Purpose: Plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) and cardiac troponin T levels show a transient increase after marathon running. The aim of this study was to investigate whether running duration influences the patterns of changes in cardiac biomarkers. Methods: Twenty participants with fast and slow finishing times were included in the study. Blood samples were taken before the marathon race, immediately after, and 24 hours after the race. Samples were analyzed for NT-proBNP and cardiac troponin T concentration. Furthermore, a complete blood cell count was performed. Results: After the marathon race, the fast and slow runners showed similar changes of NT-proBNP and cardiac troponin T (ie, a transient increase). Curve estimation regression analysis showed a curvilinear relationship (quadratic model) between running times and NT-proBNP increments immediately after the race, with less of an increase in the very fast and the very slow runners (r2 = .359, P = .023). NT-proBNP ...
We conducted a single centre blinded study with follow up of patients admitted to a hospital coronary care unit with chest pain. Management decisions were based on clinical, electrocardiographic, and routine biochemical marker results (daily serum creatine kinase, aspartate transaminase, and hydroxybutyrate dehydrogenase activities). An additional sample was taken 12-24 hours after admission, when the cardiac troponin T concentration is at its most efficient for diagnosing myocardial damage in these patients.11 All management decisions were made without knowledge of the patients troponin T status.. Full clinical details of each patient were recorded on a form. Follow up for cardiac events was by examination of hospital records, necropsy reports when available and death certificates, questionnaires, and telephone contact when required. Survival status and cause of death were established for all patients. Cause of death was classified according to American Heart Association ...
TY - JOUR. T1 - High-sensitivity cardiac troponin I at presentation in patients with suspected acute coronary syndrome: a cohort study. AU - High-STEACS investigators. AU - Shah, Anoop S V. AU - Anand, Atul. AU - Sandoval, Yader. AU - Lee, Kuan Ken. AU - Smith, Stephen W. AU - Adamson, Philip D. AU - Chapman, Andrew R.. AU - Langdon, Timothy. AU - Sandeman, Dennis. AU - Vaswani, Amar. AU - Strachan, Fiona E.. AU - Ferry, Amy. AU - Stirzaker, Alexandra G. AU - Reid, Alan. AU - Gray, Alasdair J. AU - Collinson, Paul O. AU - McAllister, David A. AU - Apple, Fred S. AU - Newby, David E. AU - Mills, Nicholas L. N1 - Date of Acceptance: 15/09/2015. PY - 2015/12/19. Y1 - 2015/12/19. N2 - Background: Suspected acute coronary syndrome is the commonest reason for emergency admission to hospital and is a large burden on health-care resources. Strategies to identify low-risk patients suitable for immediate discharge would have major benefits.Methods: We did a prospective cohort study of 6304 consecutively ...
We investigated the effect of 7 Hypertrophic Cardiomyopathy (HCM)-causing mutations in troponin T (TnT) on troponin function in thin filaments reconstituted with actin and human cardiac tropomyosin. We used the quantitative in vitro motility assay to study Ca(2+)-regulation of unloaded movement and its modulation by troponin I phosphorylation. Troponin from a patient with the K280N TnT mutation showed no difference in Ca(2+)-sensitivity when compared with donor heart troponin and the Ca(2+)-sensitivity was also independent of the troponin I phosphorylation level (uncoupled). The recombinant K280N TnT mutation increased Ca(2+)-sensitivity 1.7-fold and was also uncoupled. The R92Q TnT mutation in troponin from transgenic mouse increased Ca(2+)-sensitivity and was also completely uncoupled. Five TnT mutations (Δ14, Δ28 + 7, ΔE160, S179F and K273E) studied in recombinant troponin increased Ca(2+)-sensitivity and were all fully uncoupled. Thus, for HCM-causing mutations in TnT, Ca(2+)-sensitisation
Judd E. Hollander, MD, says all hes heard for the past five years is that an assay will be out at the end of the year. And once you get halfway through the year, it will be out next year, says Dr. Hollander, chair of the Department of Emergency Medicine and associate dean of strategic health initiatives at Sidney Kimmel Medical College of Thomas Jefferson University.. Robert Christenson, PhD, DABCC, professor of pathology at the University of Maryland School of Medicine, sees the odds as good that the FDA will clear one such assay this year. He predicts it will be a Roche or an Abbott assay.. Agim Beshiri, MD, Abbotts senior medical director of global medical and scientific affairs for diagnostics, says, The requirements for U.S. regulatory approval for any troponin test are very high, and the complexity is enhanced with high-sensitivity troponin methods. It is not possible to predict when these tests will become available.. Dr. deFilippi. The FDA appears to have two concerns, says ...
Troponin assays are a relatively common laboratory diagnostic request in emergency medical admissions. Following cardiac injury these macromolecules diffuse into the cardiac interstitium with subsequent detection in the peripheral circulation. We have previously shown that a clinical decision to request high-sensitivity cardiac troponin T (hscTnT) was a prognostic marker and semi-quantitative mortality predictor in unselected emergency medical admissions [1]. Cardiac-specific troponins are useful because they convey prognostic information that can influence therapeutic decisions, [2] not alone for the diagnosis of acute coronary syndromes [3], but also in non-cardiac presentations [4-17].. ...
To the Editor We read with interest the systematic review and meta-analysis by Bruins Slot et al concerning early diagnosis of myocardial infarction (MI) using heart-type fatty acid-binding protein (H-FABP).1 We agree with their summary that when used in isolation, H-FABP may not offer a diagnostic advantage over the current troponin standard. However, it should be noted that in five of the included studies constituting 1573 patients (42% of the pooled cohort), no … ...
A number of studies have demonstrated a role for troponin T in the modulation of muscle activation, particularly in fishes. Cod Gadus morhua show longitudinal variation in the activation of their white muscle (Davies et al., 1995). Thys et al. (1998) demonstrated that this shift in muscle contractile properties correlates with a longitudinal pattern of expression of two isoforms of TnT. Similarly, Thys et al. (2001) showed a significant rostral-caudal shift in both muscle activation and TnT expression in the white muscle of largemouth bass. In both cod and bass, the anterior muscle is kinetically faster and expresses relatively greater amounts of an isoform of TnT that migrates faster on PAGE gels. (TnT-2; Thys et al., 1998, 2002). For both white (cod and bass) and red (rainbow and brook trout) muscle in fishes, the kinetically faster isoform of TnT appears to be the physically smaller isoform found in each type of muscle. Other fish, such as saithe Pollachius virens (Altringham et al., 1993), ...
The existence of cardiac damage in active rheumatic carditis patients is unknown, especially in those without pericarditis. The aim of this study was to determine cardiac myocyte damage using cardiac troponin T (cTnT) measurements in active rheumatic
There is a growing interest in using biomarkers to obtain pathophysiological insight into and, possibly, to improve the management of patients with heart failure (HF). Considering that HF is a systemic disease, biomarkers reflecting cardiac and systemic abnormalities may add incremental information to cardiac-specific markers such as B-type natriuretic peptide and high-sensitivity troponin T. Growth-differentiation factor-15 (GDF-15) is a distant member of the transforming growth factor-β cytokine superfamily that is produced in the heart and vasculature in response to tissue injury and inflammation. Accumulating evidence indicates that the circulating levels of GDF-15 are associated with prognosis in patients with coronary artery disease. In the present subinvestigation from the Valsartan Heart Failure Trial (Val-HeFT), 85% of the patients with advanced, stable, chronic HF had elevated circulating levels of GDF-15. GDF-15 levels further increased during the course of 12 months in both the ...
