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

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 &lt; or = 0.0067) earlier than CK and CKMB activity and were also significantly (P &lt; 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.

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.

P2673Challenging time limits: Using a single high-sensitive troponin I to rule-out acute myocardial infarction in early presenters

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C Hansen ◽  
C Bang ◽  
K G Lauridsen ◽  
C A Frederiksen ◽  
M Schmidt ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Emergency Department ◽  
Chest Pain ◽  
Troponin I ◽  
Regional Hospital ◽  
Late Presenters ◽  
Siemens Healthcare ◽  
High Sensitive Troponin ◽  
Rule Out

Abstract Introduction According to ESC guidelines, an acute myocardial infarction (MI) can be excluded without serial troponin measurements in patients presenting with a single high-sensitive troponin below the 99th percentile and chest pain starting >6 hours prior to admission. However, it is unclear if single-testing of high-sensitive troponin can rule-out MI in early presenters. Purpose To investigate the diagnostic performance of a single value of high-sensitive cardiac troponin I (hs-cTnI) at presentation for ruling-out MI in patients presenting with chest pain to the Emergency Department irrespective of chest pain onset. Methods We conducted a substudy of preliminary data from the RACING-MI trial. We included patients presenting with chest pain suggestive of MI to the Emergency Department of a Regional Hospital. We used the Siemens hs-cTnI (Siemens Healthcare, TNIH, Limit of detection: 2.21 ng/L) and a diagnostic cut-off value <3 ng/L to rule-out MI at presentation. Two physicians independently adjudicated the final diagnosis based on all clinical information. Patients were stratified based on time from chest pain onset to hospital admission as very early (0–3 hours), early (3–6 hours) and late presenters (>6 hours). Results We included 989 patients with available hs-cTnI results at admission. MI was confirmed in 82 (8.3%) patients. Using hs-cTnI <3 ng/L as diagnostic cut-off value at presentation, 302 (30.5%) patients without MI were classified as rule-out. Overall, the negative predictive value (NPV) for MI was 100% (95% CI 98.7–100). Based on chest pain onset, 33.8% of patients were classified as very early, 12.8% as early, and 42.7% as late presenters, with 10.7% patients with unreported/unknown onset. NPV was 100% (95% CI 96.5–100) for very early, 100% (95% CI 88.3–100) for early and 100% (95% CI 97.3–100) for late presenters. Conclusions Using a single hs-cTnI value <3ng/L as diagnostic cut-off to rule-out MI seems to be safe and to allow rapid rule-out of MI in patients presenting with chest pain to the emergency department, even in very early presenters. ClinicalTrials.gov Identifier: NCT03634384. Acknowledgement/Funding Randers Regional Hospital, A.P Møller Foundation, Boserup Foundation, Korning Foundation, Højmosegård Grant, Siemens Healthcare (TNIH assays), etc.

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.

Autoantibody prevalence with an improved immunoassay for detecting cardiac troponin-specific autoantibodies

2014 ◽  
Vol 52 (2) ◽  
Author(s):  
Tanja Savukoski ◽  
Tuomo Ilva ◽  
Juha Lund ◽  
Pekka Porela ◽  
Noora Ristiniemi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Emergency Department ◽  
Chest Pain ◽  
Cardiac Troponin ◽  
Troponin I ◽  
State Of The Art ◽  
Cardiac Troponin I ◽  
High Prevalence ◽  
Sandwich Type ◽  
Pain Patients

AbstractCardiac troponin-specific autoantibodies (cTnAAb) can interfere with the measurement of cardiac troponin I (cTnI) by immunoassays used for the diagnosis of myocardial infarction (MI). Here, an improved version of a previous autoantibody assay was validated and used to evaluate the cTnAAb prevalence in a cohort of consecutive chest pain patients presenting to an emergency department.Admission samples from 510 patients with suspected MI were analyzed in parallel with two sandwich-type cTnAAb assays based on different cTnI epitopes used to capture cardiac troponin-bound cTnAAbs.Sample-specific backgrounds were lower for the new assay than for the old assay (median 1225 vs. 2693 counts, p<0.001). Net signals of cTnAAb-positive samples were higher for the new assay than for the old assay (median 5076 vs. 3921 counts, p<0.001). Of all patients, 9.2% were cTnAAb-positive for the new assay and 7.3% for the old assay (p=0.013). Previous cardiac problems were not associated with cTnAAb status and cTnAAb status did not correlate with the 12-month outcome.With our new and more sensitive autoantibody assay, approximately one out of ten patients who presented to the initial cardiac triage had detectable amounts of cTnAAbs in the circulation. Because these cTnAAbs can interfere with state-of-the-art cTnI assays, their high prevalence should be acknowledged by clinical chemists, physicians, and kit manufacturers.

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 Health Outcomes Categorized by Current and Previous Definitions of Acute Myocardial Infarction in an Unselected Cohort of Troponin-Naïve Emergency Department Patients

2006 ◽  
Vol 52 (11) ◽  
pp. 2028-2035 ◽  
Author(s):  
Peter A Kavsak ◽  
Andrew R MacRae ◽  
Glenn E Palomaki ◽  
Alice M Newman ◽  
Dennis T Ko ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Emergency Department ◽  
Health Outcomes ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Survival Rates ◽  
World Health ◽  
Separate Analysis ◽  
Health Organization

Abstract Background: In a population originally classified for acute myocardial infarction (AMI) by the World Health Organization (WHO) definition, we compared the health outcomes after retrospectively reclassifying with the European Society of Cardiology and the American College of Cardiology (ESC/ACC) AMI definition, using the peak cardiac troponin I (cTnI) concentrations. The health outcomes were based on the WHO definition and occurred in an era that preceded the use of cardiac troponin biomarkers. Methods: For 448 patients who presented to the emergency department with symptoms suggestive of cardiac ischemia in 1996, we obtained data for all-cause mortality and recurrent AMI for up to 1 year after the initial presentation. We performed retrospective analysis of the patients’ frozen plasma samples to measure cTnI (AccuTnI®, Beckman Coulter). Results: At 30, 120, and 360 days, the risk for AMI/death in patients positive for AMI by only the ESC/ACC criteria was significantly lower than the risk in patients positive by both ESC/ACC and WHO criteria, and significantly higher than in patients negative according to both criteria. In a separate analysis, patients with a peak cTnI &gt;0.10 μg/L were at greater risk for AMI/death than patients with cTnI concentrations of 0.04–0.10 μg/L. Patients negative by both definitions or with peak cTnI concentrations &lt;0.04 μg/L had the highest event-free survival rates (92% and 94%, respectively) at 1 year. Conclusion: In a troponin-naïve population, patients classified as positive for AMI by only the ESC/ACC criteria have a prognosis that appears to be intermediate between those classified positive by both the WHO and ESC/ACC definitions and those who meet neither criteria.

Sign in / Sign up

Export Citation Format

Share Document