Does extracellular cardiac troponin I play a pathogenic role independently of autoantibodies?

2016 ◽  
Vol 130 (24) ◽  
pp. 2277-2278
Author(s):  
Charles S. Redwood
Keyword(s):  
Cell Adhesion ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Cardiac Contractility ◽  
Myocardial Damage ◽  
Cardiac Troponin I ◽  
Pathogenic Role ◽  
Nuclear Factor Kappa Beta ◽  
Cell Adhesion Molecule 1

Cardiac troponin I (cTnI) is a key component of the Ca2+-regulatory mechanism of cardiac contractility. It is released into the circulation upon ischaemia and has become established as one of the principal diagnostic biomarkers of myocardial damage. The release of cTnI results in the generation of autoantibodies, and these have been suggested to play a pathogenic role. However, in this Edition of Clinical Science, Han, Y. et al. suggests that cTnI can act independently of immunological involvement, with the protein being found to increase infarct size caused by ischaemia/reperfusion (I/R) prior to the development of cTnI antibody. In vitro work shows that cTnI can induce increases in vascular cell adhesion molecule 1 (VCAM-1) expression and cell adhesion, with toll-like receptor 4 (TLR4) and nuclear factor kappa beta (NF-κB) involved in the downstream signalling.

scholarly journals Frontal QRS-T angle as a predictive marker for myocardial damage in acute carbon monoxide poisoning

2021 ◽  
pp. 096032712110434
Author(s):  
Yusuf K Tekin ◽  
Gülaçan Tekin ◽  
Naim Nur ◽  
İlhan Korkmaz ◽  
Sefa Yurtbay
Keyword(s):  
Carbon Monoxide ◽  
Creatine Kinase ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Myocardial Damage ◽  
Cardiac Troponin I ◽  
Arterial Oxygen ◽  
Co Poisoning ◽  
Arterial Blood ◽  
Creatine Kinase Mb

Introduction The present study was undertaken to investigate the prognostic value of the frontal QRS-T angle associated with adverse cardiac outcomes in patients with carbon monoxide (CO) poisoning in early stages in the emergency department. Materials and methods The data of 212 patients with CO poisoning who were admitted to the ED between January 2010 and May 2020 were retrospectively analyzed. The frontal QRS-T angle was obtained from the automatic reports of the EKG device. Results Compared to patients without myocardial damage, among patients with myocardial damage, statistically high creatinine, creatine kinase MB, cardiac troponin I, and frontal QRS-T angle values were found ( p < 0.001 for all parameters), while the saturation of arterial blood pH and arterial oxygen values were found to be lower ( p = 0.002 and p < 0.001, respectively). The frontal QRS-T angle values were correlated with creatine kinase, creatine kinase-MB, cardiac troponin I, and oxygen saturation (SpO2) in arterial blood (r = 0. 232, p = 0.001; r = 0. 253, p = < 0.001; r = 0. 389, p = < 0.001; r = −0. 198, p = 0.004, respectively). The optimum cut-off value of the frontal QRS-T angle was found to be 44.5 (area under the curve: 0.901, 95% confidence interval: 0.814–0.988, sensitivity: 87%, specificity: 84%). Conclusions The frontal QRS-T angle, a simple and inexpensive parameter that can be easily obtained from 12-lead surface electrocardiography, can be used as an early indicator in the detection of myocardial damage in patients with CO poisoning.