Cardiac conditions. Certain subtypes of troponin (cardiac troponin I and T) are very sensitive and specific indicators of damage to the heart muscle (myocardium). They are measured in the blood to differentiate between unstable angina and myocardial infarction (heart attack) in patients with chest pain or acute coronary syndrome. A patient who had suffered from a myocardial infarction would have an area of damaged heart muscle and so would have elevated cardiac troponin levels in the blood. This can also occur in patients with coronary vasospasm.. It is important to note that cardiac troponins are a marker of all heart muscle damage, not just myocardial infarction. Other conditions that directly or indirectly lead to heart muscle damage can also increase troponin levels. Severe tachycardia (for example due to supraventricular tachycardia) in an individual with normal coronary arteries can also lead to increased troponins for example, presumably due to increased oxygen demand and inadequate ...
TY - JOUR. T1 - High population prevalence of cardiac troponin I measured by a high-sensitivity assay and cardiovascular risk estimation. T2 - The MORGAM Biomarker Project Scottish Cohort. AU - Zeller, Tanja. AU - Tunstall-Pedoe, Hugh. AU - Saarela, Olli. AU - Ojeda, Francisco. AU - Schnabel, Renate B.. AU - Tuovinen, Tarja. AU - Woodward, Mark. AU - Struthers, Allan. AU - Hughes, Maria. AU - Kee, Frank. AU - Salomaa, Veikko. AU - Kuulasmaa, Kari. AU - Blankenberg, Stefan. PY - 2014/2/1. Y1 - 2014/2/1. N2 - Our aim was to test the prediction and clinical applicability of high-sensitivity assayed troponin I for incident cardiovascular events in a general middle-aged European population. Methods and results High-sensitivity assayed troponin Iwasmeasured in the Scottish HeartHealth ExtendedCohort (n = 15 340) with 2171 cardiovascular events (including acute coronary heart disease and probable ischaemic strokes), 714 coronary deaths (25% of all deaths),1980myocardial infarctions, and797strokesof all ...
Methods and Results-Cp was measured at ARIC visit 4 (1996-1998). We studied 9240 individuals without HF or CVD at ARIC visit 4 and followed them for a mean of 10.5 years. Genome-wide association study was performed to identify genetic determinants of Cp levels and evaluate their association with incident HF in ARIC participants. Cp levels (mean±SD) were higher in women versus men (335±79 versus 258±44 mg/L; P,0.0001), women on versus not on hormone-replacement therapy (398±89 versus 291±60 mg/L; P,0.0001), and African Americans versus whites (299±63 versus 293±74 mg/L; P=0.0005). After adjusting for traditional risk factors, high-sensitivity C-reactive protein, N-terminal pro-B-type natriuretic peptide, and high-sensitivity cardiac troponin T, higher levels of Cp were associated with HF (hazard ratio, 1.44; 95% confidence interval, 1.13-1.83) and mortality (hazard ratio, 1.38; 95% confidence interval, 1.11-1.63). A locus on the ceruloplasmin gene on chromosome 3 was significantly ...
Background: High sensitivity cardiac troponin I (hs-cTnI) assays are being approved for use in the United States (US). Our objective was to determine the efficacy of a 2 hour acute myocardial infarction (AMI) rule-out/rule-in European derived hs-cTnI algorithm when applied to patients in the US when the second sample was drawn 2-3 hours later in the High Sensitivity Cardiac Troponin I in the US (HIGH-US) study. Methods: Adults presenting with any suspicion for AMI were included. Patients with STEMI were excluded. Baseline and 2-3 hour plasma samples were analyzed in a core laboratory (University of Maryland) using the Siemens Atellica hs-cTnI assay (99th % 45.0 ng/L). AMI was independently adjudicated using all 30 day clinical materials available. Results: 2505 patients were enrolled with 1916 having complete data for the 2-3 hour algorithm analyses. Subjects had a mean age of 56.7 ± 12.9 years and 1419 (56.5%) were males Past medical history included hypertension in 1730 (69.1%), coronary artery
This study sought to identify differences in coronary anatomic pathology in patients with unstable angina and elevated versus nonelevated serum troponin T values. Previous studies have shown a worse prognosis in unstable angina patients with elevated
Image via Wikipedia Troponin Troponin is a complex of three regulatory proteins. Troponin T-Attaches troponin complex to Tropomyosin Troponin I-Binds troponin complex to actin Troponin C-Calcium binding troponin Tropomyosin Covers the sites where myosin heads bind actin. Troponin-Tropomyosin complex inhibits …. Read more ». ...
We have previously demonstrated the strong prognostic value of cardiac troponin in patients with high clinical suspicion for non-ST-segment elevation ACS (14). The present study demonstrates that, in the important group of patients presenting with symptoms of ACS who were later found to not have angiographically significant CAD, the presence of an elevated troponin is also associated with an adverse prognosis. This finding challenges the idea that these are false-positive troponin results and that these patients may be regarded as low-risk for subsequent cardiovascular events. Elevation of troponin in these patients may result from coronary atherothrombosis not evident using standard angiography or from other ischemic and non-ischemic mechanisms.. In the current study, 6% of patients who satisfied clinical criteria for ACS and had elevated troponin early after presentation were found not to have significant angiographic coronary stenosis. Despite the absence of significant coronary stenosis, ...
Coronary artery disease (CAD) is one of the leading causes of morbidity and mortality worldwide. Life threatening manifestations such as acute myocardial infarction (AMI) and sudden cardiac death are the most important causes of death in many countries. Cardiac troponin is a biomarker with a high specificity for cardiac necrosis and is recommended for diagnosis of acute myocardial infarction by the Universal definition of myocardial infarction. Since a new generation of high-sensitivity cardiac troponin assays has become commercially available a few years ago, myocardial infarction can be detected earlier and even small AMIs, that were classified as unstable angina pectoris (UAP) with the less sensitive assays, are detectable now. On the other side, more patients with acute or chronic myocardial damage not due to AMI are identified now. Thereby, the reason for elevated troponin levels should be sought actively, because high troponin levels were associated with adverse outcome - independent of ...
TY - JOUR. T1 - Decreased left ventricular ejection fraction in transgenic mice expressing mutant cardiac troponin T-Q92, responsible for hypertrophic cardiomyopathy. AU - Lim, Do Sun. AU - Oberst, Leslie. AU - McCluggage, Meghan. AU - Youker, Keith. AU - Lacy, Jeffrey. AU - DeMayo, Francesco. AU - Entman, Mark L.. AU - Roberts, Robert. AU - Michael, Lloyd H.. AU - Marian, Ali J.. PY - 2000. Y1 - 2000. N2 - The causality of mutant sarcomeric proteins in hypertrophic cardiomyopathy (HCM) is well established. The current emphasis is to elucidate the pathogenesis of HCM in transgenic animal models. We determined the left ventricular ejection fraction (LVEF) in transgenic mice expressing mutant cardiac troponin T (cTnT)-Q92, known to cause HCM in humans. Transgenes were constructed by placing wild-type (R92) or mutant (Q92) full-length human cTnT cDNAs 3 into a 5.5-kb murine [α-myosin heavy chain (MyHC)] promoter injected into fertilized zygotes. Three wild-type and six mutant lines were produced. ...
Association of high-sensitivity cardiac troponin I concentration with cardiac outcomes in patients with suspected acute coronary syndrome. Chapman, Andrew R., Lee, Kuan Ken, McAllister, David A., Cullen, Louise, Greenslade, Jaimi H., Parsonage, William, Worster, Andrew, Kavsak, Peter A., Blankenberg, Stefan, Neumann, Johannes, Söerensen, Nils A., Westermann, Dirk, Buijs, Madelon M., Verdel, Gerard J. E., Pickering, John W., Than, Martin P., Twerenbold, Raphael, Badertscher, Patrick, Sabti, Zaid, Mueller, Christian, Anand, Atul, Adamson, Philip, Strachan, Fiona E., Ferry, Amy, Sandeman, Dennis, Gray, Alasdair, Body, Richard, Keevil, Brian, Carlton, Edward, Greaves, Kim, Korley, Frederick K., Metkus, Thomas S., Sandoval, Yader, Apple, Fred S., Newby, David E., Shah, Anoop S. V. and Mills, Nicholas L. (2017) Association of high-sensitivity cardiac troponin I concentration with cardiac outcomes in patients with suspected acute coronary syndrome. JAMA - Journal of the American Medical Association, ...
