scholarly journals Troponin T and I Assays Show Decreased Concentrations in Heparin Plasma Compared with Serum: Lower Recoveries in Early than in Late Phases of Myocardial Injury

2000 ◽  
Vol 46 (6) ◽  
pp. 817-821 ◽  
Author(s):  
Willie Gerhardt ◽  
Gunnar Nordin ◽  
Ann-Katrin Herbert ◽  
Birgitta Linåker Burzell ◽  
Anders Isaksson ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Chest Pain ◽  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Troponin I ◽  
Troponin T ◽  
Serum Samples ◽  
Heparin Plasma ◽  
Time Courses ◽  
Serial Samples

Abstract Background: Heparinized plasma samples allow more rapid analysis than serum samples, but preliminary studies showed lower cardiac troponin T (cTnT) results in plasma. We undertook a multicenter study to characterize this effect for cTnT and cardiac troponin I (cTnI). Methods: Blood samples were collected with and without heparin at five hospitals. cTnT was measured by a “third generation” assay (Elecsys®), and cTnI was measured by a commercial immunoassay (IMMULITE®). Results: Mean cTnT was 15% lower in heparin sampling tubes than in serum. Measured concentrations of cardiac troponins also decreased with increasing heparin concentrations added to sera. Heparin-induced losses were greater in early than in late phases after onset of chest pain. Addition of heparin (∼100 IU/mL) to serial samples from nine acute myocardial infarction patients produced mean cTnT losses of 33% at 1–12 h after onset of chest pain, 17% at 13–48 h, and 7% after 48 h. The changing heparin effects were seen for both cTnT and cTnI during time courses of individual patients with myocardial infarction. Conclusion: We suggest that binding of heparin to troponins decreases immunoreactivity, especially in early phases of myocardial injury. The resulting losses may depend on the antibodies used in each troponin assay.

scholarly journals Characterization of cardiac troponin subunit release into serum after acute myocardial infarction and comparison of assays for troponin T and I

1998 ◽  
Vol 44 (6) ◽  
pp. 1198-1208 ◽  
Author(s):  
Alan H B Wu ◽  
Yue-Jin Feng ◽  
Robert Moore ◽  
Fred S Apple ◽  
Paul H McPherson ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Cross Reactivity ◽  
Binary Complex ◽  
Serum Samples ◽  
Binary And Ternary Complexes ◽  
The Cross

Abstract We examined the release of cardiac troponin T (cTnT) and I (cTnI) into the blood of patients after acute myocardial infarction (AMI). Three postAMI serum samples were applied in separate analytical runs onto a calibrated gel filtration column (Sephacryl S-200), and the proteins were separated by molecular weight. Using commercial cTnT and cTnI assays measured on collected fractions, we found that troponin was released into blood as a ternary complex of cTnT-I-C, a binary complex of cTnI-C, and free cTnT, with no free cTnI within the limits of the analytical methodologies. The serum samples were also examined after incubation with EDTA and heparin. EDTA broke up troponin complexes into individual subunits, whereas heparin had no effect on the assays tested. We added free cTnC subunits to 24 AMI serum samples and found no marked increase in the total cTnI concentrations, using an immunoassay that gave higher values for the cTnI-C complex than free cTnI. To characterize the cross-reactivity of cTnT and cTnI assays, purified troponin standards in nine different forms were prepared, added to serum and plasma pools, and tested in nine quantitative commercial and pre-market assays for cTnI and one approved assay for cTnT. All nine cTnI assays recognized each of the troponin I forms (complexed and free). In five of these assays, the relative responses for cTnI were nearly equimolar. For the remainder, the response was substantially greater for complexed cTnI than for free cTnI. Moreover, there was a substantial difference in the absolute concentration of results between cTnI assays. The commercial cTnT assay recognized binary and ternary complexes of troponin on a near equimolar basis. We conclude that all assays are useful for detection of cardiac injury. However, there are differences in absolute cTnI results due to a lack of mass standardization and heterogeneity in the cross-reactivities of antibodies to various troponin I forms.

