scholarly journals Measurement of Cardiac Troponins

2001 ◽  
Vol 38 (5) ◽  
pp. 423-449 ◽  
Author(s):  
Paul O Collinson ◽  
Frances G Boa ◽  
David C Gaze
Keyword(s):  
Gold Standard ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Regulatory Mechanism ◽  
Troponin T ◽  
Myocardial Damage ◽  
Myocardial Cell ◽  
Cell Necrosis ◽  
Form Part ◽  
Cardiac Troponins

The cardiac troponins form part of the regulatory mechanism for muscle contraction. Specific cardiac isoforms of cardiac troponin T and cardiac troponin I exist and commercially available immunoassay systems have been developed for their measurement. A large number of clinical and analytical studies have been performed and the measurement of cardiac troponins is now considered the ‘gold standard’ biochemical test for diagnosis of myocardial damage. There have been advances in understanding the development and structure of troponins and their degradation following myocardial cell necrosis. This has contributed to the understanding of the problems with current assays. Greater clinical use has also highlighted areas of analytical and clinical confusion. The assays are reviewed based on manufacturers' information, current published material as well as the authors' in-house experience.

Cardiac troponins and mortality in type 1 and 2 myocardial infarction

2017 ◽  
Vol 55 (2) ◽  
Author(s):  
Giuseppe Lippi ◽  
Fabian Sanchis-Gomar ◽  
Gianfranco Cervellin
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Post Discharge ◽  
Assay Sensitivity ◽  
Percentage Difference ◽  
Cardiac Troponins

AbstractBackground:The pathogenesis of different types of myocardial infarction (MI) differs widely, so that accurate and timely differential diagnosis is essential for tailoring treatments according to the underlying causal mechanisms. As the measurement of cardiac troponins is a mainstay for diagnosis and management of MI, we performed a systematic literature analysis of published works which concomitantly measured cardiac troponins in type 1 and 2 MI.Methods:The electronic search was conducted in Medline, Scopus and Web of Science using the keywords “myocardial infarction” AND “type(-)2” OR “type II” AND “troponin” in “Title/Abstract/Keywords”, with no language restriction and date limited from 2007 to the present.Results:Overall, 103 documents were identified, but 95 were excluded as precise comparison of troponin values in patients with type 1 and 2 MI was unavailable. Therefore, eight studies were finally selected for our analysis. Two studies used high-sensitivity (HS) immunoassays for measuring cardiac troponin T (HS-TnT), one used a HS immunoassay for measuring cardiac troponin I (HS-TnI), whereas the remaining used conventional methods for measuring TnI. In all studies, regardless of type and assay sensitivity, troponin values were higher in type 1 than in type 2 MI. The weighted percentage difference between type 1 and 2 MI was 32% for TnT and 91% for TnI, respectively. Post-discharge mortality obtained from pooling individual data was instead three times higher in type 2 than in type 1 MI.Conclusions:The results of our analysis suggest that the value of cardiac troponins is consistently higher in type 1 than in type 2 MI.

scholarly journals Cardiac Troponins are Among Targets of Doxorubicin-Induced Cardiotoxicity in hiPCS-CMs

2019 ◽  
Vol 20 (11) ◽  
pp. 2638 ◽  
Author(s):  
Michaela Adamcova ◽  
Veronika Skarkova ◽  
Jitka Seifertova ◽  
Emil Rudolf
Keyword(s):  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Early Recognition ◽  
Morphological Changes ◽  
Cancer Therapeutics ◽  
Diagnostic Strategies ◽  
Human Cardiomyocytes ◽  
Induced Pluripotent ◽  
Cardiac Troponins

