scholarly journals Proteolytic Digestion of Serum Cardiac Troponin I as Marker of Ischemic Severity

2018 ◽  
Vol 3 (3) ◽  
pp. 450-455 ◽  
Author(s):  
Somaya Zahran ◽  
Vivian P Figueiredo ◽  
Michelle M Graham ◽  
Richard Schulz ◽  
Peter M Hwang
Keyword(s):  
Cardiac Troponin ◽  
Troponin I ◽  
Thrombus Formation ◽  
Cardiac Troponin I ◽  
Total Serum ◽  
Proteolytic Degradation ◽  
Troponin Level ◽  
Proteolytic Digestion ◽  
Severity Of Injury ◽  
Clinically Significant

Abstract Background The serum troponin assay is the biochemical gold standard for detecting myocardial infarction (MI). A major diagnostic issue is that some believe troponin levels can rise with reversible injury, in the absence of radiologically detectable infarct. Hypothesis Because cell death activates intracellular proteases, troponin released by irreversible infarct will be more proteolyzed than that released by milder processes. Our goal was to quantify proteolytic digestion of cardiac troponin I in patients with varying degrees of myocardial injury. Methods Serum or plasma samples from 29 patients with cardiac troponin I elevations were analyzed for proteolytic degradation, using 3 different sandwich ELISAs designed to specifically detect the N-terminal, core, or C-terminal regions of cardiac troponin I. Results As predicted, the degree of proteolytic digestion increased with increasing severity of injury, as estimated by the total troponin level, and this trend was more pronounced for C-terminal (vs N-terminal) degradation. The highest degree of proteolytic digestion was observed in patients with ST-elevation MI; the least, in type 2 MI (supply–demand ischemia rather than acute thrombus formation). Conclusions The proteolytic degradation pattern of cardiac troponin I may be a better indicator of clinically significant MI than total serum troponin level. Distinguishing between intact and degraded forms of troponin may be useful for (a) identifying those patients with clinically significant infarct in need of revascularization, (b) monitoring intracellular proteolysis as a possible target for therapeutic intervention, and (c) providing an impetus for standardizing the epitopes used in the troponin I assay.

Elevated Cardiac Troponin Levels in Critically Ill Patients: Prevalence, Incidence, and Outcomes

2006 ◽  
Vol 15 (3) ◽  
pp. 280-288 ◽  
Author(s):  
Wendy Lim ◽  
Deborah J. Cook ◽  
Lauren E. Griffith ◽  
Mark A. Crowther ◽  
P. J. Devereaux
Keyword(s):  
Myocardial Infarction ◽  
Intensive Care Unit ◽  
Critically Ill ◽  
Critically Ill Patients ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Cardiac Troponin I ◽  
Troponin Level ◽  
Elevated Troponin ◽  
Electrocardiographic Changes

• Background Levels of cardiac troponin, a sensitive and specific marker of myocardial injury, are often elevated in critically ill patients. • Objectives To document elevated levels of cardiac troponin I in patients in a medical-surgical intensive care unit and the relationship between elevated levels and electrocardiographic findings and mortality. • Methods A total of 198 patients expected to remain in the intensive care unit for at least 72 hours were classified as having myocardial infarction (cardiac troponin I level ≥1.2 μg/L and ischemic electrocardiographic changes), elevated troponin level only (≥1.2 μg/L and no ischemic electrocardiographic changes), or normal troponin levels. Events were classified as prevalent if they occurred within 48 hours after admission and as incident if they occurred 48 hours or later after admission. Factors associated with mortality were examined by using regression analysis. • Results A total of 171 patients had at least one troponin level measured in the first 48 hours. The prevalence of elevated troponin level was 42.1% (72 patients); 38 patients (22.2%) had myocardial infarction, and 34 (19.9%) had elevated troponin level only. After the first 48 hours, 136 patients had at least 1 troponin measurement. The incidence of elevated troponin level was 11.8% (16 patients); 7 patients (5.1%) met criteria for myocardial infarction, and 2 (1.5%) had elevated troponin level only. Elevated levels of troponin I at any time during admission were associated with mortality in the univariate but not the multivariate analysis. • Conclusions Elevated levels of cardiac troponin I in critically ill patients do not always indicate myocardial infarction or an adverse prognosis.

scholarly journals Prognostic Value of Initial Elevation in Cardiac Troponin I Level in Critically Ill Patients Without Acute Coronary Syndrome

2015 ◽  
Vol 35 (2) ◽  
pp. e1-e10 ◽  
Author(s):  
Michael Liu ◽  
Merita Shehu ◽  
Edmund Herrold ◽  
Henry Cohen
Keyword(s):  
Intensive Care Unit ◽  
Acute Coronary Syndrome ◽  
Intensive Care ◽  
Critically Ill ◽  
Critically Ill Patients ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Cardiac Troponin I ◽  
Troponin Level ◽  
Coronary Syndrome