Abstract 219: Histidine Substituted Cardiac Troponin I (a164h) Improves Survival And Protects Cardiac Contractility During Acute Hypoxia In The Aged Murine Heart.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Nathan Palpant ◽  
Sharlene Day ◽  
Kimber Converso ◽  
Joseph Metzger
Keyword(s):  
Cardiac Troponin ◽  
Troponin I ◽  
Acute Hypoxia ◽  
Cardiac Contractility ◽  
Systolic Pressure ◽  
Calcium Sensitivity ◽  
The Elderly ◽  
Cardiac Troponin I ◽  
Pump Failure ◽  
Myofilament Calcium Sensitivity

Contractile dysfunction associated with ischemia is a significant cause of morbidity and mortality particularly in the elderly. Strategies designed to protect the aged heart from ischemia-mediated pump failure are needed. We have generated transgenic (Tg) mice expressing a modified form of adult cardiac troponin I, the Ca ++ -activated molecular switch of the myofilament. Consonant with the fetal isoform, this transgene encodes a histidine substitution (A164H) in the critical switch domain of TnI thus increasing myofilament calcium sensitivity in a pH-dependent manner. We hypothesized that aged mice (24 months), intrinsically susceptible to myocardial dysfunction, would retain improved cardiac contractility at baseline and during an acute hypoxic challenge by means of myofilament-mediated calcium sensitization. Methods/Results: At baseline, by echocardiography, Tg hearts had increased systolic function, with a 26% higher mean ejection fraction compared to nontransgenic (Ntg) mice: 75 ± 3% [Tg: n = 13] vs. 63 ± 4% [Ntg: n = 12], P < 0.05, with no differences in diastolic function between the groups. To study the effects of acute hypoxia on cardiac hemodynamics mice underwent microconductance Millar catheterization while ventilated with 12% oxygen. Aged Tg mice had improved survival compared to Ntg mice: time to pump failure (65% of baseline peak systolic pressure) 11.59 ± 1.25 min. [Tg: n = 3] vs. 4.11 ± 1.90 min. [Ntg: n = 3], P < 0.05. After four minutes of hypoxia, Tg mice had markedly improved cardiac contractility compared to Ntg mice with increased stroke volume (30.05 ± 4.49 uL [Tg] vs. 13.23 ± 3.21 uL [Ntg], P < 0.05), end systolic pressure (106.09 ± 11.81 mmHg [Tg] vs. 64.49 ± 4.05 mmHg [Ntg], P < 0.05) and rate of positive left ventricular pressure development (12958.66 ± 2544.68 mmHg/sec [Tg] vs. 5717.00 ± 745.67 mmHg/sec [Ntg], P = 0.05). Conclusion: An alteration in myofilament calcium sensitivity via a pH-responsive histidine button in cardiac troponin I augments baseline heart function in Tg mice over their lifetime. During acute hypoxia, cTnI A164H improves survival in aged mice by maintaining cardiac contractility, and thus holds promise for the design of gene therapeutics to treat pump failure associated with acute ischemic events in the elderly.

Evaluation of Myocardial Damage After Electroconvulsive Therapy: Analyses of High-Sensitive Cardiac Troponin I and N-Terminal pro-B-type Natriuretic Peptide

2018 ◽  
Vol 52 (02) ◽  
pp. 92-93
Author(s):  
Laura Kranaster ◽  
Johanna Badstübner ◽  
Suna Aksay ◽  
Jan Bumb ◽  
Rayan Suliman ◽  
...  
Keyword(s):  
Natriuretic Peptide ◽  
Electroconvulsive Therapy ◽  
Cardiac Troponin ◽  
Cardiovascular Events ◽  
Troponin I ◽  
Myocardial Damage ◽  
Cardiac Troponin I ◽  
Safe Procedure ◽  
Increased Risk ◽  
Before And After

AbstractElectroconvulsive therapy (ECT) is a remarkably safe procedure. However, there might exist a subgroup of patients with an increased risk for cardiovascular events. The cardiac-specific enzymes high-sensitive cardiac troponin I (hscTnI) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) were measured before and after ECT in 23 patients. No relevant increase of hscTnI after ECT was found. Mean NT-proBNP levels were higher after ECT and in three patients a new NT-proBNP elevation after ECT was identified. In conclusion, our small study did not find any evidence for myocardial damage due to ECT by measuring hsTnI, but an increase of NT-proBNP, whose clinical relevance could only be speculated, yet.

