Rapid and specific immunoassay for cardiac troponin I in the diagnosis of myocardial damage

1997 ◽  
Vol 27 (1) ◽  
pp. 60-64 ◽  
Author(s):  
M. Panteghini ◽  
R. Bonora ◽  
F. Pagani
2021 ◽  
pp. 096032712110434
Author(s):  
Yusuf K Tekin ◽  
Gülaçan Tekin ◽  
Naim Nur ◽  
İlhan Korkmaz ◽  
Sefa Yurtbay

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.


2018 ◽  
Vol 52 (02) ◽  
pp. 92-93
Author(s):  
Laura Kranaster ◽  
Johanna Badstübner ◽  
Suna Aksay ◽  
Jan Bumb ◽  
Rayan Suliman ◽  
...  

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.


2019 ◽  
Vol 47 (8) ◽  
pp. 3623-3635
Author(s):  
Hong-mei Zhou ◽  
Xiao-yan Ling ◽  
Yun-jian Ni ◽  
Cheng Wu ◽  
Zhi-peng Zhu

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.


Author(s):  
Siti Fatonah ◽  
Anik Widijanti ◽  
Tinny Endang Hernowati

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.


2016 ◽  
Vol 130 (24) ◽  
pp. 2277-2278
Author(s):  
Charles S. Redwood

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.


1998 ◽  
Vol 13 (4) ◽  
pp. 378-384 ◽  
Author(s):  
Luc Jacquet ◽  
Philippe Noirhomme ◽  
Gebrin El Khoury ◽  
Martin Goenen ◽  
Marianne Philippe ◽  
...  

2016 ◽  
Vol 49 (03) ◽  
pp. 406-409 ◽  
Author(s):  
Arindam Bose ◽  
Chandra B. Chhabra ◽  
Shobha Chamania ◽  
Nanda Hemvani ◽  
Dhananjay S. Chitnis

ABSTRACTMyocardial infarction (MI) following high voltage electric burn is very rare, and its pathogenesis remains controversial. Electrical burns represent only 4% of all burns. Hence, clinical managements have taken a slow pace in developing. The recent guidelines laid down by the cardiology societies include cardiac troponin I (cTnI) as the gold standard marker for the assessment of myocardial damage assessment. Two patients were admitted to our hospital at the different time with the same kind of high voltage electric burn. Both patients had complained with chest discomfort during admission, and cardiac parameter assessment was done for both the patients. cTnI was also measured for both patients, and marked increase in the values was seen within 5 h of onset of myocardial damage and got into normal range within 72 h. Myocardial damage following electric burn needs to be suspected and assessed as early as possible. Hence, cTnI should be the valuable tool to detect the severity of myocardial damage incurred in the electric burn cases.


2014 ◽  
Vol 9 (9-10) ◽  
pp. 354-354
Author(s):  
Tatjana Zekic ◽  
Luka Bastiancic ◽  
Stanislav Laginja ◽  
Dragana Grohovac ◽  
Tomislav Jakljevic ◽  
...  

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