Modern diagnostic strategies for early recognition of cancer therapeutics-related cardiac dysfunction involve cardiac troponins measurement. Still, the role of other markers of cardiotoxicity is still unclear. The present study was designed to investigate dynamics of response of human cardiomyocytes derived from induced pluripotent stem cells (hiPCS-CMs) to doxorubicin with the special emphasis on their morphological changes in relation to expression and organization of troponins. The hiPCS-CMs were treated with doxorubicin concentrations (1 and 0.3 µM) for 48 h and followed for next up to 6 days. Exposure of hiPCS-CMs to 1 µM doxorubicininduced suppression of both cardiac troponin T (cTnT) and cardiac troponin I (cTnI) gene expression. Conversely, lower 0.3 µM doxorubicin concentration produced no significant changes in the expression of aforementioned genes. However, the intracellular topography, arrangement, and abundance of cardiac troponin proteins markedly changed after both doxorubicin concentrations. In particular, at 48 h of treatment, both cTnT and cTnI bundles started to reorganize, with some of them forming compacted shapes extending outwards and protruding outside the cells. At later intervals (72 h and onwards), the whole troponin network collapsed and became highly disorganized following, to some degree, overall changes in the cellular shape. Moreover, membrane permeability of cardiomyocytes was increased, and intracellular mitochondrial network rearranged and hypofunctional. Together, our results demonstrate complex effects of clinically relevant doxorubicin concentrations on hiPCS-CM cells including changes in cTnT and cTnI, but also in other cellular compartments contributing to the overall cytotoxicity of this class of cytostatics.

scholarly journals NILAI DIAGNOSTIK UJI TROPONIN I KUANTITATIF METODE IMMUNOKROMATOGRAFI

2018 ◽  
Vol 14 (1) ◽  
pp. 20
Author(s):  
Siti Fatonah ◽  
Anik Widijanti ◽  
Tinny Endang Hernowati
Keyword(s):  
Cardiac Troponin ◽  
Biochemical Markers ◽  
Acute Coronary Syndromes ◽  
Troponin I ◽  
Myocardial Damage ◽  
Diagnostic Value ◽  
Cardiac Troponin I ◽  
Coronary Syndromes ◽  
Sensitivity Specificity ◽  
Cardiac Troponins

Cardiac troponins are the most sensitive and specific biochemical markers of myocardial damage but there is no standardization of WHO for cardiac troponin I, resulting in a variability for diagnostic value. It is necessary to determine diagnostic value for a new kitof troponin I. To evaluate a new quantitative immunochromatography assay for troponin I at a various cut off level. A cross sectionalstudy was conducted in 64 patients with acute myocardial infarction (AMI) and 55 non-AMI as control from February to September2007. The level of cardiac troponin I (cTnI) was measured and determined it diagnostic value at a various cut off level. The sensitivity,specificity, PPV and NPV of this assay were 91%, 91%, 92% and 89% at cut off level of 1,0 ng/ml (according to the kit), respectively.The cut off of cTnI were divided into five levels: 0.8, 1.0, 1.2, 1.5, and 2.0 with the area under curve were 0.923, 0.908, 0.912, and0.897, respectively. The sensitivity were 94%, 91%, 86%, 81% and 72%, respectively, the specificity were 91%, 91%, 96%, 98% and98%, respectively. This rapid diagnostic test is sensitive and specific to diagnose an acute coronary syndromes.

Elevated Cardiac Troponin in the Setting of Periodic Symptomatology: A Case Report

2020 ◽  
Vol 154 (Supplement_1) ◽  
pp. S89-S90
Author(s):  
J M Rohr ◽  
S Pirruccello ◽  
A Sofronescu
Keyword(s):  
Chest Pain ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Clinical Chemistry ◽  
Package Insert ◽  
Clinical Diagnostics ◽  
Heterophile Antibody ◽  
Tertiary Center ◽  
Cardiac Troponins