BackgroundCardiac troponin I levels are often obtained to help rule out acute coronary syndrome.ObjectiveTo determine if elevation of troponin level within 24 hours for patients without acute coronary syndrome admitted to the intensive care unit provides important prognostic information. METHODS Patients without acute coronary syndrome admitted to the intensive care unit were prospectively divided into 2 groups according to highest serum level of cardiac troponin I within 24 hours of admission (elevated > 0.049 ng/mL; control ≤ 0.049 ng/mL). Hospital mortality, incidence of intubation, and other parameters were compared between the 2 groups.ResultsPatients with elevated troponin level (n = 40) had higher mortality than did control patients (n = 50) (35% vs 12%; P = .01). Compared with control patients, patients with elevated levels were more likely to be intubated (41% vs 17%; P = .02).ConclusionCritically ill patients without acute coronary syndrome with elevated levels of cardiac troponin I at admission had higher mortality and more intubations than did control patients.

scholarly journals Potential Use of Quercetin as Protective Agent against Hydroxychloroquine Induced Cardiotoxicity

2021 ◽  
Vol 2 (3) ◽  
pp. 185-192
Author(s):  
Mona G Amer ◽  
Nader M Mohamed
Keyword(s):  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Serum Levels ◽  
Treated Group ◽  
Cardiac Troponin I ◽  
Male Rats ◽  
Total Serum ◽  
Protective Agent ◽  
Prophylactic Measure

The aim of this study is to investigate the protective effects of Quercetin (QCT) on Hydroxychloquine (HCQ)-induced myocardial affection in rats. HCQ has been found to produce toxic effects including cardiac manifestation. Adding QCT to HCQ ameliorates its effects and prevents cardiac manifestations. For this purpose, eighty adult male rats were divided into four groups (n = 20). Group 1 (control) and group 2 (QCT-treated). Group 3 (HCQ treated) received 20 mg/kg of HCQ and group 4 (QCT + HCQ treated) received quercetin (50 mg/kg; orally) combined with HCQ for 4 weeks. Cardiac troponin-I and oxidative markers (Malondialdehyde (MDA), and total serum antioxidant) were estimated in serum. In addition, histopathological and morphometric changes of the rat heart were assessed. The HCQ treated group showed increased serum levels of cardiac troponin-I, MDA and decreased serum levels of total antioxidant. Pathological picture of myocardial hypertrophy and degeneration together with depleted cardiac tissue expression of troponin T were also observed. The characteristic features were presence of whorled myelin bodies and curvilinear bodies by EM examination. These parameters improved better in the group receiving combination of QCT together with HCQ. So, Adding QCT to HCQ could be prophylactic measure against its cardiotoxic effect compared with HCQ treatment alone.

False-Positive AxSYM Cardiac Troponin I Results in a 53-Year-Old Woman

2002 ◽  
Vol 126 (5) ◽  
pp. 606-609
Author(s):  
Ronald J. Knoblock ◽  
Christopher M. Lehman ◽  
Ruth A. Smith ◽  
Fred S. Apple ◽  
William L. Roberts
Keyword(s):  
Polyethylene Glycol ◽  
Rheumatoid Factor ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Protein A ◽  
Cardiac Troponin I ◽  
Heterophile Antibody ◽  
Clinically Significant ◽  
Polyethylene Glycol Precipitation ◽  
Number Of Classes

Abstract A number of classes of endogenous antibodies, including heterophile, rheumatoid factor, and autoantibodies, can interfere with immunoassay measurements of many different analytes. Heterophile and rheumatoid factor antibody interferences have been described previously for the AxSYM cardiac troponin I assay. Several commercial products have been developed to neutralize heterophile antibody interferences. We describe a patient with multiple apparently falsely elevated cardiac troponin I results that were unique to the AxSYM analyzer. These cardiac troponin I results diluted linearly. When treated with 2 different heterophile-blocking reagents, the magnitudes of the falsely elevated results increased 17- and 26-fold, and these results also demonstrated dilution linearity. This interfering substance could be removed by passage through an immobilized protein A column and by polyethylene glycol precipitation. It does not appear to be a classic heterophile antibody, nor is it a paraprotein. Laboratorians must remain constantly vigilant for immunoassay interferences that lead to clinically significant inaccurate results and must recognize that accepted methods for detecting and neutralizing the interference may be ineffective.

scholarly journals Degradation of cardiac troponin I: implication for reliable immunodetection

