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Troponin

Troponin is a complex of three regulatory proteins (troponin C, troponin I, and troponin T) that is integral to the control of muscle contraction in striated muscle.
Thoponin plays a crucial role in the calcium-mediated regulation of the actin-myosin interaction, which facilitates skeletal and cardiac muscle movement.
Measurement of troponin levels is a key diagnostic tool for the detection of myocardial infarction and other cardiac injuries.
PubCompare.ai's AI-powered platform can help researchers enhance the reproducibility and accuracy of their troponin analysis by providing access to relevant scientific protocols and enabling intelligent comparisons to identify optimal methods and products.

Most cited protocols related to «Troponin»

1
Genetic Study of Early-Onset Myocardial Infarction
Cited 46 times
We conducted a genetic association study with three stages as displayed in Figure 1. Stage 1 consisted of the Myocardial Infarction Genetics Consortium (MIGen), a collection of 2,967 cases of early-onset MI (in men ≤50 years old or women ≤60 years old) and 3,075 age- and sex-matched controls free of MI from six international sites: Boston and Seattle in the United States as well as Sweden, Finland, Spain, and Italy (Table 1). At each site, MI was diagnosed on the basis of autopsy evidence of fatal MI or a combination of chest pain, electrocardiographic evidence of MI, or elevation of one or more cardiac biomarkers (creatine kinase or cardiac troponin). The mean age at the time of MI was 41 years among male cases and 47 years among female cases.
We took forward SNPs into two stages of replication (Stages 2 and 3, Figure 1). 1441 SNPs were tested in Stage 2 based on two criteria: i) strength of statistical evidence in Stage 1 (1433 SNPs from loci with P < 10-3 in Stage 1) or ii) belonging to one of eight reported loci from recent genome-wide association studies for coronary artery disease (a common SNP from each of 9p21.3, near CXCL12, SMAD3, MTHFD1L, MIA3, near CELSR2/PSRC1/SORT1, 2q36, and PCSK9)3 (link),7 (link).
Stage 2 consisted of in silico comparisons with four recently completed GWAS for MI consisting of a symmetric effective sample size of up to 3,942 cases of MI and 3,942 controls. These studies included the Wellcome Trust Case Control Consortium Coronary Heart Disease study3 (link), German MI Family Study I3 (link), PennCATH, and MedStar (Supplementary Table 1). In each Stage 2 study, the analysis was restricted to the phenotype of MI with an age of onset threshold of <66 years for men or women. Although this age cutoff is slightly less restrictive than that used in Stage 1, this cutoff is at or below the mean age of first MI in the US (65 years for men and 70 years for women).
Thirty-three SNPs were taken forward to Stage 3, which consisted of genotyping an additional 6 studies with a symmetric effective sample size of up to 5,469 cases of MI and 5,469 controls. These six studies included Acute MI Gene Study/Dortmund Health Study, Verona Heart Study29 (link), Mid-America Heart Institute Study30 (link), Irish Family Study31 (link), German MI Family Study II, and INTERHEART32 (link) (European ancestry and South Asian ancestry each analyzed separately) (Supplementary Table 2). Stage 3 was comprised of 25 SNPs with the best combined statistical evidence for MI from Stages 1 and 2 (P < 10-5) and the eight previously-reported SNPs discussed above. In each Stage 3 study, the analysis was restricted to the phenotype of MI and in four of the six studies, an age of onset threshold was established at <66 years for men or women.
Genome-wide association of early-onset myocardial infarction with common single nucleotide polymorphisms, common copy number variants, and rare copy number variants. (2009). Nature genetics, 41(3), 334-341.
Publication 2009
Asian Persons Autopsy Biological Markers CELSR2 protein, human Chemokine CXCL12 Chest Pain Coronary Artery Disease Creatine Kinase DNA Replication Electrocardiography Europeans Genes Genetic Association Studies Genome-Wide Association Study Heart Heart Disease, Coronary Males migen Myocardial Infarction PCSK9 protein, human Phenotype Single Nucleotide Polymorphism SMAD3 protein, human SORT1 protein, human Troponin Woman
2
Ruling Out Myocardial Infarction with CTA
Cited 31 times

