Cardiac troponin T in diagnosis of acute myocardial infarction

1991 ◽  
Vol 37 (6) ◽  
pp. 845-852 ◽  
Author(s):  
Johannes Mair ◽  
Erika Artner-Dworzak ◽  
Peter Lechleitner ◽  
Jörn Smidt ◽  
Ina Wagner ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Striated Muscle ◽  
Troponin T ◽  
Venous Blood ◽  
Reference Interval ◽  
Laboratory Diagnosis ◽  
Fibrinolytic Therapy ◽  
Tissue Type ◽  
Enzyme Linked Immunosorbent Assay

Abstract Troponin T is a structurally bound protein found in striated muscle cells. We tested concentrations of its cardiac-specific isotype in peripheral venous blood samples serially drawn from 72 patients with confirmed myocardial infarction. Fifty-nine patients received thrombolytic treatment with intravenous streptokinase, urokinase, or recombinant tissue-type plasminogen activator; because of contraindications, the remaining 13 patients did not. Concentrations of troponin T in plasma, measured by an enzyme-linked immunosorbent assay, started increasing within a few hours after the onset of symptoms (median, 4 h; range, 1-10 h). The sensitivity of troponin T for detecting myocardial infarction was 100% from 10 to 120 h after the onset of symptoms; sensitivity on the seventh day after admission was 84%. Concentrations were increased for up to three weeks in some patients with late or high peak values. Successful reperfusion in Q-wave infarction obviously influences the release of troponin T into plasma, with all such cases showing peak values less than or equal to 26 h (median, 14 h) after the onset of symptoms. Troponin T concentrations in these patients returned to within the reference interval more rapidly than in nonreperfused subjects. In the 13 patients without fibrinolytic therapy, troponin T tended to peak approximately 48 h (median) after the onset of chest pain. Troponin T concentrations in patients for whom thrombolysis was unsuccessful resembled those in patients without fibrinolytic therapy. The specificity of the assay was 96% as tested in samples of 96 emergency-room patients. The reference interval (less than 0.5 micrograms/L) was established from samples of 100 healthy blood donors. Troponin T measurements are a specific and sensitive method for the early and late diagnosis of acute myocardial infarction and could, therefore, provide a new criterion in laboratory diagnosis of its occurrence.

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.

Fibrin Metabolism in Patients with Acute Myocardial Infarction During and After Treatment with Tissue-Type Plasminogen Activator

1988 ◽  
Vol 60 (03) ◽  
pp. 428-433 ◽  
Author(s):  
Michael E Ring ◽  
Samuel M Butman ◽  
Denise C Bruck ◽  
William M Feinberg ◽  
James J Corrigan
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Molecular Markers ◽  
Plasminogen Activator ◽  
Degradation Products ◽  
Fibrinolytic Therapy ◽  
Tissue Type ◽  
Tissue Type Plasminogen Activator ◽  
Fibrin Degradation Products ◽  
Type Plasminogen Activator

SummaryIn order to define some of the determinants of successful thrombolysis and reocclusion during fibrinolytic therapy for acute myocardial infarction (AMI), specific molecular markers of fibrin metabolism were serially measured in 15 patients with AMI treated with tissue-type plasminogen activator (t-PA). Fibrin formation was assessed by measurement of fibrinopeptide A (FpA) and fibrinolysis by assay of B-P peptides 1—42 and 15—42 and crosslinked fibrin degradation products (XDP). At baseline, FpA levels were high while markers of fibrinolysis were near normal. Following a 90-minute infusion of t-PA (0.5—1.1 mg kg−1 hr−1), all markers of fibrinolysis increased. Levels of FpA remained elevated despite heparin at the initiation of cardiac catheterization. None of these markers discriminated between patients with successful reperfusion from those without. At 4 hours, B-β 15—42 peptide and XDP levels remained elevated suggesting persistence of fibrinolysis beyond the short circulatory half-life of t-PA. FpA levels at 4 hours were lower in patients who underwent acute coronary angioplasty compared to those who received additional low dose t-PA (12.3 ± 4.5 vs. 30.4 ± 5.5 ng/ ml, p <0.05). By 48 hours, markers of fibrinolysis had returned toward normal except in 2 patients with persistently elevated B-P 15—42 peptide levels who suffered reocclusion on days 5 and 6 (75 and 44 vs. 29 ± 3 nM, p <0.005). In conclusion, molecular markers of fibrin metabolism during fibrinolytic therapy may provide clinically relevant data.