The timing of troponin elevation after an ischemic event is another topic of research, as serial troponin measurements have been found to be an effective tool to detect developing myocardial injury. Initial research on troponins has shown cTnT and cTnI are most commonly elevated 4 to 9 hours after myocardial injury, with a peak at 12 to 24 hours. These enzymes may remain elevated in the blood for 7 to 14 days [3]. Thus, the time from onset of chest pain is crucially important for ED practitioners to discern, as troponin elevations may not be detected with commonly used assays if the insult occurred immediately prior (i.e., less than two hours) to presentation. To account for this discrepancy, practitioners will frequently observe patients who lack the electrocardiographic (ECG) changes indicative of ST-segment myocardial infarctions in addition to having a negative initial troponin. The observation period usually involves repeat physical examinations and telemetry monitoring along with repeat ...
PIOMBO, Alfredo C et al. Clinical Significance of High Troponin T with Normal Creatine Kinase Levels on Ventricular Function in Acute Coronary SyndromesClinical Significance of High Troponin T with Normal Creatine Kinase Levels on Ventricular Function in Acute Coronary Syndromes Background. Rev. argent. cardiol. [online]. 2012, vol.80, n.2, pp. 145-150. ISSN 1850-3748.. The role of elevated troponins to predict changes on ventricular function in patients with high creatine kinase (CK) levels has been well established; yet, little is known about the clinical significance of high troponin levels with normal CK levels. Objectives To analyze the relation between Troponin T (TnT) levels and global and regional left ventricular function in patients with acute coronary syndromes (ACS) with normal CK and CK-MB levels. Material and Methods We included patients admitted to the coronary care unit due to ACS within 48 hours from symptoms onset with elevated TnT levels measured by quantitative determination ...
TY - JOUR. T1 - Cardiac troponin I in pediatrics. T2 - Normal values and potential use in the assessment of cardiac injury. AU - Hirsch, R.. AU - Landt, Y.. AU - Porter, S.. AU - Canter, C. E.. AU - Jaffe, A. S.. AU - Ladenson, J. H.. AU - Grant, J. W.. AU - Landt, M.. PY - 1997/1/1. Y1 - 1997/1/1. N2 - Objective: To establish normal values and determine the impact of congenital or acquired heart disease on serum cardiac troponin I (cTnl). Methods: Concentrations of cTnl were measured in two groups of children. Group A represented ambulatory pediatric patients with no apparent cardiac disease (n = 120) and patients in stable condition with known congenital or acquired cardiac abnormalities (n = 96); group B was composed of patients admitted to intensive care units with normal echocardiograms (n = 16), with abnormal echocardiograms (n = 36), and those with blunt chest trauma who were thought to have cardiac contusions (n = 7). Results: The cTnl concentrations were generally less than 2.0 ng/ml in ...
The results of the study by Stewart and colleagues confirm previous findings showing that successful coronary reperfusion leads to an accelerated increase in the levels of plasma markers of myocardial injury in patients treated with thrombolytic therapy for MI (1-3). Changes in the level of myoglobin have been found in almost all previous studies to be useful in detecting coronary reperfusion but may lack specificity because this marker is not cardiac-specific. Rapid increases in CKMB, MB isoforms, and troponin may offer enhanced specificity but may be less sensitive because early changes in levels of these compounds are less marked than those of myoglobin. Differences also exist in the performance of the available assays for these markers. This is important for development of clinical criteria for failure of reperfusion. Nonetheless, available data suggest that using ratios of 60- and 90-minute levels to the initial levels of some of these markers is reasonably accurate for assessing the ...
When measured with the old assays, elevated troponin levels could be detected between 6 and 12 hours after the myocardial damage event, peaking at 24 hours followed by a gradual decline after two weeks.. In recent years there has been the introduction of a new type of troponin, troponin to high sensitivity, with different sensitivity and specificity, which made it possible to overcome the large limit of classical troponins of being detectable in the blood only several hours after the ischemic event and which improved the diagnostic accuracy, being able to diagnose subendocardial or transmural infarction with two samples veins performed just 3 hours apart from each other.. It was a remarkable one increase of the sensitivity for IMA (from 63.7% to 90.7%), compared to a slight reduction of the specificity (from 97.2% to 90.7%). However, the tissue specificity of troponin hs for damage to cardiomyocytes, which is always very high, must always be distinguished from clinical specificity for AMI, which ...
Hypertrophic cardiomyopathy (HCM) is defined as the presence of a hypertrophied, nondilated left ventricle in the absence of another causative disease (1). It is estimated to affect 1 in 500 persons, with highly variable clinical and pathologic presentations and penetrance (2,3). The severity of disease varies from a lifelong asymptomatic course to a sentinel event of sudden cardiac death (SCD) at a young age. A growing realization that the implanted cardioverter defibrillator (ICD) is effective in the primary and secondary prevention of SCD has provided an added impetus to discover new approaches for the identification and risk stratification of susceptible individuals in whom the prophylactic implantation of an ICD might be life saving (4).. In addition to this phenotypic variability, there is profound heterogeneity in the genetic substrate for HCM. To date, nine genes encoding various components of the cardiac sarcomere have been implicated in HCM: cardiac beta-myosin heavy chain (MYH7) ...
TY - GEN. T1 - A Multi-Stage decision support Algorithm to Rule-Out patientswith suspected Acute Myocardial Infarction (AMI). AU - Navarro-Paredes, Cesar. AU - Shand, James A. AU - McEneaney, David. AU - McLaughlin, James. PY - 2016/5/27. Y1 - 2016/5/27. N2 - Objective: Provide a multi-stage rule-out algorithm to stratify patients admitted to the Emergency Room (ER) with chest pain of presumed ischemic origin. The aim is to keep at-risk patients in the ER providing a proper care while minimizing overcrowding. The algorithm uses data from biomarkers -heart-type fatty acid-binding protein (H-FABP), high sensitivity cardiac troponin T (hs-cTnT) measured at different times (presentation, 1, 2, 3, 6, 12 and 24 hours) together with ECG at presentation.Methods: Data in a randomly selected training set of 296 patients were retrospectively analysed. 182 cases comprised a test set. STEMI were not considered since biomarkers are not routinely measured for these cases. H-FABP and hs-cTnT were statistically ...
The IFCC Committee on Clinical Applications of Cardiac Bio-Markers (C-CB) has directives and initiatives focused on providing evidence-based educational resources to aid and improve understanding around key analytical and clinical aspects of cardiac biomarkers used in clinical practice and the research setting. As a task force, we have previously published position statements and recommendations focused on use and analytical aspects of high-sensitivity cardiac troponin assays. The current educational document is the first from the C-CB highlighting important biochemical, analytical, and clinical aspects as they relate to the natriuretic peptides (NPs), including B-type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP), with a focus on heart failure. ...