scholarly journals Lower Cardiac Troponin T and I Results in Heparin-Plasma Than in Serum

2000 ◽  
Vol 46 (9) ◽  
pp. 1338-1344 ◽  
Author(s):  
Hugo Stiegler ◽  
Yuriko Fischer ◽  
Jaime F Vazquez-Jimenez ◽  
Jürgen Graf ◽  
Karsten Filzmaier ◽  
...  
Keyword(s):  
Cardiac Troponin ◽  
Heart Surgery ◽  
Troponin I ◽  
Troponin T ◽  
Open Heart Surgery ◽  
Cardiac Troponin T ◽  
Serum Samples ◽  
Coronary Syndrome ◽  
Heparin Plasma

Abstract Background: The use of plasma rather than serum for determination of cardiac troponins can improve turnaround time and potentially avoid incomplete serum separation that may produce falsely increased results. We investigated the influence of incomplete serum separation and the effect of heparin-plasma on cardiac troponin concentrations. Methods: Serum and heparin-plasma samples were drawn simultaneously from 100 patients (50 patients with acute coronary syndrome and 50 patients after open heart surgery) and measured on three different analytical systems, two for determination of cardiac troponin I (cTnI; Abbott AxSYM and Bayer ACS:Centaur) and one for cardiac troponin T (cTnT; Roche Elecsys cTnT STAT). Serum samples were reanalyzed after a second centrifugation to assess the influence of incomplete serum separation. Results: Mean results (± 95% confidence interval) in heparin-plasma compared with serum were 101% ± 2% (AxSYM cTnI), 94% ± 3% (ACS:Centaur cTnI), and 99% ± 3% (Elecsys cTnT). Differences >20% were seen in 11% of results on the ACS:Centaur, 9% of results on Elecsys cTnT, and 2% of results on the AxSYM. For the Elecsys cTnT assay, the magnitude of the difference between serum and plasma was independent of the absolute concentration and confined to individual samples, and was reversed by treatment with heparinase. A second centrifugation had no effect on serum results by any of the assays. Conclusion: The concentrations of troponins measured in heparin-plasma are markedly lower than in serum in some cases.

scholarly journals Full-Size Cardiac Troponin I and Its Proteolytic Fragments in Blood of Patients with Acute Myocardial Infarction: Antibody Selection for Assay Development

2018 ◽  
Vol 64 (7) ◽  
pp. 1104-1112 ◽  
Author(s):  
Ivan A Katrukha ◽  
Alexander E Kogan ◽  
Alexandra V Vylegzhanina ◽  
Alexey V Kharitonov ◽  
Natalia N Tamm ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Cardiac Troponin I ◽  
Amino Acid Residues ◽  
Serum Samples ◽  
Before And After ◽  
Stable Part ◽  
Serial Samples

Abstract BACKGROUND In the blood of patients with acute myocardial infarction (AMI), cardiac troponin I (cTnI) presents as an intact molecule with a repertoire of proteolytic fragments. The degradation of cTnI might negatively influence its precise immunodetection. In this study we identified cTnI fragments and calculated their ratio in the blood of patients at different times after AMI to discriminate the most stable part(s) of cTnI. METHODS Serial serum samples were collected from AMI patients within 1 to 36 h after the onset of chest pain both before and after stenting. cTnI and its fragments were immunoextracted from serum samples and analyzed by Western blotting with monoclonal antibodies (mAbs) specific to the different epitopes of cTnI and by 2 in-house immunoassays specific to the central and terminal portions of cTnI. RESULTS Intact cTnI and its 11 major fragments were detected in blood of AMI patients. The ratio of the fragments in serial samples did not show large changes in the period 1–36 h after AMI. mAbs specific to the epitopes located approximately between amino acid residues (aar) 34 and 126 stained all extracted cTnI. mAbs specific to aar 23–36 and 126–196 recognized approximately 80% to 90% (by abundance) of cTnI. CONCLUSIONS In addition to mAbs specific to the central part of cTnI (approximately aar 34–126), antibodies specific to the adjacent epitopes (approximately aar 23–36 and 126–196) could be used in assays because they recognize ≥80% of cTnI in patients' blood samples within the first 36 h after AMI.