EARLY SPONTANEOUS FIBRINOLYSIS IS RELATED TO THE EXTENSION OF ACUTE MYOCARDIAL INFARCTION

1987 ◽  
Author(s):  
M Hanss ◽  
D Rousson ◽  
P Touboul ◽  
M Dechavanne
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Plasma Levels ◽  
Early Stage ◽  
Venous Blood ◽  
Peak Level ◽  
Enzyme Linked Immunosorbent Assay ◽  
Significant Linear Correlation ◽  
Coefficient Corrélation ◽  
Two Parameters

The relative importance of spontaneous fibrinolysis was studied during the early stage of acute myocardial infarction (AMI). Ten consecutive male patients (52.1 ± 5.7 years old) with AMI and without haemodynamic or rythmic complications were selected. Blood samples were obtained less than 5 hours (3.4 ± 0.8 hours) after the onset of symptoms. Enzyme linked immunosorbent assay procedures were performed to quantify the D-dimer antigen (Dd-Ag) and tissue plasminogen activator antigen (tPA-Ag) plasma levels. The creatine phosphokinase (CPK) peak level was measured in serum as an index of the AMI extension. Mean ± S.D. (range) levels were respectively 368 ± 342 (118-1100) μg/1 for Dd-Ag, 12.9 ± 9.4 (4.5 - 29.1) μg/1 for tPA-Ag and 1117 ± 856 (256-2800) U/l for CPK. Coefficient correlation (r) between these parameters are given in the table.A significant linear correlation was observed between tPA-Ag and Dd-Ag. Moreover, plasma levels of these two parameters were inversely correlated to the logarithm of the CPK peak level. Thus abnormaly high tPA-Ag levels are detected in plasma from peripheric venous blood when likely marked fibrin lysis occurs and if AMI size is limited.These data suggest that impaired fibrinolysis is probably involved in the .progression of coronary occlusion during the early stage of AMI.

Pharmacokinetics and Haemostatic Status During Consecutive Infusions of Recom binant Tissue-Type Plasminogen Activator in Patients with Acute Myocardial Infarction

1989 ◽  
Vol 61 (03) ◽  
pp. 497-501 ◽  
Author(s):  
E Seifried ◽  
P Tanswell ◽  
D Ellbrück ◽  
W Haerer ◽  
A Schmidt
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Plasminogen Activator ◽  
Peak Plasma ◽  
Peak Plasma Concentration ◽  
Tissue Type ◽  
Tissue Type Plasminogen Activator ◽  
Precise Control ◽  
Type Plasminogen Activator

SummaryPharmacokinetics and systemic effects of recombinant tissue type plasminogen activator (rt-PA) were determined during coronary thrombolysis in 12 acute myocardial infarction patients using a consecutive intravenous infusion regimen. Ten mg rt-PA were infused in 2 minutes resulting in a peak plasma concentration (mean ±SD) of 3310±950 ng/ml, followed by 50 mg in 1 h and 30 mg in 1.5 h yielding steady state plasma levels of. 2210±470 nglml and 930±200 ng/ml, respectively. All patients received intravenous heparin. Total clearance of rt-PA was 380±74 ml/min, t,½α was 3.6±0.9 min and t,½β was 16±5.4 min.After 90 min, in plasma samples containing anti-rt-PA-IgG to inhibit in vitro effects, fibrinogen was decreased to 54%, plasminogen to 52%, α2-antiplasmin to 25%, α2-macroglobulin to 90% and antithrombin III to 85% of initial values. Coagulation times were prolonged and fibrin D-dimer concentrations increased from 0.40 to 2.7 μg/ml. It is concluded that pharmacokinetics of rt-PA show low interpatient variability and that its short mean residence time in plasma allows precise control of therapy. Apart from its moderate effect on the haemostatic system, rt-PA appears to lyse a fibrin pool in addition to the coronary thrombus.

Systemic Thrombin Generation and Activity Resistant to Low Molecular Weight Heparin Administered Prior to Streptokinase in Patients with Acute Myocardial Infarction

1997 ◽  
Vol 77 (01) ◽  
pp. 057-061 ◽  
Author(s):  
Dennis W T Nilsen ◽  
Lasse Gøransson ◽  
Alf-Inge Larsen ◽  
Øyvind Hetland ◽  
Peter Kierulf
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Molecular Weight ◽  
Body Weight ◽  
Low Molecular Weight Heparin ◽  
Troponin T ◽  
Bleeding Complications ◽  
Control Group ◽  
Low Molecular Weight ◽  
Creatine Kinase Mb

SummaryOne hundred patients were included in a randomized open trial to assess the systemic factor Xa (FXa) and thrombin inhibitory effect as well as the safety profile of low molecular weight heparin (LMWH) given subcutaneously in conjunction with streptokinase (SK) in patients with acute myocardial infarction (MI). The treatment was initiated prior to SK, followed by repeated injections every 12 h for 7 days, using a dose of 150 anti-Xa units per kg body weight. The control group received unfractionated heparin (UFH) 12,500 IU subcutaneously every 12 h for 7 days, initiated 4 h after start of SK infusion. All patients received acetylsalicylic acid (ASA) initiated prior to SK.Serial blood samples were collected prior to and during the first 24 h after initiation of SK infusion for determination of prothrombin fragment 1+2 (Fl+2), thrombin-antithrombin III (TAT) complexes, fibrinopeptide A (FPA) and cardiac enzymes. Bleeding complications and adverse events were carefully accounted for.Infarct characteristics, as judged by creatine kinase MB isoenzyme (CK-MB) and cardiac troponin T (cTnT), were similar in both groups of patients.A comparable transient increase in Fl+2, TAT and FPA was noted irrespective of heparin regimen. Increased anti-Xa activity in patients given LMWH prior to thrombolytic treatment had no impact on indices of systemic thrombin activation.The incidence of major bleedings was significantly higher in patients receiving LMWH as compared to patients receiving UFH. However, the occurrence of bleedings was modified after reduction of the initial LMWH dose to 100 anti-Xa units per kg body weight.In conclusion, systemic FXa- and thrombin activity following SK-infusion in patients with acute MI was uninfluenced by conjunctive LMWH treatment.