Troponin plays a central role in regulation of muscle contraction. It is the Ca2+ switch of striated muscles including the heart and in the cardiac muscle is physiologically modulated by PKA-dependent phosphorylation at Ser22 and 23. Many cardiomyopathy-related mutations affect Ca2+ regulation and/or disrupt the relationship between Ca2+ binding and phosphorylation. Unlike the mechanism of heart activation, the modulation of Ca2+-sensitivity by phosphorylation of the cardiac specific N-terminal segment of TnI (1-30) is structurally subtle and has proven hard to investigate. The crystal structure of cardiac troponin describes only the relatively stable core of the molecule and the crucial mobile parts of the molecule are missing including TnI C terminal region, TnI (1-30), TnI (134-149) (inhibitory peptide) and the C-terminal 28 amino acids of TnT that are intrinsically disordered.Recent studies over the years have been performed to answer this matter by building structural models of cardiac troponin
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Elevated cardiac troponin levels were highly predictive of both in-hospital and long-term mortality in patients admitted for CAP.
Elevated troponin in kidney disease. Troponin can be elevated in acute and chronic kidney disease. Here are some reasons why troponin can be elevated.
Free Essay: Cardiac Troponins are specific to the cardiac myocyte and have central role in diagnosing ACS. They are found to be specific and sensitive, in...
Objective. To investigate oxidative stress and myocardial injury at different stages of coronary artery bypass grafting (CABG). Design. Twenty patients underwent CABG with use of cardiopulmonary bypass (CPB) and with intermittent sampling of plasma and urine. Main markers were: 8-iso-PGF(2 alpha) (oxidative stress); troponin T (myocardial injury); and 15-keto-dihydro-PGF2 alpha and hsCRP (inflammation). Results. Plasma 8-iso-PGF2 alpha increased after start of surgery, but there was no further rise during CPB or after aortic cross-clamp release and no significant myocardial arterio-venous differences. An increase in troponin T was seen early after the operation, but no relationship was established between 8-iso-PGF2 alpha and troponin T. 8-iso-PGF2 alpha levels were elevated by preoperative withdrawal of acetylsalicylic acid (ASA) but reduced by intraoperative use of heparin. 15-keto-dihydro-PGF2 alpha was elevated during operation and hsCRP following operation. Conclusions. In the present study ...
T helper 17 (Th17) cells have crucial functions in mucosal immunity and the pathogenesis of several chronic inflammatory diseases. The lineage-specific transcription factor, RORγt, encoded by the RORC gene modulates Th17 polarization and function, as well as thymocyte development. Here we define several regulatory elements at the human RORC locus in thymocytes and peripheral CD4+ T lymphocytes, with CRISPR/Cas9-guided deletion of these genomic segments supporting their role in RORγt expression. Mechanistically, T cell receptor stimulation induces cyclosporine A-sensitive histone modifications and P300/CBP acetylase recruitment at these elements in activated CD4+ T cells. Meanwhile, NFAT proteins bind to these regulatory elements and activate RORγt transcription in cooperation with NF-kB. Our data thus demonstrate that NFAT specifically regulate RORγt expression by binding to the RORC locus and promoting its permissive conformation. The master transcription factor RORγt, encoded by the RORC gene,
RATIONALE: Subcellular Ca2+ indicators have yet to be developed for the myofilament where disease mutation or small molecules may alter contractility through myofilament Ca2+ sensitivity. Here, we develop and characterize genetically encoded Ca2+ indicators restricted to the myofilament to directly visualize Ca2+ changes in the sarcomere. OBJECTIVE: To produce and validate myofilament-restricted Ca2+ imaging probes in an adenoviral transduction adult cardiomyocyte model using drugs that alter myofilament function (MYK-461, omecamtiv mecarbil, and levosimendan) or following cotransduction of 2 established hypertrophic cardiomyopathy disease-causing mutants (cTnT [Troponin T] R92Q and cTnI [Troponin I] R145G) that alter myofilament Ca2+ handling. METHODS AND RESULTS: When expressed in adult ventricular cardiomyocytes RGECO-TnT (Troponin T)/TnI (Troponin I) sensors localize correctly to the sarcomere without contractile impairment. Both sensors report cyclical changes in fluorescence in paced
Horjen, Anja Wiedswang; Ulimoen, Sara Reinvik; Norseth, Jon; Svendsen, Jesper Hastrup; Smith, Pål; Arnesen, Harald; Seljeflot, Ingebjørg & Tveit, Arnljot (2018). High-sensitivity troponine I in persistent atrial fibrillation - relation to NT-proBNP and markers of inflammation and haemostasis. Scandinavian Journal of Clinical and Laboratory Investigation. ISSN 0036-5513. 78(5), s 386- 392 . doi: 10.1080/00365513.2018.1481224 Show summary Purpose: As cardiac troponins emerge as prognostic markers in atrial fibrillation (AF), it is important to identify mechanisms initiating and perpetuating cardiac troponin release, including its relations to other circulating biomarkers, in AF populations. We studied associations between high-sensitivity troponin I (hs-TnI) and markers representing myocardial wall tension, inflammation and haemostasis in persistent AF. Methods: In a double blind, placebo-controlled study, 171 patients referred for electrical cardioversion for persistent AF were randomised to ...
What are other reasons other than heart attack for increased level of troponin - What are other reasons other than heart attack for increased level of troponin? Any heart problem. Troponin is an enzyme released by damaged heart muscle. While the major cause is a heart attack, and large increases are usually due to this, almost any condition affecting the heart can cause small increases. Viral infections of the heart, pulmonary embolus or medial procedures such as angioplasty often result in increases of troponin.
TY - JOUR. T1 - Cost-effectiveness of cardiac biomarkers as screening test in acute chest pain. AU - Shams-Vahdati, Samad. AU - Vand-Rajavpour, Zahra. AU - Paknezhad, Seyed-Pouya. AU - Piri, Reza. AU - Moghaddasi-Ghezeljeh, Elnaz. AU - Mirabolfathi, Saba. AU - Naghavi-Behzad, Mohammad. PY - 2014. Y1 - 2014. N2 - INTRODUCTION: Acute chest pain is an important and frequently occurring symptom in patients. Chest pain is often a sign of ischemic heart disease. Associated findings of electrocardiograph (ECG) are rather heterogeneous, and traditional cardiac biomarkers such as Creatine Kinase-MB (CK-MB) suffer from low cardiac specificity and sensitivity. In this study cost effectiveness of cardiac biomarkers single quantitative measurement was examined.METHODS: The present descriptive-analytic study conducted on patients who were asked for troponin I and CK-MB. All patients who referred to Emergency unit of Tabriz Imam Reza educational-medical center during January 2012 to July the 2013 were included ...
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Troponin proteins are released when the heart muscle has been damaged, such as occurs with a heart attack. The more damage there is to the heart, the greater the amount of troponin T and I there will be in the blood. The most common reason to perform this test is to see if a heart…
Background: Myocardial biomarker testing with some form of troponin assay has become standard of care for diagnosing acute myocardial infarction (AMI) among patients presenting with symptoms consistent with acute coronary syndrome. However, in order to not miss anyone, troponin assays may be ordered on patients presenting with non-cardiac diagnoses, but the frequency, justification and outcome of this practice are unknown.. Methods: During the year 2007, in a large multi-hospital integrated health system, all patients with a troponin-I (trpI) measurement obtained were studied. Baseline clinical characteristics, primary and secondary admit and discharge diagnoses, as well as maximum trpI were collected and analyzed. A trpI level ,0.4 was considered consistent with AMI. Independent predictors of a positive trpI were determined by logistic regression analysis.. Results: At least one trpI test was obtained in a total of 22,410 unique encounters in 18,730 unique patients (age=67±16 years, ...
Troponin levels Article by an interventional cardiologist describing the usefulness of measuring blood troponin levels in investigating heart disease
Troponin levels Article by an interventional cardiologist describing the usefulness of measuring blood troponin levels in investigating heart disease
Troponin elevation can occur from a number causes although there is no imaging involved, it is useful for the radiologist to have a basic understanding of their causes (especially when interpreting imaging findings associated with troponin elevat...
