of 16% to 19% and specificities of 96% to 100%; serial biomarker tests had sensitivities of 31% to 45% and specificities of 95% to 98%. Considering only the diagnosis of AMI, presentation biomarker tests had summary sensitivities of 37% to 49% and summary specificities of 87% to 97%; serial biomarker tests had summary sensitivities of 79% to 93% and summary specificities of 85% to 96%. Variation of test sensitivity was best explained by test timing. Longer symptom duration or time between serial tests yielded higher sensitivity. CONCLUSION The limited evidence available to evaluate the diagnostic accuracy of biomarkers for ACI suggests that biomarkers have very low sensitivity to diagnose ACI. Thus, biomarkers alone will greatly underdiagnose ACI and will be inadequate to make triage decisions. For AMI diagnosis alone, multiple testing of individual biomarkers over time substantially improves sensitivity, while retaining high specificity, at the expense of additional time. Further high-quality studies are needed on the clinical effect of using biomarkers for patients with ACI in the ED and on optimal timing of serial testing and in combination with other tests.