Equivalent early sensitivities of myoglobin, creatine kinase MB mass, creatine kinase isoform ratios, and cardiac troponins I and T for acute myocardial infarction

1995 ◽  
Vol 41 (9) ◽  
pp. 1266-1272 ◽  
Author(s):  
J Mair ◽  
D Morandell ◽  
N Genser ◽  
P Lechleitner ◽  
F Dienstl ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Creatine Kinase ◽  
Chest Pain ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Turnaround Time ◽  
Serum Marker ◽  
Creatine Kinase Mb

Abstract Early sensitivities of creatine kinase (CK), CKMB (activity and mass), CKMM and CKMB isoform ratios, myoglobin, cardiac troponin I (cTnI), and cardiac troponin T (cTnT) were compared to find the most sensitive serum marker for acute myocardial infarction (AMI) during the first hours after onset of chest pain. In a prospective study we investigated 37 consecutive patients with AMI who were admitted to the coronary care unit within 4 h after onset of chest pain. Blood samples were drawn every hour for the first 10 h after admission. CKMB mass concentrations, CKMM and CKMB isoform ratios, myoglobin, cTnI, and cTnT increased significantly (P < or = 0.0067) earlier than CK and CKMB activity and were also significantly (P < or = 0.046) and markedly more sensitive on admission. Differences in early sensitivities of myoglobin, CKMB mass, CK isoform ratios, cTnI, and cTnT were small and not significant. Therefore, turnaround time and practicality for emergency determination of methods, specificities of markers, the required specificity in the individual patient, and costs mainly determine the choice among myoglobin, CKMB mass, CK isoforms, cTnI, and cTnT.

Role of Biochemical Markers in Detection of Myocardial Infarction

2021 ◽  
Vol 15 (11) ◽  
pp. 3346-3348
Author(s):  
Fareeha Cheema ◽  
Zahid Mahmood ◽  
Nasir Iqbal ◽  
Hassan Jamil ◽  
Saima Rubab Khan ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Emergency Department ◽  
Chest Pain ◽  
Cardiac Troponin ◽  
Biochemical Markers ◽  
Troponin I ◽  
Troponin T ◽  
Care Hospital ◽  
Observational Cohort