The ST2 cardiac biomarker is a protein biomarker of cardiac stress encoded by the IL1RL1 gene. ST2 signals the presence and severity of adverse cardiac remodeling and tissue fibrosis, which occurs in response to myocardial infarction, acute coronary syndrome, or worsening heart failure. ST2 provides prognostic information that is independent of other cardiac biomarkers such as BNP, NT-proBNP, highly sensitive troponin, GDF-15, and galectin-3. One study indicated that discrimination is independent of age, body mass index, history of heart failure, anemia and impaired renal failure or sex. ST2 is a member of the interleukin 1 receptor family. The ST2 protein has two isoforms and is directly implicated in the progression of cardiac disease: a soluble form (referred to as soluble ST2 or sST2) and a membrane-bound receptor form (referred to as the ST2 receptor or ST2L). When the myocardium is stretched, the ST2 gene is upregulated, increasing the concentration of circulating soluble ST2. The ligand ...
Elevated troponin levels can be the result of the heart beating too fast, high blood pressure in the lung arteries, congestive heart failure, inflammation in the heart and cardiomyapothy, states...
Background While electroconvulsive therapy is widely regarded as a lifesaving and safe procedure, evidence regarding its effects on myocardial cell injury is sparse. The objective of this investigation was to determine the incidence and magnitude of new cardiac troponin elevation after electroconvulsive therapy using a novel high-sensitivity cardiac troponin I assay. Methods This was a prospective cohort study in adult patients undergoing electroconvulsive therapy in a single academic center (up to three electroconvulsive therapy treatments per patient). The primary outcome was new high-sensitivity cardiac troponin I elevation after electroconvulsive therapy, defined as an increase of high-sensitivity cardiac troponin I greater than 100% after electroconvulsive therapy compared to baseline with at least one value above the limit of quantification (10 ng/l). Twelve-lead electrocardiogram and high-sensitivity cardiac troponin I values were obtained before and 15 to 30 min after electroconvulsive ...
BACKGROUND: Measurement of high-sensitivity cardiac troponin levels is increasingly used in non-ST-elevation acute coronary syndrome (NSTE-ACS). However, studies investigating the distribution and prognostic implications of high-sensitivity troponin levels in men and women separately are currently lacking.. METHODS: Cardiac troponin I (cTnI) levels were determined using a high-sensitivity assay (Abbott Laboratories, Abbott Park, IL) in 1,677 male and 1,073 female NSTE-ACS patients participating in the GUSTO IV study. The prognostic associations of cTnI to outcome (30-day composite end point of recurrent myocardial infarction and 1-year mortality) were assessed in multivariable models, using cTnI both as a continuous variable and dichotomized at different sets of single and gender-specific 99th percentiles.. RESULTS: Median cTnI levels were 947 and 175 ng/L in men and women, respectively (P , .001). The adjusted odds ratios for cTnI (ln) were similar in men and women. The adjusted odds ratios for ...
TY - JOUR. T1 - Can amyotrophic lateral sclerosis chronically elevate troponin T?. AU - Mach, Lukas. AU - Konecny, Tomas. AU - Jaffe, Allan S.. AU - Sorenson, Eric J.. AU - Reeder, Guy S.. N1 - Funding Information: Supported by European Regional Development Fund - Project FNUSA-ICRC (No. CZ.1.05/1.1.00/02.0123 ), European Social Fund and the State Budget of the Czech Republic . Publisher Copyright: © 2014 The Czech Society of Cardiology. Copyright: Copyright 2017 Elsevier B.V., All rights reserved.. PY - 2015/8/1. Y1 - 2015/8/1. N2 - A 57-year-old woman with progressive amyotrophic lateral sclerosis (ALS) presented repeatedly with atypical chest pain over a period of 4 years. Her initially normal cardiac troponin T (cTnT) value became progressively elevated during subsequent visits in the absence of clinically overt heart disease, and in the absence of alternative explanations for cTnT elevation. In this one patient there appeared to be a relationship between her rising levels of cTnT and ...
Troponin I is a cardiac and skeletal muscle protein useful in the laboratory diagnosis of heart attack. It occurs in different plasma concentration but the same circumstances as troponin T - either test can be performed for confirmation of cardiac muscle damage and laboratories usually offer one test or the other. Troponin I is a part of the troponin protein complex, where it binds to actin in thin myofilaments to hold the actin-tropomyosin complex in place. Because of it, myosin cannot bind actin in relaxed muscle. When calcium binds to the troponin C it causes conformational changes which lead to dislocation of troponin I and finally tropomyosin leaves the binding site for myosin on actin leading to contraction of muscle. The letter I is given due to its inhibitory character. The tissue specific subtypes are: Slow-twitch skeletal muscle isoform troponin I, TNNI1 (1q31.3, 191042) Fast-twitch skeletal muscle isoform troponin I, TNNI2 (11p15.5, 191043) Cardiac troponin I, TNNI3 (19q13.4, 191044) ...
TY - JOUR. T1 - Factors associated with and prognostic implications of cardiac troponin elevation in decompensated heart failure with preserved ejection fraction. T2 - Findings from the American Heart Association Get With the Guidelines-Heart Failure program. AU - Pandey, Ambarish. AU - Golwala, Harsh. AU - Sheng, Shubin. AU - DeVore, Adam D.. AU - Hernandez, Adrian F.. AU - Bhatt, Deepak L.. AU - Heidenreich, Paul A.. AU - Yancy, Clyde W.. AU - de Lemos, James A.. AU - Fonarow, Gregg C.. PY - 2017/2/1. Y1 - 2017/2/1. N2 - IMPORTANCE: Elevated levels of cardiac troponins are associated with adverse clinical outcomes among patients with heart failure (HF) and reduced ejection fraction. However, the clinical significance of troponin elevation in the setting of decompensated HF with preserved ejection fraction (HFpEF) is not well established. OBJECTIVE: To determine the clinical predictors of troponin elevation and its association with in-hospital and long-term outcomes among patients with ...
Purpose: To investigate whether there is a differential response at rest and following exercise to conditions of genuine high altitude (GHA), normobaric hypoxia (NH), hypobaric hypoxia (HH), and normobaric normoxia (NN). Method: Markers of sympathoadrenal and adrenocortical function [plasma normetanephrine (PNORMET), metanephrine (PMET), cortisol], myocardial injury [highly sensitive cardiac troponin T (hscTnT)], and function [N-terminal brain natriuretic peptide (NT-proBNP)] were evaluated at rest and with exercise under NN, at 3375 m in the Alps (GHA) and at equivalent simulated altitude under NH and HH. Participants cycled for 2 h [15-min warm-up, 105 min at 55% Wmax (maximal workload)] with venous blood samples taken prior (T0), immediately following (T120) and 2-h post-exercise (T240). Results: Exercise in the three hypoxic environments produced a similar pattern of response with the only difference between environments being in relation to PNORMET. Exercise in NN only induced a rise in ...
TY - JOUR. T1 - Relationship of cardiac troponin to systolic global longitudinal strain in hypertrophic cardiomyopathy. AU - Agarwal, Anushree. AU - Yousefzai, Rayan. AU - Shetabi, Kambiz. AU - Samad, Fatima. AU - Aggarwal, Saurabh. AU - Cho, Chi. AU - Bush, Michelle. AU - Jan, M. Fuad. AU - Khandheria, Bijoy K.. AU - Paterick, Timothy E.. AU - Tajik, A. Jamil. PY - 2017/10/1. Y1 - 2017/10/1. N2 - Background: A high proportion of stable hypertrophic cardiomyopathy (HCM) patients have elevated serum cardiac troponin I (cTnI), but its clinical and echocardiographic determinants are unknown. Our objective was to determine the prevalence and clinical predictors of positive troponin (cTnI+) in a well-defined population of HCM patients using a highly sensitive assay. Methods: We retrospectively interrogated medical records of 167 stable HCM patients from 1/2011 to 3/2014. cTnI ,0.04 ng/mL was considered positive. Results: Thirty-four percent were troponin-positive (median cTnI was 0.1 [0.07, 0.2] ...