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Publication 2009
Angina Pectoris Chest Pain Coronary Arteriosclerosis Ethics Committees, Research Heart Inpatient Myocardial Infarction Outpatients Ovum Implantation Patients Physicians Stents Troponin X-Ray Computed Tomography
3
Evaluating Troponin Thresholds for Myocardial Infarction
Cited 27 times

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Publication 2015
Biological Assay Cardiac Death Cardiovascular Diseases Electrocardiography Heart Hypersensitivity Myocardial Infarction Myocardial Ischemia Patients ST Segment Elevation Myocardial Infarction Troponin Troponin I Troponin T
4
Recruiting Consecutive MI Patients
Cited 22 times
The goal of TRIUMPH was to recruit a consecutive cohort of MI patients from each enrolling center. Because an important component of the study was to perform a detailed patient interview, patients needed to be prospectively identified as early as possible during their hospitalization. All patients with a positive troponin, as established by the norms of the recruiting center, were screened for possible inclusion. For sites with large volumes of MI patients, a systematic sampling strategy (e.g. screening every second or every third MI case based on the time of the first positive cardiac enzyme blood test and not convenience) was performed. Because the timing of consecutive positive laboratory tests is not influenced by patient characteristics or disease severity, no selection biases should have been introduced.
Once a patient was identified, a brief screening form was completed to establish eligibility. Only patients with a Type 1 acute MI34 (link) (i.e. spontaneous MI related to ischemia due to a primary coronary event) were eligible for enrollment. Patients had to fulfill the following criteria for eligibility: (1) ≥18 years, (2) elevated troponin level (cardiac enzyme elevation as a complication of elective coronary revascularization did not qualify), (3) clinical features of ischemia (e.g. prolonged ischemic signs/symptoms, electrocardiographic ST changes in ≥2 consecutive leads), and (4) initial presentation to the enrolling institution or transfer within the first 24 hours of original presentation. This latter criterion ensured that the primary clinical decision making was conducted at the enrolling site. Incarcerated patients were not eligible, and all patients signed an informed consent that was approved by each institution.
Arnold S.V., Chan P.S., Jones P.G., Decker C., Buchanan D.M., Krumholz H.M., Ho P.M, & Spertus J.A. (2011). Translational Research Investigating Underlying disparities in acute Myocardial infarction Patients’ Health status (TRIUMPH): Design and Rationale of a Prospective Multicenter Registry. Circulation. Cardiovascular Quality and Outcomes, 4(4), 467-476.
Publication 2011
BLOOD Cardiac Events Electrocardiography Eligibility Determination Enzymes Heart Hospitalization Ischemia Myocardial Revascularization Patients Signs and Symptoms Test, Clinical Enzyme Troponin
5
Acute Coronary Syndrome Diagnosis Protocol
Cited 21 times
We prospectively identified consecutive patients presenting to the Royal Infirmary of Edinburgh, United Kingdom, from 1 August to 31 October 2012, in whom the attending doctor suspected an acute coronary syndrome. Patients not resident in the south east of Scotland were excluded from the study. We obtained information about the patients and their clinical outcomes through the TrakCare software application (InterSystems, Cambridge, MA) as previously described.9 (link)
10 (link)
Serum troponin concentrations were measured on admission and repeated six or 12 hours after the onset of symptoms13 (link)
14 (link) using both a contemporary sensitive troponin I assay and a high sensitivity troponin I assay. Clinical decisions were based on the results of the contemporary assay only, with clinicians blinded to the results of the high sensitivity assay.
Shah A.S., Griffiths M., Lee K.K., McAllister D.A., Hunter A.L., Ferry A.V., Cruikshank A., Reid A., Stoddart M., Strachan F., Walker S., Collinson P.O., Apple F.S., Gray A.J., Fox K.A., Newby D.E, & Mills N.L. (2015). High sensitivity cardiac troponin and the under-diagnosis of myocardial infarction in women: prospective cohort study. The BMJ, 350, g7873.
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Publication 2015
Acute Coronary Syndrome Biological Assay Hypersensitivity Patients Physicians Serum Troponin Troponin I

Most recents protocols related to «Troponin»