scholarly journals Pre-cardiopulmonary bypass administration of dexmedetomidine decreases cardiac troponin I level following cardiac surgery with sevoflurane postconditioning

2019 ◽  
Vol 47 (8) ◽  
pp. 3623-3635
Author(s):  
Hong-mei Zhou ◽  
Xiao-yan Ling ◽  
Yun-jian Ni ◽  
Cheng Wu ◽  
Zhi-peng Zhu
Keyword(s):  
New York ◽  
Cardiac Surgery ◽  
Cardiopulmonary Bypass ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Myocardial Damage ◽  
Heart Association ◽  
Cardiac Troponin I ◽  
Sevoflurane Postconditioning ◽  
Ctni Level

Objective This study was performed to determine the effect of dexmedetomidine (DEX) administration on myocardial damage in cardiac surgery with sevoflurane postconditioning. Methods We retrospectively examined all cardiac valve replacement surgeries from 1 April 2016 to 30 April 2017. Eligible patients were divided into two groups based on whether DEX was infused. DEX infusion was permitted only between intubation and the beginning of cardiopulmonary bypass (CPB). Sevoflurane was inhaled via the standard postconditioning procedure starting at aortic declamping. The cardiac troponin I (cTnI) level was measured at different time points. The postoperative outcomes and complications were also analyzed. Results One hundred patients were included in the study (DEX group, n = 53; non-DEX group, n = 47). Increased cTnI levels were significantly correlated with the New York Heart Association classification, CPB time, and DEX use. DEX use and the CPB time were potential independent factors contributing to changes in the cTnI level. The cTnI level at 6, 12, and 24 hours postoperatively was remarkably lower in the DEX than non-DEX group by 1.14, 7.83, and 5.86 ng/mL, respectively. Conclusions DEX decreased the cTnI level after CPB when sevoflurane postconditioning was used, especially at 6, 12, and 24 hours postoperatively.

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.

scholarly journals Regulation of the rat cardiac troponin I gene by the transcription factor GATA-4

1997 ◽  
Vol 322 (2) ◽  
pp. 393-401 ◽  
Author(s):  
Anne M. MURPHY ◽  
W. Reid THOMPSON ◽  
Ling Fan PENG ◽  
Lawrence JONES
Keyword(s):  
Transcription Factor ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Cardiac Cells ◽  
Cardiac Troponin I ◽  
Luciferase Expression ◽  
Specific Gene ◽  
Upstream Sequence ◽  
I Gene

Troponin I is a thin-filament contractile protein expressed in striated muscle. There are three known troponin I genes which are expressed in a muscle-fibre-type-specific manner in mature animals. Although the slow skeletal troponin I isoform is expressed in fetal and neonatal heart, the cardiac isoform is restricted in its expression to the myocardium at all developmental stages. To study the regulation of this cardiac-specific and developmentally regulated gene in vitro, the rat cardiac troponin I gene was cloned. Transient transfection assays were performed with troponin I–luciferase fusion plasmids to characterize the regulatory regions of the gene. Proximal regions of the upstream sequence were sufficient to support high levels of expression of the reporter gene in cardiocytes and relatively low levels in other cell types. The highest luciferase activity in the cardiocytes was noted with a plasmid that included the region spanning -896 to +45 of the troponin I genomic sequence. Co-transfection of GATA-4, a recently identified cardiac transcription factor, with troponin I–luciferase constructs permitted high levels of luciferase expression in non-cardiac cells. Electrophoretic mobility-shift assays demonstrated specific binding of GATA-4 to oligonucleotides representative of multiple sites of the troponin I sequence. Mutation of a proximal GATA-4 DNA-binding site decreased transcriptional activation in transfected cardiocytes. These results indicate that the proximal cardiac troponin I sequence is sufficient to support high levels of cardiac-specific gene expression and that the GATA-4 transcription factor regulates troponin I–luciferase expression in vitro.

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