TY - JOUR. T1 - Phosphorylation of cardiac troponin by guanosine 3. T2 - 5-monophosphate-dependent protein kinase. AU - Blumenthal, D. K.. AU - Stull, J. T.. AU - Gill, G. N.. PY - 1978. Y1 - 1978. N2 - Homogeneous cGMP-dependent protein kinase catalyzes the rapid incorporation of phosphate, specifically into the inhibitory subunit of purified cardiac troponin with a maximal incorporation of 1 mol of phosphate/mol of troponin. When troponin was incubated in the presence of both cGMP- and cAMP-dependent protein kinases, a maximal incorporation of 1 mol of phosphate/mol of troponin was observed which suggested phosphorylation of the same site by the two kinases. Both cyclic nucleotide-dependent kinases had similar K(m) values for troponin, but the V(max) value for the phosphorylation reaction catalyzed by cAMP-dependent protein kinase was 12-fold greater than the value obtained for cGMP-dependent protein kinase.. AB - Homogeneous cGMP-dependent protein kinase catalyzes the rapid incorporation of ...
Results The direct numeric result from hs-cTnT measurement cannot merely be substituted for a cTnT measurement in the Mayo AL staging system. The performance of the receiver operator curve derived an hs-cTnT cut-point of 54 ng/L which improves on the value of 35 ng/L validated with the prior iteration of the assay. An alternate staging option using hs-cTnT alone-using the two thresholds 14 ng/L and 54 ng/L-performs as well as either the original Mayo AL staging system or other systems incorporating hs-cTnT. On multivariate analysis, an hs-cTnT alone staging system was independent of period of diagnosis, type of therapy, and NT-proBNP value, the last of which dropped out of the model. Alternate models were explored, but none performed better than the original system or the new hs-cTnT system. Thus, hs-cTnT can be used alone for the staging of disease prognosis.. ...
Background: One of the complications of diabetes, as a chronic metabolic disorder, is cardiovascular diseases.  Objective This study aims to investigate the effect of an eight-week High-Intensity Interval Training (HIIT) program on serum Cardiac troponin I (CtnI) level in streptozotocin-induced diabetic rats.  Methods: In this experimental clinical trial, 30 rats were randomly assigned into ...
Patients presenting to the emergency department (ED) with chest pain must be evaluated quickly. Rapid serum troponin measurement is an important part of ED practice that can provide decisive information for patient management. Reducing delays in troponin testing has been reported to result in shorter length of stay in the ED and more rapid initiation of anti-ischemic treatment. Emergency departments and chest pain centers should, therefore, have effective procedures for ensuring optimal turnaround time (TAT) for troponin testing and a process for ongoing monitoring to ensure that performance meets expectations. QT15 is enhanced for 2019 with additional time intervals to help pinpoint process time challenges. Laboratories use this monitor to help meet CAP Laboratory Accreditation Program Checklist statement GEN.20316 QM Indicators of Quality. The American College of Cardiology and the American Heart Association recommend troponin as the preferred diagnostic biomarker in their Acute Coronary ...
SEA478Hu, ELISA Kit for Cardiac Troponin I (cTnI), TNNI3; TNNC1; CMH7; C-TnI; Troponin I Type 3; Troponin I Type 3, Cardiac | Products for research use only!
The contractile response of the heart can be altered by disease-related protein modifications to numerous contractile proteins. By utilizing an IAANS labeled fluorescent troponin C, [Formula: see text], we examined the effects of ten disease-related troponin modifications on the Ca(2+) binding properties of the troponin complex and the reconstituted thin filament. The selected modifications are associated with a broad range of cardiac diseases: three subtypes of familial cardiomyopathies (dilated, hypertrophic and restrictive) and ischemia-reperfusion injury. Consistent with previous studies, the majority of the protein modifications had no effect on the Ca(2+) binding properties of the isolated troponin complex. However, when incorporated into the thin filament, dilated cardiomyopathy mutations desensitized (up to 3.3-fold), while hypertrophic and restrictive cardiomyopathy mutations, and ischemia-induced truncation of troponin I, sensitized the thin filament to Ca(2+) (up to 6.3-fold). Kinetically,
McGraw-Hill, New York, 1995, pp. 3799- 876. Part Three Renal Disease Acute and chronic renal failure are reported in Cases 5 and 9, respectively (both edited by (MGS); Cases 6, 7, 8, and 11 (all edited by MGS) present cases of renal transplant cyclosporin toxicity, glomerular nephritis, nephrotic syndrome, and syndrome of inappropriate secretion of antidiuretic hormone (SIADH), respectively; and a case of renal osteodystrophy is presented in Case 10 (edited by AMG). Tietzs Applied L aboratory Medicine, Second Edition. The cardiac troponins are the serum markers of choice to differentiate myocardial infarction from skeletal muscle damage. Cardiac troponin I or T are contractile proteins of the myofibril, and thus the presence of these proteins in serum is consistent and specific for damage to myocardial tissue. Cardiac troponins are elevated within 4- 6 hours of injury, peak at 12 - 36 hours, and remain elevated for 4- 10 days. A characteristic rise or fall of cTnI or cTnT in the correct ...
Calcium binding proteins are biologically important for their ability to convert changes in calcium ion concentration to functional changes in proteins. All calcium binding proteins use a calcium sensing motif that changes the protein conformation and dynamics when associated with calcium ions. Dysfunction in calcium binding proteins has been linked to many diseases such as cancer and heart disease. In this study, models of mutated proteins were generated and Molecular Dynamics simulations were used to study Annexin and Cardiac Troponin C (cTnC). Annexin A1 is an important protein that is known to induce membrane aggregation, while cardiac Troponin C (cTnC) regulates cardiac muscle contraction. This study focuses on the impact of mutations on Annexin A1 and cTnC with the objective to gain insight of how these changes are made by mutations. The ultimate goal of this research is to use the knowledge of the effects of point mutations on calcium binding proteins dynamics to treat disease. Multiple ...
We performed a meta-analysis of published trials to determine the predictive value of cardiac troponin I (cTnI) and T (cTnT) levels for adverse events (death and myocardial infarction) in acute coronary syndrome without ST elevation (ACS). The accumulated odds ratio (OR) for adverse events (30 days) in ACS with elevated cTnI (n = 5,759) and cTnT (n = 5,483) was 4.9 (95% confidence interval, CI, 3.9-6.2) and 4.6 (95% CI 3.8-5.5), respectively. Trials that mandated timed serum sampling (6 or more hours after symptom onset) had an improved predictive value for elevated cTnI (n = 2,807, OR 8.8; 95% CI 5.9-13.2) and cTnT (n = 1,990, OR 8.5; 95% CI 5.9-12.5). In conclusion, cTnI and cTnT provide similar information in ACS. The risk of adverse events is 4-fold higher in patients with suspected ACS and elevated serum cTn. For patients with an elevated timed (6-hour) sample the risk is over 8-fold higher.