1
Timing of DOAC Initiation and Outcomes
Patients were categorized based on long-term anticoagulant (DOAC, warfarin, or enoxaparin). To examine the timing of DOAC initiation with outcomes, patients receiving a DOAC were categorized as having initiation <48, 48-72, and >72 h from thrombolysis. The primary outcome was hospital LOS (days). Secondary outcomes included ICU LOS, hospital LOS after oral anticoagulation initiation, in-hospital bleeding events, 30-day readmission, 90-day major and minor bleeding,12 (link) VTE/stroke, and mortality. Clinical and demographic measures included age, sex, semi-quantitative RV size on echocardiogram, simplified pulmonary embolism severity index, and continuous measures of serum creatinine, troponin, brain natriuretic protein (BNP), weight, heart rate, systolic blood pressure, and respiratory rate.
Wolfe A., Phillips A., Tierney D.M., Melamed R., Qadri G., Lillyblad M., Smith C., St. Hill C., Stenzel A.E., Beddow D., Kirven J., Kethireddy R, & Patel L. (2023). Retrospective Analysis of Direct-Acting Oral Anticoagulants (DOACs) Initiation Timing and Outcomes After Thrombolysis in High- and Intermediate-Risk Pulmonary Embolism. Clinical and Applied Thrombosis/Hemostasis, 29, 10760296231156414.
Publication 2023
Anticoagulants Brain Cerebrovascular Accident Creatinine Echocardiography Enoxaparin Fibrinolytic Agents Patients Proteins Pulmonary Embolism Rate, Heart Respiratory Rate Serum Systolic Pressure Thirty Day Readmission Troponin Warfarin
2
Korean Acute Myocardial Infarction Registry
The study population was selected from the Korean Acute Myocardial Infarction Registry-National Institutes of Health (KAMIR-NIH) [10 (link)]. KAMIR-NIH is a nation-wide, prospective, multicenter, web-based observational cohort study aiming to develop a prognostic and surveillance index for patients with AMI. Patients who were hospitalized primarily for AMI and signed informed consents were consecutively enrolled from November 2011 to October 2015. This study was conducted according to the ethical guidelines of the Declaration of Helsinki. The study protocol was approved by the ethics committee at Chonnam National University Hospital, Republic of Korea (IRB No. CNUH-2011-172) and the institutional review boards of all participating hospitals approved the study protocol. Written informed consents were obtained from participating patients or legal representative. Data were collected by the attending physician with the assistance of a trained clinical research coordinator, via a web-based case report form in the clinical data management system of the Korea NIH. Patients, who died during index hospitalization, did not have hypertension, were prescribed neither ACEI nor ARB, or both ACEI and ARB at discharge, did not undergo echocardiographic study, and had incomplete clinical data, were excluded.
AMI was diagnosed when there was an evidence of myocardial necrosis (a rise and/or fall in cardiac biomarker, preferably cardiac troponin), and at least one of the following: (1) symptoms of ischemia, (2) new or presumed new significant ST-segment-T wave changes or a new left bundle branch block, (3) a development of pathologic Q waves in the electrocardiogram, (4) an imaging evidence of the new loss of viable myocardium or new regional wall motion abnormality, and (5) the identification of an intracoronary thrombus by angiography [11 (link)]. Hypertension was defined as values ≥140 mmHg of systolic BP (SBP) and/or ≥90 mmHg of diastolic BP (DBP) during the initial hospitalization [12 (link), 13 (link)]. Patients with a history of hypertension or antihypertensive treatment on the interview were also considered to have hypertension. Coronary reperfusion included reperfusion by percutaneous coronary intervention (PCI), thrombolysis, or coronary artery bypass graft (CABG), MI with non-obstructed coronary arteries (MINOCA) [3 (link)], and myocardial bridge. LV systolic function was evaluated by the echocardiographic study during the initial hospitalization.
Lee J.G., Joo S.J., Kim S.Y., Choi J.H., Boo K.Y., Hwang J.Y., Hur S.H, & Jeong M.H. (2023). Impact of angiotensin-converting enzyme inhibitors versus angiotensin receptor blockers on clinical outcomes in hypertensive patients with acute myocardial infarction. PLOS ONE, 18(3), e0281460.
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Publication 2023
Angiography Antihypertensive Agents Artery, Coronary Biological Markers Coronary Artery Bypass Surgery Echocardiography Electrocardiography Ethics Committees Ethics Committees, Research Fibrinolytic Agents Heart High Blood Pressures Hospitalization Ischemia Koreans Left Bundle-Branch Block Myocardial Infarction Myocardial Reperfusion Myocardium Patient Discharge Patients Percutaneous Coronary Intervention Physicians Pressure, Diastolic Reperfusion Systole Systolic Pressure Thrombus Troponin
3
Factors Influencing COVID-19 Admission Patterns
Participant characteristics were summarized descriptively. Comparisons between patients discharged home, admitted to the medical ward, or admitted directly to the ICU were made with Wilcoxson rank sum and Pearson chi-square tests for continuous and categorical variables, respectively. Impact of timing during the pandemic was assessed as days since data collection started (March 8, 2020).
All tests were 2-sided and a P value < .05 was considered statistically significant. All variables were initially assessed for significance using univariable analysis comparing: Patients discharged home versus admitted to the medical ward and; Patients admitted to the medical ward versus ICU (see Tables S1 and S2, Supplemental Digital Content, http://links.lww.com/MD/I601, which shows the results of univariable analysis). A Multivariable logistic regression was fitted separately comparing: Patients discharged home versus admitted to the medical ward and; Patients admitted to the medical ward versus ICU. We opted for 2 logistic regression models to reflect the distinct clinical decision making processes in the ED (i.e., “discharge home” vs “admit to medical ward,” and “admit to medical ward” vs “admit to ICU”).”
