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 Determination of Cardiac Troponin I Forms in the Blood of Patients with Acute Myocardial Infarction and Patients Receiving Crystalloid or Cold Blood Cardioplegia

1999 ◽  
Vol 45 (2) ◽  
pp. 213-222 ◽  
Author(s):  
Isabelle Giuliani ◽  
Jean-Pierre Bertinchant ◽  
Claude Granier ◽  
Michel Laprade ◽  
Sidney Chocron ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Troponin ◽  
Heart Surgery ◽  
Troponin I ◽  
Binary Complex ◽  
Serum Samples ◽  
Blood Cardioplegia ◽  
Cold Blood ◽  
Cold Blood Cardioplegia

Abstract To determine the forms of cardiac troponin I (cTnI) circulating in the bloodstream of patients with acute myocardial infarction (AMI) and patients receiving a cardioplegia during heart surgery, we developed three immunoenzymatic sandwich assays. The first assay involves the combination of two monoclonal antibodies (mAbs) specific for human cTnI. The second assay involves the combination of a mAb specific for troponin C (TnC) and an anti-cTnI mAb. The third assay was a combination of a mAb specific for human cardiac troponin T (cTnT) and an anti-cTnI mAb. Fifteen serum samples from patients with AMI, 10 serum samples from patients receiving crystalloid cardioplegia during heart surgery, and 10 serum samples from patients receiving cold blood cardioplegia during heart surgery were assayed by the three two-site immunoassays. We confirmed that cTnI circulates not only in free form but also complexed with the other troponin components (TnC and cTnT). We showed that the predominant form in blood is the cTnI-TnC binary complex (IC). Free cTnI, the cTnI-cTnT binary complex, and the cTnT-cTnI-TnC ternary complex were seldom present, and when present, were in small quantities compared with the binary complex IC. Similar results were obtained in both patient populations studied. These observations are essential for the development of new immunoassays with improved clinical sensitivity and for the selection of an appropriate cTnI primary calibrator.

Kinetics of high-sensitivity cardiac troponin T or troponin I compared to creatine kinase in patients with revascularized acute myocardial infarction

2015 ◽  
Vol 53 (5) ◽  
Author(s):  
Kamila Solecki ◽  
Anne Marie Dupuy ◽  
Nils Kuster ◽  
Florence Leclercq ◽  
Richard Gervasoni ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
High Sensitivity ◽  
Cardiac Troponin T ◽  
Significant Difference ◽  
Kinetics Of

AbstractCardiac biomarkers are the cornerstone of the biological definition of acute myocardial infarction (AMI). The key role of troponins in diagnosis of AMI is well established. Moreover, kinetics of troponin I (cTnI) and creatine kinase (CK) after AMI are correlated to the prognosis. New technical assessment like high-sensitivity cardiac troponin T (hs-cTnT) raises concerns because of its unclear kinetic following the peak. This study aims to compare kinetics of cTnI and hs-cTnT to CK in patients with large AMI successfully treated by percutaneous coronary intervention (PCI).We prospectively studied 62 patients with anterior AMI successfully reperfused with primary angioplasty. We evaluated two consecutive groups: the first one regularly assessed by both CK and cTnI methods and the second group by CK and hs-cTnT. Modeling of kinetics was realized using mixed effects with cubic splines.Kinetics of markers showed a peak at 7.9 h for CK, at 10.9 h (6.9–12.75) for cTnI and at 12 h for hs-cTnT. This peak was followed by a nearly log linear decrease for cTnI and CK by contrast to hs-cTnT which appeared with a biphasic shape curve marked by a second peak at 82 h. There was no significant difference between the decrease of cTnI and CK (p=0.63). CK fell by 79.5% (76.1–99.9) vs. cTnI by 86.8% (76.6–92.7). In the hs-cTnT group there was a significant difference in the decrease by 26.5% (9–42.9) when compared with CK that fell by 79.5% (64.3–90.7).Kinetic of hs-cTnT and not cTnI differs from CK. The role of hs-cTnT in prognosis has to be investigated.