TY - JOUR. T1 - Hs-troponin i followed by CT angiography improves acute coronary syndrome risk stratification accuracy and work-up in acute chest pain patients results from ROMICAT II trial. AU - Ferencik, Maros. AU - Liu, Ting. AU - Mayrhofer, Thomas. AU - Puchner, Stefan B.. AU - Lu, Michael T.. AU - Maurovich-Horvat, Pal. AU - Pope, J. Hector. AU - Truong, Quynh A.. AU - Udelson, James E.. AU - Peacock, W. Frank. AU - White, Charles S.. AU - Woodard, Pamela K.. AU - Fleg, Jerome L.. AU - Nagurney, John T.. AU - Januzzi, James L.. AU - Hoffmann, Udo. N1 - Publisher Copyright: © 2015 American College of Cardiology Foundation. Copyright: Copyright 2015 Elsevier B.V., All rights reserved.. PY - 2015/11. Y1 - 2015/11. N2 - Objectives This study compared diagnostic accuracy of conventional troponin/traditional coronary artery disease (CAD) assessment and highly sensitive troponin (hsTn) I/advanced CAD assessment for acute coronary syndrome (ACS) during the index hospitalization. Background hsTnI ...
Peer Review History: Predictive Role of Cardiac Troponin I, Creatine Kinase-Mb and Electrocardiogram in Early Assessment of Acute Cardiotoxicity in Patients Poisoned by Cardiotoxic Drugs and ...
Objectives: To assess the clinical characteristics and diagnosis of ACS for timely, management and further prevention from coronary events. Study Design: Cross sectional study. Setting: Emergency Department (ED) of Punjab Institute of Cardiology (PIC) Lahore. Period: November 2017 to January 2018. Material & Methods: Included 170 diagnosed patients of ACS of both sexes presenting within approximately four hours of symptoms. At presentation ECG and initial blood samples were taken from all patients for base line and Troponin T estimation. All the patients included in the study were properly examined and complete history was taken. Blood samples of patients for diagnosis of NSTEMI were also drawn at 8hrs of arrival. The patients were categorized into STEMI, NSTEMI and UA on the basis of history, ECG and cardiac Troponin T. Results were analyzed statistically. A p-value ≤ 0.05 was considered statistically significant. Results: A total of 170 patients with established diagnosis of ACS were ...
Prevalence and prognostic significance of preprocedural cardiac troponin elevation among pPatients with stable coronary artery disease undergoing percutaneous coronary intervention: Results from the evaluation of drug eluting stents and ischemic events registry Academic Article ...
Background: High-dose chemotherapy (HDC) has been widely utilized in high-risk breast cancer, but it may induce cardiac toxicity. Cardiac dysfunction may become evident weeks or months after HDC and, to date, no early markers of myocardial injury that are able to predict late ventricular impairment are available. We investigated the role of plasma troponin I (TnI) in this setting. Patients and methods: We measured TnI plasma concentration after HDC in 211 high-risk breast cancer women (46 ± 11 years, mean ± SD). According to TnI value (,0.5 or ≥0.5 ng/ml), patients were allocated into a troponin positive (TnI+; n = 70) and a troponin negative (TnI-; n = 141) group. All patients underwent left ventricular ejection fraction (LVEF, Echo) examination during the following 12 months. Results: LVEF progressively decreased in the TnI+ group but not in the TnI- group. In TnI+ patients a close relationship between the TnI increase, as well as the number of positive TnI assays, and the maximal LVEF ...
Ischemic heart disease is common in COPD and associated with worse prognosis. This study aimed to investigate the presence and prognostic impact of biomarkers of myocardial injury and ischemia among individuals with COPD and normal lung function, respectively. In 2002-04, all individuals with airway obstruction (FEV1/VC | 0.70, n = 993) were identified from population-based cohorts, together with age and sex-matched non-obstructive referents. At re-examination in 2005, spirometry, Minnesota-coded ECG and analyses of high-sensitivity cardiac troponin I (hs-cTnI) were performed in individuals with COPD (n = 601) and those with normal lung function (n = 755). Deaths were recorded until December 31st, 2010. Hs-cTnI concentrations were above the risk stratification threshold of ≥5 ng/L in 31.1 and 24.9% of those with COPD and normal lung function, respectively. Ischemic ECG abnormalities were present in 14.8 and 13.4%, while 7.7 and 6.6% had both elevated hs-cTnI concentrations and ischemic ECG
TY - JOUR. T1 - Diagnosing acute myocardial infarction with troponins: how low can you go?. AU - Body, R. AU - McDowell, Garry. AU - Carley, S. AU - Ferguson, J. AU - Mackway-Jones, K. PY - 2010. Y1 - 2010. N2 - Background Recent consensus guidelines state that acute myocardial infarction (AMI) may be diagnosed in the context of a troponin rise above the 99th percentile of the upper reference limit (URL) with the optimal imprecision of the assay (coefficient of variation, CV) being ≤10%. However, at the 99th percentile, modern assays do not have a CV ≤10%. Objective The authors compared the prognostic implications of placing the diagnostic troponin cut-off at the 99th percentile and at the lowest concentration with a CV ≤10% (functional sensitivity). Methods The authors prospectively recruited 804 patients presenting to the Emergency Department of a university-affiliated teaching hospital with suspected ACS. All patients underwent 12 h troponin T testing and were followed up by telephone ...
wp-content/uploads/2018/08/johns_hopkins_medicine_logo-300-x-156-300x156.jpg 0 0 admin /wp-content/uploads/2018/08/johns_hopkins_medicine_logo-300-x-156-300x156.jpg admin2015-08-06 15:04:382018-08-11 11:46:07A novel phosphorylation site, Serine 199, in the C-terminus of cardiac troponin I regulates calcium sensitivity and susceptibility to calpain-induced proteolysis ...
OBJECTIVE: We sought to establish references ranges and to test the hypothesis that biochemical tissue-specific markers for the heart in umbilical cord blood of newborns with cardiac defects and intrauterine growth restriction (IUGR) are abnormal. STUDY DESIGN: A prospective study was conducted. Serum samples of the umbilical vein (n = 280) and artery (n = 156) from 599 healthy newborns at 37(+0)-42(+0) weeks of gestation were collected. Total creatine kinase (CK), CK-MB heart type (CK-MB), cardiac troponin T (cTnT), myoglobin, N-terminal pro-B-type natriuretic peptide (NT-proBNP), and S100 were measured. Reference ranges for each marker were constructed. Concentrations of tissue-specific markers from umbilical cord blood of neonates with cardiac defects (n = 10) and IUGR (n = 41) were plotted against the established reference ranges. RESULTS: Reference ranges for each studied marker were established for both umbilical artery and vein. In fetuses with cardiac defects, both NT-proBNP (4/6 [66%] ...
TY - JOUR. T1 - Longitudinal studies of cardiac troponin I in a large cohort of healthy children. AU - Koerbin, Gus. AU - Potter, Julia. AU - Abhayaratna, W. AU - Telford, Richard. AU - Badrick, T. AU - Apple, F. AU - Jaffe, A. AU - Hickman, Peter. PY - 2012. Y1 - 2012. U2 - 10.1373/clinchem.2012.192054. DO - 10.1373/clinchem.2012.192054. M3 - Article. VL - 58. SP - 1665. EP - 1672. JO - Clinical Chemistry. JF - Clinical Chemistry. SN - 0009-9147. IS - 12. ER - ...
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The diagnosis of acute myocardial infarction is based on the rise of bio-markers for cardiac necrosis such as troponin. While troponin measurement is highly sensitive for myocardial necrosis it has several limitations that influence its clinical use. First, since the troponin test is reliable only after 4-6 hours from symptoms onset, it has only limited value in the assessment of patients presenting earlier. Second, several clinical situations, most commonly renal dysfunction, are associated with increased troponin level and therefore may decrease the specificity of the test. Third, since troponin rise indicates myocardial infarction it is not useful in the common situations where there is myocardial ischemia without necrosis.. The P53 is a tumor suppressing gene activated in different stressful situations including hypoxia. This activation is associated with accelerated transcription (up to 30-50 folds from baseline) of different genes that are involved in apoptosis, DNA repair and in stopping ...