Our key associations of interest were race, ethnicity, ADI, English as a primary language, homelessness, and illicit substance use (opiates, cocaine, methamphetamine); variables also included age, gender, and clinical comorbidities, including body mass index (mg/kg2) and clinical severity. We evaluated disease severity using clinical severity scores (sequential organ failure assessment, Charlson comorbidity index) and laboratory markers found in other risk severity scores,[27 (link),28 ] specifically, C-reactive protein (mg/L), ferritin (ug/L), D-dimer (ng/mL), creatine kinase (U/L), troponin (ng/L), procalcitonin (ng/mL), absolute lymphocyte count (K/mL), and blood urea nitrogen (mg/dL). Timing of admission was calculated as days after the first date of data collection (March 8, 2020). In our regression, we controlled for timing of admission and included the square of timing of admission to evaluate how the effect changed over time. To build our regression models, we first included a priori variables based on clinical understanding (i.e., age, sex, sequential organ failure assessment, C-reactive protein, ferritin, and troponin), and then added variables that were significant on univariable analysis.” Variables were excluded if they showed significant co-linearity (variance inflation factors over 10). We used stepwise, backward selection for our logistic regression model, using a P value of over 0.2 as a cutoff to remove variables. Potential interaction between significant variables was explored.
Additionally, we divided differences in number of admissions in 3 groups to visually evaluate changes in admission over time. Groups were created as general phases of the surge in SARS-CoV-2 admissions in our hospital, representing changes in comfort with diagnosis and clinical management of COVID-19. Changes in admission patterns over time were assessed using the Jonckheere–Terpstra test for trend. All data were analyzed using Stata Statistical Software (Release 16. College Station, TX: StataCorp LLC).
Olds P.K., Musinguzi N., Geisler B.P, & Haberer J.E. (2023). Evaluating disparities by social determinants in hospital admission decisions for patients with COVID-19 quaternary hospital early in the pandemic. Medicine, 102(10), e33178.
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Publication 2023
Cocaine COVID 19 C Reactive Protein Creatine Kinase Diagnosis Ethnicity Factor X Ferritin fibrin fragment D Index, Body Mass Lymphocyte Count Methamphetamine Opiate Alkaloids Pandemics Patients Procalcitonin SARS-CoV-2 Substance Use Troponin Urea Nitrogen, Blood
4
Defining Obstructive Coronary Artery Disease in ATTR-CM
All patients included underwent review of medical records for evidence of oeCAD by two study investigators (R.H., N.M.F.), including symptom history, cardiovascular risk factors, healthcare encounters such as ambulatory clinic visits, Emergency Department visits and hospitalizations, and cardiac investigation findings such as electrocardiogram (ECG), cardiac biomarker (troponin and N-terminal pro-B-type natriuretic peptide, NTproBNP), ECG stress test, stress imaging, coronary computed tomography angiography (CCTA), invasive coronary angiography, history of acute coronary syndrome (ACS) or myocardial infarction (MI), and/or coronary artery revascularization. The clinical indication for oeCAD evaluation, in addition to the temporal relation with ATTR-CM diagnosis (occurring before, after, or simultaneous with) was also collected.
As patients with ATTR-CM often have clinical characteristics and/or non-invasive investigation result findings that resemble oeCAD (such as chest pain, chronically elevated troponin levels, and anterior Q-waves on ECG), a strict definition of oeCAD was used for this analysis. A diagnosis of CAD required ≥ 1 of the following criteria: (1) prior history of coronary artery revascularization by either percutaneous coronary intervention (PCI) and/or coronary artery bypass grafting (CABG), (2) obstructive epicardial coronary artery stenosis of ≥ 70% by CCTA or invasive coronary angiography, or ≥ 50% of the left main coronary artery [11 (link)]. This strict criteria was selected in order to definitively confirm the presence of obstructive epicardial coronary artery disease lesions in ATTR-CM patients, and to discriminate the presence oeCAD from patients who may have microvascular coronary artery disease or findings on non-invasive evaluation (such as ECG or echocardiography) that are secondary to myocardial amyloid fibril infiltration but resemble oeCAD. Among patients with a prior history of ACS/MI, all had subsequent confirmatory invasive coronary angiography.
Hassan R., Miller R.J., Howlett J.G., White J.A, & Fine N.M. (2023). Prevalence, incidence and clinical outcomes of epicardial coronary artery disease among transthyretin amyloidosis cardiomyopathy patients. BMC Cardiovascular Disorders, 23, 124.
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Publication 2023
Acute Coronary Syndrome Amyloid Fibrils Artery, Coronary Biological Markers Chest Pain Clinic Visits Computed Tomography Angiography Coronary Angiography Coronary Artery Disease Coronary Stenosis Diagnosis Echocardiography Electrocardiography Exercise Tests Heart Hospitalization Myocardial Infarction Myocardium Patients Percutaneous Coronary Intervention pro-brain natriuretic peptide (1-76) Troponin TTR protein, human
5
Precipitating Factors and Outcomes in Heart Failure