Introduction: Acute myocardial infarction causes significant mortality and morbidity. Timely conclusion permits clinicians to risk stratify their patients and select suitable treatment. Biomarkers have been utilized to help with timely decision, whereas an expanding number of novel markers have been recognized to predict result taking after an acute myocardial infarction or acute coronary disorder. This may encourage tailoring of appropriate treatment to high-risk patients. This survey focuses on an assortment of promising biomarkers which give symptomatic and prognostic data. Objective: To compare the early demonstrative efficiency of the cardiac troponin I (cTn-I) level with that of the cardiac troponin T (cTn-T) level, as well as the creatine kinase (CK), CK-MB, and myoglobin levels, for acute myocardial infarction (AMI) in patients without an initially diagnostic ECG presenting to the Emergency department within 24 hours of the onset of their symptoms. Material and Methods Study design: Prospective Observational Cohort Settings: Punjab Institute of Cardiology Duration: Six months i.e. 1st January 2020 to 30th June 2020 Data Collection procedure: A planned, observational, cohort study was performed including chest pain patients admitted to territory care hospital. Members were sequential consenting through Emergency department with chest pain and age more than 30 years. Exclusion included having symptoms >24 hours, failure to total information collection, receipt of CPR, and ST-segment elevation on the starting ECG. Estimations included levels of Trop-I, Trop- T, CK, CK-MB, and myoglobin at the time of introduction and 1, 2, 6, and 12-24 hours after presentation as well as showing ECG and clinical follow-up. The collected data was analyzed by using SPSS version 23. Results: 140 included for study out of the 200 patients, 21 (14%) were analyzed as having acute myocardial infarction after diagnostic ECG testing. The sensitivities of all 5 biochemical markers for acute myocardial infarction were poor at the time of emergency department induction. The sensitivity of Trop-T was essentially superior to that of Trop-I over the starting 2 hours (3.2-33.1), but both markers' sensitivities were low (<60%) during this time outline. The Trop-I was significantly more particular for acute myocardial infarction than was the Trop-T, but not essentially better than CK-MB or myoglobin. Likelihood proportion analysis appeared that the biochemical markers with the most elevated positive ratios for acute myocardial infarction amid the primary 2 hours taking after emergency department admission were myoglobin and CK-MB. From 6 through 24 hours, the positive probability proportions for Trop I, CK-MB, and myoglobin were predominant to those of CK and Trop-T. Conclusion: Trop-I, CK-MB, and myoglobin are essentially more particular for acute myocardial infarction than are CK and Trop-T. Myoglobin is the biochemical marker having the most elevated combination of sensitivity, specificity, and negative predictive value for acute myocardial infarction inside 2 hours of emergency department induction. Not one or the other Trop-I nor Trop-T offers significant advantages over myoglobin and CK-MB within the early less than 2 hours starting screening for acute myocardial infarction. The cardiac troponins are of advantage in recognizing acute myocardial infarction greater than 6 hours after presentation. Key words: Myocardial Infarction, CKMB, Trop t, Trop I, Myoglobin

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 Thrombin-Mediated Degradation of Human Cardiac Troponin T

2017 ◽  
Vol 63 (6) ◽  
pp. 1094-1100 ◽  
Author(s):  
Ivan A Katrukha ◽  
Alexander E Kogan ◽  
Alexandra V Vylegzhanina ◽  
Marina V Serebryakova ◽  
Ekaterina V Koshkina ◽  
...  
Keyword(s):  
Sample Preparation ◽  
Serum Sample ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Specific Inhibitor ◽  
Cardiac Troponin T ◽  
Amino Acid Residues ◽  
Serum Samples ◽  
Heparin Plasma ◽  
Normal Human

AbstractBACKGROUNDCardiac troponin T (cTnT) is an acknowledged biomarker of acute myocardial infarction (AMI) that is known to be prone to proteolytic degradation in serum. Such degradation is usually explained by the action of μ-calpain, although there could be other candidates for that role. In the current study, we explored the hypothesis that thrombin-mediated cTnT cleavage occurs as a result of the serum sample preparation.METHODScTnT degradation was studied by using immunoblotting and mass spectrometry (MS) analysis.RESULTSThe comparison of cTnT isolated from AMI heparin plasma and serum samples showed that cTnT in the plasma samples was mainly present as the full-sized molecule (approximately 35 kDa), while in serum samples it was present as a 29-kDa fragment. The incubation of recombinant cTnT, or native ternary cardiac troponin complex with thrombin or in normal human serum (NHS), resulted in the formation of a 29-kDa product that was similar to that detected in AMI serum samples. No cTnT degradation was observed when thrombin or NHS was pretreated with hirudin, a specific inhibitor of thrombin, or during incubation of troponin in normal heparin plasma. When the products of thrombin-mediated cTnT proteolysis were analyzed by MS, 2 fragments consisting of amino acid residues (aar) 2–68 and 69–288 were identified, which suggests that thrombin cleaves cTnT between R68 and S69.CONCLUSIONSThe results of this study suggest that the 29-kDa fragment of cTnT in AMI serum samples mainly appears due to the cleavage by thrombin during serum sample preparation.

scholarly journals Biological variation of cardiac troponins in chronic kidney disease