1998 ◽  
Vol 44 (12) ◽  
pp. 2433-2440 ◽  
Author(s):  
Aleksei G Katrukha ◽  
Anastasia V Bereznikova ◽  
Vladimir L Filatov ◽  
Tatiana V Esakova ◽  
Olga V Kolosova ◽  
...  
Keyword(s):  
Cardiac Troponin ◽  
Troponin I ◽  
Cardiac Troponin I ◽  
Immunological Methods ◽  
Proteolytic Degradation ◽  
Necrotic Tissue

Abstract We have analyzed by different immunological methods the proteolytic degradation of cardiac troponin I (cTnI) in human necrotic tissue and in serum. cTnI is susceptible to proteolysis, and its degradation leads to the appearance of a wide diversity of proteolytic peptides with different stabilities. N- and C-terminal regions were rapidly cleaved by proteases, whereas the fragment located between residues 30 and 110 demonstrated substantially higher stability, possibly because of its protection by TnC. We conclude that antibodies selected for cTnI sandwich immunoassays should preferentially recognize epitopes located in the region resistant to proteolysis. Such an approach can be helpful for a much needed standardization of cTnI immunoassays and can improve the sensitivity and reproducibility of cTnI assays.

Coronary Angiographic Findings in Patients With Clinical Unstable Angina According to Cardiac Troponin I and T Concentrations in Serum

2002 ◽  
Vol 126 (4) ◽  
pp. 448-451
Author(s):  
Mauro Panteghini ◽  
Claudio Cuccia ◽  
Franca Pagani ◽  
Claudia Turla ◽  
Graziella Bonetti ◽  
...  
Keyword(s):  
Coronary Angiography ◽  
Unstable Angina ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Thrombus Formation ◽  
Cardiac Troponin I ◽  
Surrogate Markers ◽  
Significant Release ◽  
Angiographic Findings

Abstract Context.—Elevated cardiac troponin levels have been reported to identify unstable angina patients at high risk. Objective.—To examine the relation of cardiac troponin I (cTnI) and cardiac troponin T (cTnT) levels to findings of coronary angiography in these patients. Methods.—Samples for troponin estimation were taken every 4 hours throughout the first 48 hours after admission before angiography in 34 patients with primary unstable angina. Patients were considered to be troponin positive if the marker was increased (>0.04 μg/L for cTnT and >0.03 μg/L for cTnI) in at least one sample collected. Results.—An increased troponin (I or T) concentration was documented in 14 patients (41.2%). Twelve patients (35.3%) had elevations of both markers, whereas the remaining 2 patients had elevations of cTnI or cTnT alone. Patients with or without increased troponin levels did not differ with respect to degree of coronary disease at angiography. However, patients with elevated troponin concentrations had more complex lesion characteristics. In 69% of patients with increased cTnI levels and in 77% of patients with increased cTnT levels, type B2 or C lesions were documented with presence of ulcerated plaques and thrombus formation. In contrast, only 23% of the patients with elevated cTnI or cTnT levels had type A lesions compared with 71% of patients with negative troponin concentrations. Conclusions.—Patients with unstable angina who have significant release of cTnI and/or cTnT have evidence of more complex lesions on coronary angiography, supporting the hypothesis that both troponins might be used without distinction as surrogate markers for microembolization from thrombus formation on a disrupted plaque.

Left atrial thrombosis secondary to blunt cardiac injury in two dogs

2019 ◽  
Vol 7 (2) ◽  
pp. e000803
Author(s):  
Isabella Ballocco ◽  
Maria Luisa Pinna Parpaglia ◽  
Francesca Corda ◽  
Giovanna Serra ◽  
Andrea Corda
Keyword(s):  
Cardiac Troponin ◽  
Left Atrial ◽  
Troponin I ◽  
Motor Vehicle ◽  
Thrombus Formation ◽  
Cardiac Injury ◽  
Serum Levels ◽  
Cardiac Troponin I ◽  
Vehicle Accidents ◽  
Blunt Cardiac Injury

Two dogs, victims of motor vehicle accidents, were hospitalised at our Veterinary Teaching Hospital with multiple injuries. Electrocardiographic abnormalities were observed in both dogs: case 1 showed ventricular arrhythmias, while case 2 manifested second degree atrioventricular block. Increased cardiac troponin-I serum levels and echocardiographic alterations compatible with left atrial wall lesions and thrombosis were detected. Based on these symptoms, the dogs were diagnosed with traumatic blunt cardiac injury. Both patients had left atrial thrombus formation, but only case 1 underwent antiplatelet therapy and experienced thromboembolic spread. Blunt cardiac injury and related consequences should be considered in traumatised patients. ECG together with cardiac troponin-I measurement and echocardiography could help clinicians to diagnose and monitor the condition.

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