Cardiomyopathies (CM) are the leading cause of death in America, and can develop from mutations in sarcomeric proteins, leading to altered protein structure and function. Current therapies target upstream signaling pathways to treat the symptoms of heart failure, but are associated with increased mortality by affecting downstream signaling pathways and other muscle types. Rational drug design can develop therapies to treat CM at the protein level. However, a detailed knowledge of how sarcomeric proteins regulate muscle contraction is required. Muscle contraction occurs through a cyclic interaction between actin thin and myosin thick filaments, regulated by intracellular Ca2+ concentration. Troponin (Tn), the Ca2+-binding protein in muscle, allosterically regulates actin and myosin interactions (crossbridge formation) by facilitating the release of two troponin I (TnI) actin binding sites at high Ca2+, the inhibitory region (IR) and the second actin binding site (SABS). The mechanism to remove TnI
Drug maker, Roche, is recalling two of its Elecsys Troponin Immunoassays, the U.S. Food & Drug Administration (FDA) just announced. The recall has been deemed a Class I by the agency, its most severe and involving a situation in which there exists a reasonable probability that the use of, or exposure to, the recalled, violative product-in this case, the Roche Elecsys Troponin Assays-will cause serious adverse health consequences or death.. The Elecsys Troponin I and Elecsys Troponin I STAT Immunoassays are used to determine heart damage as an aid when diagnosing a heart attack.. With certain types of plasma samples, doctors may receive a falsely low result that can be up to a maximum of 50% lower than the actual concentration of Troponin I. These incorrect results may cause serious adverse health consequences, which include death.. Specifically, Roche is recalling its Elecsys Troponin I and Elecsys Troponin I STAT Immunoassays with the following lot numbers: 163176, 163177. The recalled Assays ...
Muscle contraction is initiated by the binding of Ca2+ to the thin filament. This signal somehow results in a changed interaction between the myosin head and actin. Since Ca2+ binds to troponin C, a protein which is not in direct contact with either myosin or actin, the signal must be propagated via the other regulatory proteins, troponin I, troponin T and tropomyosin. The nature of these interactions is not well understood. In solution Ca-binding proteins containing E-F hands analogous to troponin C undergo large structural changes. The conformational freedom of troponin C in complex with the proteins of the thin filament is greatly restricted and changes are more subtle. They involve changes in the mobility of constituent proteins and their relative geometries. The questions asked and the general strategy to answer them is similar to those described above for energy transduction-identify and describe the motions within the proteins, and correlate them with thin filament activation. The ...
The extent of cTnAAb interference in different cTnI assay configurations and the molecular characteristics of cTnAAbs were investigated in publications I and II, respectively. The findings showed that cTnI midfragment targeting immunoassays used predominantly in clinical practice are affected by cTnAAb interference which can be circumvented by using a novel 3+1-type assay design with three capture antibodies against the N-terminus, midfragment and C-terminus and one tracer antibody against the C-terminus. The use of this assay configuration was further supported by the epitope specificity study, which showed that although the midfragment is most commonly targeted by cTnAAbs, the interference basically encompasses the whole molecule, and there may be remarkable individual variation at the affected sites. In publications III and IV, all the data obtained in previous studies were utilized to develop an improved version of an existing cTnAAb assay and a sensitive cTnI assay free of this specific ...
Troponin I Rapid Test Card is an immunochromatography based one step in vitro test. It is designed for qualitative determination of cardiac Troponin I (cTnI) in human serum or plasma specimens as an aid in the diagnosis of myocardial infarction. ...
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This work focuses on the study and evaluation of the retrievals of aerosol complex refractive index (m = mr + imi) and single scattering albedo (SSA) from the inversion of multi-wavelength lidar measurements, particularly of three backscattering coefficients (β) at 355, 532 and 1064 nm and two extinction coefficients (α) at 355 and 532 nm, typically known as the stand-alone 3β + 2α lidar inversion. The focus is on the well-known regularization technique for spherical particles. It is well known that constraints in the range of refractive indices allowed in the inversion are essential, both for the real (mr) and imaginary (mi) parts, due to the under-determined nature of the problem. Usually these constraints are fixed for a given set of inversions. Using a large database of AERONET retrievals, correlations between retrieved mr and mi are observed and those correlations together with results from the GOCART model are used to define optimized, case-dependent, constraints in the stand-alone 3β ...
A normal troponin level in the blood is so low that it is not detectable, according to MedlinePlus. The normal troponin value varies depending on the laboratory, measurements and samples used. Its...
By Asli Tanindi and Mustafa Cemri Hello All, My preceptor recently asked me a questions that I believe all my followers should quickly review - what are the causes of troponin elevation in conditions other than acute coronary syndromes? Quick List: -Chronic renal failure -Advanced heart failure -Subarachnoid hemorrhage (SAH) -Ischemic cerebrovascular accident -Acute pulmonary…
Title : Cardiovascular Clinical Trialists (CVCT) Forum - Paris 2012 : Journal editors viewpointsSpeaker: John JARCHO, Boston, USA, NEJMDiscussant: Rita REDBERG, San Francisco, USA, Arch Intern MedAbstract : Biomarker studies have proliferated widely, but the actual impact of most such studies on the practice of medicine is modest. One major underlying problem is a lack of clarity (on the part of both investigators and readers) about what biomarker data can be expected to contribute. In many cases, studies merely demonstrate a statistical association between a putative biomarker and a clinical correlate, but the implications of this association are not made explicit. In some cases, there is an expectation that a new biomarker, if found to correlate with disease, will reveal previously unsuspected or unproven aspects of disease pathogenesis; but scientific discovery is achieved by an association study alone. Novel biomarkers may occasionally improve diagnosis, as with high-sensitivity troponin assays, or
TY - JOUR. T1 - Biological Variation of Creatinine, Cystatin C, and eGFR over 24 Hours. AU - Hilderink, Judith M.. AU - van der Linden, Noreen. AU - Kimenai, Dorien M.. AU - Litjens, Elisabeth J. R.. AU - Klinkenberg, Lieke J. J.. AU - Aref, Breshna M.. AU - Aziz, Fahra. AU - Kooman, Jeroen P.. AU - Rennenberg, Roger J. M. W.. AU - Bekers, Otto. AU - Koopmans, Richard P.. AU - Meex, Steven J. R.. PY - 2018/5. Y1 - 2018/5. KW - GLOMERULAR-FILTRATION-RATE. KW - CHRONIC KIDNEY-DISEASE. KW - CARDIAC TROPONIN-T. KW - COOKED-MEAT MEAL. KW - SERUM CREATININE. KW - CLINICAL-CHEMISTRY. KW - CRITICAL-APPRAISAL. KW - INDIVIDUALS. KW - VARIABILITY. KW - ANALYTES. U2 - 10.1373/clinchem.2017.282517. DO - 10.1373/clinchem.2017.282517. M3 - Article. VL - 64. SP - 851. EP - 860. JO - Clinical Chemistry. JF - Clinical Chemistry. SN - 0009-9147. IS - 5. ER - ...
Myocardial ischemia with subsequent reperfusion (MI/R) can lead to significant myocardial damage. Ischemia initiates inflammation at the blood-microvascular endothelial cell interface and contributes significantly to both acute injury and repair of the damaged tissue. We have found that MI/R injury in mice is associated with a cellular immune response to troponin. Myocardial cells exclusively synthesize troponin and release the troponin into the bloodstream following injury. Mucosally administered proteins induce T cells that secrete anti-inflammatory cytokines such as IL-10 and transforming growth factor β at the anatomical site where the protein localizes. We found that nasal administration of the three subunits of troponin (C, I and T isoforms), given prior to or 1 h following MI/R, decreased infarct size by 40% measured 24 h later. At 1.5 months following MI/R, there was a 50% reduction in infarct size and improvement in cardiac function as measured by echocardiography. Protection was ...