2020 ◽  
Vol 57 (2) ◽  
pp. 162-169
Author(s):  
RA Jones ◽  
J Barratt ◽  
EA Brettell ◽  
P Cockwell ◽  
RN Dalton ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Biological Variation ◽  
Cardiac Troponin I ◽  
Cardiac Troponin T ◽  
Reference Change Value

Background Patients with chronic kidney disease often have increased plasma cardiac troponin concentration in the absence of myocardial infarction. Incidence of myocardial infarction is high in this population, and diagnosis, particularly of non ST-segment elevation myocardial infarction (NSTEMI), is challenging. Knowledge of biological variation aids understanding of serial cardiac troponin measurements and could improve interpretation in clinical practice. The National Academy of Clinical Biochemistry (NACB) recommended the use of a 20% reference change value in patients with kidney failure. The aim of this study was to calculate the biological variation of cardiac troponin I and cardiac troponin T in patients with moderate chronic kidney disease (glomerular filtration rate [GFR] 30–59 mL/min/1.73 m2). Methods and results Plasma samples were obtained from 20 patients (median GFR 43.0 mL/min/1.73 m2) once a week for four consecutive weeks. Cardiac troponin I (Abbott ARCHITECT® i2000SR, median 4.3 ng/L, upper 99th percentile of reference population 26.2 ng/L) and cardiac troponin T (Roche Cobas® e601, median 11.8 ng/L, upper 99th percentile of reference population 14 ng/L) were measured in duplicate using high-sensitivity assays. After outlier removal and log transformation, 18 patients’ data were subject to ANOVA, and within-subject (CVI), between-subject (CVG) and analytical (CVA) variation calculated. Variation for cardiac troponin I was 15.0%, 105.6%, 8.3%, respectively, and for cardiac troponin T 7.4%, 78.4%, 3.1%, respectively. Reference change values for increasing and decreasing troponin concentrations were +60%/–38% for cardiac troponin I and +25%/–20% for cardiac troponin T. Conclusions The observed reference change value for cardiac troponin T is broadly compatible with the NACB recommendation, but for cardiac troponin I, larger changes are required to define significant change. The incorporation of separate RCVs for cardiac troponin I and cardiac troponin T, and separate RCVs for rising and falling concentrations of cardiac troponin, should be considered when developing guidance for interpretation of sequential cardiac troponin measurements.

Cardiac Troponin I and T Concentrations in Patients with Cocaine-Associated Chest Pain

1996 ◽  
Vol 33 (3) ◽  
pp. 183-186 ◽  
Author(s):  
Mary McLaurin ◽  
Fred S Apple ◽  
Timothy D Henry ◽  
Scott W Sharkey
Keyword(s):  
Skeletal Muscle ◽  
Chest Pain ◽  
Cardiac Troponin ◽  
Muscle Injury ◽  
Troponin I ◽  
Troponin T ◽  
Acute Chest Pain ◽  
Cardiac Troponin I ◽  
Skeletal Muscle Injury ◽  
Rule Out

Patients with cocaine-related chest pain with electrocardiographic (ECG) abnormalities are often admitted to rule out acute myocardial infarction (AMI). Cardiac troponin I and T should be superior to measurement of creatine kinase (CK)—MB for detecting cardiac injury in patients with coexisting skeletal muscle injury. We prospectively evaluated 19 consecutive patients with acute chest pain related to cocaine use who were hospitalized to rule out AMI. The admission ECG was abnormal in 16 of 19 patients. Total CK and CK—MB were elevated during the hospital course in 14 and 3 patients, respectively. Cardiac troponin I and cardiac troponin T levels were within normal limits in all patients demonstrating that recent myocardial injury did not occur. Clinically, no patient had an AMI. Cocaine-induced thoracic skeletal muscle injury or transient cocaine-induced coronary vasospasm should be considered as alternative sources of chest pain in these patients.

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