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 Sensitivity and specificity of cardiac troponin-T in diagnosis of acute myocardial infarction

2017 ◽  
Vol 4 (1) ◽  
pp. 244 ◽  
Author(s):  
Dharmveer Sharma ◽  
Poonam Gupta ◽  
Sagar Srivastava ◽  
Harshit Jain
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Striated Muscle ◽  
Troponin T ◽  
T Test ◽  
Specific Marker ◽  
Enzymatic Markers ◽  
Better Than

Background: Myocardial Infarction is the irreversible necrosis of the heart muscle secondary to prolong lack of oxygen supply. Troponin T is a structurally bound protein found in striated muscle cells. They have rapidly attained central role in diagnosis, prognostication and planning of therapeutic strategies in MI patients. The objective of this study was to evaluate the status of Troponin T in MI patients and its role in diagnosis compare to normal subjects.Methods: The study was conducted at M. L .N. Medical College, Allahabad, Uttar Pradesh India. A total of 136 cases were included in our study. Out of these, 86 were patients of AMI and 50 were healthy controls. They were evaluated by measurement of various parameters including enzymatic markers such as CPK-MB, SGOT, LDH1, and LDH2 and non-enzymatic markers such as troponin-T and myoglobin. Apart from these, LDL, VLDL and HDL levels were also kept under evaluation.Results: Troponin-T test was better than CPK-MB or SGOT in diagnosing myocardial infarction. In our study, sensitivity (67.3%) and specificity (73.8%) of troponin-T test was higher than CPK-MB (56.2% and 45.7%) and SGOT (34.2% and 58.3%) respectively. Troponin-T test was better than CPK-MB or SGOT after 2 hours of onset of myocardial infarction. Troponin- T and I: both kind of evaluations are available and are well evaluated. However troponin T estimation is more standardized and thus more popular. The positivity of troponin-T test also varied with area of infarct.Conclusions: High LDL and VLDL were seen while at the same time HDL level was lowered. An Increase in the level of myoglobin (non-specific marker), Cardiac troponin I and T and among the enzymatic markers elevated levels of CPK-MB, LDH and SGOT were observed in patients of MI against the normal subjects. In case of LDH both LDH 1 and LDH 2 were observed and a flipped pattern was noted. Bedside troponin-T test is highly sensitive and specific in the diagnosis of acute myocardial infarction and can be used in emergency and ambulatory settings. Qualitative troponin-T test is reliable above serum level of ≥ 0.10 ng/ml.

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.

Early Diagnostic Efficiency of Cardiac Troponin I and Troponin T for Acute Myocardial Infarction

1997 ◽  
Vol 4 (1) ◽  
pp. 13-21 ◽  
Author(s):  
John F. Tucker ◽  
Richard A. Collins ◽  
Alfred J. Anderson ◽  
Jacqueline Hauser ◽  
John Kalas ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Cardiac Troponin I ◽  
Diagnostic Efficiency ◽  
Early Diagnostic

Evaluation of First-Draw Whole Blood, Point-of-Care Cardiac Markers in the Context of the Universal Definition of Myocardial Infarction: A Comparison of a Multimarker Panel to Troponin Alone and to Testing in the Central Laboratory

2011 ◽  
Vol 135 (4) ◽  
pp. 459-463
Author(s):  
Elizabeth Lee-Lewandrowski ◽  
James L Januzzi ◽  
Ricky Grisson ◽  
Asim A Mohammed ◽  
Grant Lewandrowski ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Point Of Care ◽  
Cardiac Troponin T ◽  
Central Laboratory ◽  
Universal Definition ◽  
Definition Of

Abstract Context.—Previous studies evaluating point-of-care testing (POCT) for cardiac biomarkers did not use current recommendations for troponin cutoff values or recognize the recent universal definition of acute myocardial infarction. Traditionally, achieving optimal sensitivity for the detection of myocardial injury on initial presentation required combining cardiac troponin and/or creatine kinase isoenzyme MB with an early marker, usually myoglobin. In recent years, the performance of central laboratory combining cardiac troponin assays has improved significantly, potentially obviating the need for a multimarker panel to achieve optimum sensitivity. Objective.—To compare 2 commonly used POCT strategies to a fourth generation, central laboratory cardiac troponin T assay on first-draw specimens from patients being evaluated for acute myocardial infarction in the emergency department. The 2 strategies included a traditional POCT multimarker panel and a newer POCT method using cardiac troponin I alone. Design.—Blood specimens from 204 patients presenting to the emergency department with signs and/or symptoms of myocardial ischemia were measured on the 2 POCT systems and by a central laboratory method. The diagnosis for each patient was determined by retrospective chart review. Results.—The cardiac troponin T assasy alone was more sensitive for acute myocardial infarction than the multimarker POCT panel with equal or better specificity. When compared with a POCT troponin I, the cardiac troponin T was also more sensitive, but this difference was not significant. The POCT troponin I alone also had the same sensitivity as the multimarker panel. Conclusions.—Testing for combining cardiac troponin alone using newer, commercially available, central laboratory or POCT assays performed with equal or greater sensitivity to acute myocardial infarction as the older, traditional, multimarker panel. In the near future, high-sensitivity, central laboratory troponins will be available for routine clinical use. As a result, the quality gap between central laboratories and older POCT methods will continue to widen, unless the performance of the POCT methods is improved.

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

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