Abstract Introduction/Objective Serial cardiac troponin measurement is a sensitive method to identify recent cardiac injury and is a necessary function of the clinical chemistry laboratory. We present a case of out-of-range cardiac troponin I (cTnI) elevation which remained spuriously elevated for at least 30 days. Methods Cardiac troponins were measured on a DxI (Beckman Coulter), Vitros 5600 (Ortho Clinical Diagnostics), iSTAT (Abbott), and Cobas e602 (Roche) according to the manufacturers’ instructions with appropriate controls. Heterophile antibody blocking (Scantibodies Laboratories) was performed according to the package insert. Results A 58-year-old male with a medical history significant for chronic non-ischemic cardiomyopathy with open valvular repair (ejection fraction 15-20%), chronic atrial fibrillation, and Hodgkin’s lymphoma in remission presented to a rural clinic with chest pain and a cTnI of 0.8 ng/mL (reference <0.04 ng/mL). He was transferred to our tertiary center for open revision. The patient’s cTnI (measured on a Beckman Coulter DxI) was above linearity threshold (>71.00 ng/mL) starting day 1 after surgery. The patient self-discharged against medical advice on day 16. On day 21 he experienced new chest pain and dyspnea and was readmitted with a cardiac troponin T (cTnT) of >35 ng/mL (iSTAT; reference <0.08 ng/mL) and cTnI again above threshold. This value remained elevated for the next five days despite abated symptoms. To address the discordant laboratory and physical findings, dilutional cTnI measurements on serum from day 30 demonstrated linearity. Heterophile antibody testing was negative. cTnI on the DxI machine remained >71.00 ng/mL but was separately measured as 3.4 ng/mL (Vitros 5600, reference <0.08 ng/mL). cTnT was found to be 1.05 ng/mL (Cobas e602; reference 0.00 ng/mL). Comparative examination of all methodologies was unrevealing. Conclusion This case demonstrates a spurious elevation of cardiac troponins which remarkably demonstrated linearity on serial dilution. Multiple testing methodologies were necessary to prove fallacy. The cause of the result remains unclear. The clinical pathologist should be aware of possible false positives and investigate unlikely continuous cardiac troponin elevations.

scholarly journals Inconsistent Findings of Cardiac Troponin T and I in Clinical Routine Diagnostics: Factors of Influence

2021 ◽  
Vol 10 (14) ◽  
pp. 3148
Author(s):  
Abass Eidizadeh ◽  
Laura Fraune ◽  
Andreas Leha ◽  
Rolf Wachter ◽  
Abdul R. Asif ◽  
...  
Keyword(s):  
Sensitivity And Specificity ◽  
Cardiac Troponin ◽  
Roc Analysis ◽  
Troponin I ◽  
Troponin T ◽  
Clinical Routine ◽  
Routine Diagnostics ◽  
Negative Results ◽  
Factors Of Influence ◽  
Cardiac Troponins

Cardiac troponins are crucial for the diagnosis of acute myocardial infarction. Despite known differences in their diagnostic implication, there are no recommendations for only one of the two troponins, cardiac troponin I (cTnI) and troponin T (cTnT) so far. In an everyday routine diagnostic, cTnT (Roche) as well as cTnI (Abbott) were measured in 5667 samples from 3264 patient cases. We investigated the number of identical or discrepant troponin findings. Regarding cTnI, we considered both, sex-dependent and unisex cutoffs. In particular, the number of cTnT positive and cTnI negative results was strikingly high in 14.0% of cTnT positive samples and increases to 23.8% by using sex-specific cTnI cutoffs. This group was considerably greater than the group of cTnI positive and cTnT negative results, also after elimination of patients with an eGFR < 60 mL/min/1.73 m2. Comparing the troponin cases with a dynamic increase or decrease between two measurements, we saw a balanced number of discrepant cases (between cTnT+/cTnI− and cTnT−/cTnI+), which was, however, still present. Using ROC analysis, sex-dependent cutoffs improved sensitivity and specificity of cTnI. This study shows in a large cohort that comparing the two cardiac troponins does not amount to identical analytical results. Consideration of sex-dependent cutoffs may improve sensitivity and specificity.

scholarly journals Cardiac Troponin I as Compared to Troponin T for the Detection of Myocardial Damage in Horses

2015 ◽  
Vol 29 (1) ◽  
pp. 348-354 ◽  
Author(s):  
N. Van Der Vekens ◽  
A. Decloedt ◽  
S. Ven ◽  
D. De Clercq ◽  
G. van Loon
Keyword(s):  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Myocardial Damage ◽  
Cardiac Troponin I

scholarly journals ДІАГНОСТИКА ХРОНІЧНОЇ СЕРЦЕВОЇ НЕДОСТАТНОСТІ СОБАК – ІСНУЮЧІ МЕТОДИ ТА ПОДАЛЬШІ ПЕРСПЕКТИВИ

2016 ◽  
Vol 18 (3(71)) ◽  
pp. 130-133
Author(s):  
R. Trofimjak ◽  
L. Slivinska
Keyword(s):  
Molecular Weight ◽  
Heart Disease ◽  
Cardiac Troponin ◽  
Cell Injury ◽  
Troponin I ◽  
Myocardial Cell ◽  
Response To Therapy ◽  
Cardiac Biomarkers ◽  
Myocardial Cell Injury ◽  
Cardiac Troponins