scholarly journals Sample Timing, Diagnosis of Subclinical Thyroid Dysfunction and Mortality in Acute Myocardial Infarction: ThyrAMI1 Study

2019 ◽  
Vol 105 (4) ◽  
pp. e1299-e1306 ◽  
Author(s):  
Salman Razvi ◽  
Owain Leng ◽  
Avais Jabbar ◽  
Arjola Bano ◽  
Lorna Ingoe ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Thyroid Function ◽  
Thyroid Dysfunction ◽  
Reference Interval ◽  
Reference Ranges ◽  
Diagnosis And Prognosis ◽  
Time Period ◽  
All Cause Mortality ◽  
The Impact

Abstract Objective The objective of this study was to determine the impact of blood sample timing on the diagnosis of subclinical thyroid dysfunction (SCTD) and mortality in patients with acute myocardial infarction (AMI). Patients, Design, and Main Outcome Measures Patients with AMI had thyroid function evaluated on admission between December 2014 and December 2016 and those with abnormal serum thyrotropin (TSH) had repeat thyroid function assessed at least a week later. The association between sample timing and SCTD was evaluated by logistic regression analysis. Secondary outcomes were confirmation of SCTD on repeat testing and all-cause mortality up to June 2018. Results Of the 1806 patients [29.2% women, mean (± standard deviation) age of 64.2 (±12.1) years] analyzed, the prevalence of subclinical hypothyroidism (SCH) was 17.2% (n = 311) and subclinical hyperthyroidism (SHyper) was 1.2% (n = 22) using a uniform TSH reference interval. The risk of being diagnosed with SCTD varied by sample timing in fully-adjusted models. The risk of SCH was highest between 00.01 and 06.00 hours and lowest between 12.01 and 18.00 hours, P for trend &lt;.001, and risk of SHyper was highest between 12.01 hours and 18.00 hours and lowest between 00.01 hours and 06.00 hours. Furthermore, time of the initial sample was associated with the risk of remaining in a SCH state subsequently. Mortality in SCH patients was not elevated when a uniform TSH reference interval was utilized. However, when time period–specific TSH reference ranges were utilized, the mortality risk was significantly higher in SCH patients with HR (95% CI) of 2.26 (1.01–5.19), P = .04. Conclusions Sample timing impacts on the diagnosis and prognosis of SCH in AMI patients. If sample timing is not accounted for, SCH is systemically misclassified, and its measurable influence on mortality is lost.

scholarly journals Use of Circulating MicroRNAs to Diagnose Acute Myocardial Infarction

2012 ◽  
Vol 58 (3) ◽  
pp. 559-567 ◽  
Author(s):  
Yvan Devaux ◽  
Mélanie Vausort ◽  
Emeline Goretti ◽  
Petr V Nazarov ◽  
Francisco Azuaje ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Chest Pain ◽  
Troponin T ◽  
Correct Diagnosis ◽  
Patient Treatment ◽  
Healthy Controls ◽  
Clinical Model ◽  
Acute Mi ◽  
St Elevation

Abstract BACKGROUND Rapid and correct diagnosis of acute myocardial infarction (MI) has an important impact on patient treatment and prognosis. We compared the diagnostic performance of high-sensitivity cardiac troponin T (hs-cTnT) and cardiac enriched microRNAs (miRNAs) in patients with MI. METHODS Circulating concentrations of cardiac-enriched miR-208b and miR-499 were measured by quantitative PCR in a case-control study of 510 MI patients referred for primary mechanical reperfusion and 87 healthy controls. RESULTS miRNA-208b and miR-499 were highly increased in MI patients (&gt;105-fold, P &lt; 0.001) and nearly undetectable in healthy controls. Patients with ST-elevation MI (n= 397) had higher miRNA concentrations than patients with non–ST-elevation MI (n = 113) (P &lt; 0.001). Both miRNAs correlated with peak concentrations of creatine kinase and cTnT (P &lt; 10−9). miRNAs and hs-cTnT were already detectable in the plasma 1 h after onset of chest pain. In patients who presented &lt;3 h after onset of pain, miR-499 was positive in 93% of patients and hs-cTnT in 88% of patients (P= 0.78). Overall, miR-499 and hs-cTnT provided comparable diagnostic value with areas under the ROC curves of 0.97. The reclassification index of miR-499 to a clinical model including several risk factors and hs-cTnT was not significant (P = 0.15). CONCLUSION Circulating miRNAs are powerful markers of acute MI. Their usefulness in the establishment of a rapid and accurate diagnosis of acute MI remains to be determined in unselected populations of patients with acute chest pain.

Sign in / Sign up

Export Citation Format

Share Document