The article analyzes the current scientific work related to the study of processes of chronic heart failure (CHF), and the use of biomarkers in the diagnosis of heart disease in dogs. Thoracic radiography, electrocardiography, and echocardiography are used to diagnose heart disease in dogs but despite the use of non–invasive methods, there is uncertainty about the severity of the disease and prognosis for each patient individually. In veterinary practice for the diagnosis of myocardial lesions in animals are clinically valuable, highly sensitive and simple to use cardiac biomarkers. A biomarker is typically a substance in the blood that can be objectively measured and indicates a biologic or pathologic process or response to therapy.1 There are scores of cardiac biomarkers,but this article will focus on the 2 most clinically useful ones in the dog and cat:cardiac troponin I (cTnI) and N–terminal pro–B–type natriuretic peptide (NT–proBNP). The cardiac troponins I, T, and C (cTnI, cTnT, and cTnC) are thin filament–associated regulatory proteins of the heart muscle. Cardiac troponin I («I» for inhibition) is uniquely expressed in the myocardium and is a potent inhibitor of the process of actin–myosin cross–bridge formation. The molecular weight is 24.000 D. Cardiac troponin T («T» for tropomyosin binding) has a molecular weight of 37.000 D and binds the troponin complex to tropomyosin. Cardiac troponin C («C» for calcium) binds to calcium and starts, therefore, the crossbridge cycle. As with cTnI, approximately 95% of cTnT in man and dogs is myofibril bound and about 5% is cytosolically dissolved. Mechanisms for an elevation in circulating cardiac troponins include an increase of myocyte membrane permeability (initial release of the cytosolic troponin pool) or cell necrosis (release of myofibrilbound troponins). Four to six hours after acute myocardial cell injury, the cardiac troponin concentration in blood increases in a biphasic pattern. Plasma half–life of cardiac troponins is approximately two hours, and elimination mainly occurs via the reticuloendothelial system (cTnI and cTnT) and renal loss (cTnT). Cardiac troponins are phylogenetically highly preserved proteins with a more than 95% total structural agreement between mammals. Therefore, established human serologic tests for troponin analysis may be used reliably in pets as well. Myocardial cell injury, manifested anatomically as inflammation (endomyocarditis, myocarditis, perimyocarditis), acute degeneration, apoptosis, or necrosis or hemodynamically as transient or permanent cardiac contractile dysfunction, is a frequent consequence of physical myocardial trauma (cardiac contusion), cardiomyopathy, metabolic or toxic myocardial damage (anthracyclines, catecholamines, bacterial endotoxins, tumor necrosis factor), myocardial ischemia or infarction. However, early diagnosis of myocardial injury may be important from a therapeutic and prognostic perspective. 

scholarly journals Cardiac Troponins in Patients with Renal Dysfunction

1998 ◽  
Vol 35 (3) ◽  
pp. 380-386 ◽  
Author(s):  
P O Collinson ◽  
L Hadcocks ◽  
Y Foo ◽  
S B Rosalki ◽  
P J Stubbs ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Detection Limit ◽  
Renal Dysfunction ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Multiple Organ ◽  
Chronic Renal Impairment ◽  
Cardiac Troponins

Cardiac troponin T (cTnT) and cardiac troponin I (cTnI) were measured in 198 patients with renal dysfunction [132 men: median (range) age 66·1 (8·2-90·3) years]. cTnT was measured by two methods: ELISA and Enzymun (Boehringer Mannheim UK, Lewes, UK), both with a detection limit of 0·05 μg/L in 179 and 78 patients, respectively. cTnI was measured in 80 patients by the OPUS plus and OPUS Magnum systems (Dade-Behring, Milton Keynes, UK) with a detection limit of 0·5 μg/L. Patients were classified as having chronic renal impairment (CRI), chronic renal failure (CRF), acute renal failure including those with multiple organ failure on renal replacement therapy (ARF), and patients with chronic renal failure treated with haemodialysis (HD). Cardiac troponins were detectable in the serum of patients with renal dysfunction. cTnT was detectable in 113/179 (63·1%) and 33/78 (42·3%) by the ELISA and Enzymun methods respectively. cTnI was detectable in 17/80 (21·3%). cTnT (ELISA and Enzymun methods) and cTnI were detectable with increased frequency in the CRF, HD and ARF patient groups compared with the CRI group. Cardiac troponin concentrations did not correlate with serum creatine kinase (CK) activity, CK-MB, or urea or creatinine levels. Serial cardiac troponin measurements may be required to confirm or exclude a diagnosis of acute coronary syndromes in patients with renal dysfunction.

scholarly journals Cardiac Troponins and Renal Function in Nondialysis Patients with Chronic Kidney Disease

2005 ◽  
Vol 51 (11) ◽  
pp. 2059-2066 ◽  
Author(s):  
Nasir A Abbas ◽  
R Ian John ◽  
Michelle C Webb ◽  
Michelle E Kempson ◽  
Aisling N Potter ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Left Ventricular ◽  
Reference Limit ◽  
Coronary Syndrome ◽  
Stage 4 ◽  
Cardiac Troponins

Abstract Background: Serum cardiac troponin concentrations are commonly increased in end-stage renal disease (ESRD) in the absence of an acute coronary syndrome (ACS). The data on cardiac troponin I (cTnI) are more variable than those for cardiac troponin T (cTnT). There is little information on cardiac troponin concentrations in patients with chronic kidney disease (CKD) who have not commenced dialysis. Methods: We studied 222 patients: 56 had stage 3 (moderate CKD); 70 stage 4 (severe CKD); and 96 stage 5 (kidney failure). Patients underwent echocardiography and were followed prospectively for a median of 19 months; all-cause mortality was recorded. Results: Overall, serum cTnT was increased above the 99th percentile reference limit in 43% of all CKD patients studied, compared with 18% for cTnI. Serum cTnT and cTnI concentrations were more commonly increased in the presence of more severe CKD (11 and 6 patients in stage 3, 27 and 8 in stage 4, and 57 and 24 in stage 5 (P &lt;0.0001 and &lt;0.02, respectively). Among 38 patients with detectable cTnI, 32 had detectable cTnT (rs = 0.67; P&lt;0.0001). There was evidence that decreasing estimated glomerular filtration rate increased the odds of having detectable cTnT (P &lt;0.001) but not cTnI (P = 0.128). There was no evidence to support an adjusted association of detectable cardiac troponins with increasing left ventricular mass index. Increased cTnT (P = 0.0097), but not cTnI, was associated with decreased survival. Conclusions: Increased cTnT and cTnI concentrations are relatively common in predialysis CKD patients, in the absence of an ACS, including among those with stage 3 disease. The presence of left ventricular hypertrophy alone does not explain these data. Detectable cTnT was a marker of decreased survival.

scholarly journals Different intracellular compartmentations of cardiac troponins and myosin heavy chains: a causal connection to their different early release after myocardial damage

1998 ◽  
Vol 44 (9) ◽  
pp. 1912-1918 ◽  
Author(s):  
Jürgen Bleier ◽  
Karl-Paul Vorderwinkler ◽  
Jürgen Falkensammer ◽  
Peter Mair ◽  
Otto Dapunt ◽  
...  
Keyword(s):  
Coronary Sinus ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Artery Bypass ◽  
Myocardial Damage ◽  
Right Atrial ◽  
Causal Connection ◽  
Early Release ◽  
The Impact

Abstract We investigated the net myocardial release of creatine kinase isoenzyme MB (CKMB), myoglobin, cardiac troponin T (cTnT), cardiac troponin I (cTnI), and cardiac β-type myosin heavy chain (β-MHC) into the coronary circulation after cardioplegic cardiac arrest in humans. Cardiac markers were measured in paired arterial, central venous, and coronary sinus blood in 19 patients undergoing elective coronary artery bypass grafting (CABG) before aortic cross-clamping and 1, 5, 10, and 20 min after aortic declamping. cTnT and cTnI were released into the coronary sinus in parallel to each other and almost simultaneously to myoglobin and CKMB within 20 min of reperfusion. In contrast, no β-MHC was released in the same patients during the study period. The average soluble cTnT and cTnI pools in right atrial appendages of 11 patients with right atrial and right ventricular pressures within reference values were comparable and were ∼8% of total myocardial troponin content. The soluble β-MHC pool was &lt;0.1% in all patients. Our results demonstrate the impact of the different intracellular compartmention of regulatory and contractile proteins on their early release from damaged myocardium.

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