Precipitating factors: enrolling physicians were asked to report potential precipitating factors from among several predefined reasons: ACS/MI, arrhythmia, infection, uncontrolled hypertension, non-compliance, worsening renal function, and anemia. More than one precipitating factor could be assigned to each patient when applicable, according to the clinician’s judgment.

The following definitions were applied: ‘ACS/MI,’ as defined by the ESC, in the presence of ECG changes and/or a dynamic rise in standard Troponin readings [9 (link)], ‘infection’ in the presence of fever and/or other indications of infection at initial admission (leukocytosis, increased inflammatory markers, clinical or microbiological evidence of infection); ‘atrial fibrillation’ in the presence of AF (new onset or recurrent) with ventricular rate ≥110/min; ‘hypertension’ in the presence of high systolic blood pressure (≥160 mmHg) at admission; ‘anemia’ if hemoglobin level on admission was ≤ 8.0 gm/dl; ‘renal dysfunction’ if serum creatinine level on admission was ≥ 1.5 mg/dl; and ‘non-compliance’ if a significant deviation from nutritional or treatment recommendations is seen (either in patients with a prior diagnosis of HF or in patients who have medical problems that if became uncontrolled due to non-compliance could precipitate HF).

In-hospital and long-term all-cause mortality and duration of hospital stay

Relevant confounders including demographics (such as age and gender) and signs and symptoms at admission (such as heart failure status, presence or absence of pulmonary edema, and/or cardiogenic shock) and modes of presentation (own transport vs ambulance).

Bendary A., Hassanein M., Bendary M., Smman A., Hassanin A, & Elwany M. (2023). The predictive value of precipitating factors on clinical outcomes in hospitalized patients with decompensated heart failure: insights from the Egyptian cohort in the European Society of Cardiology Heart Failure long-term registry. The Egyptian Heart Journal, 75, 16.
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Publication 2023
Ambulances Anemia Atrial Fibrillation Cardiac Arrhythmia Congestive Heart Failure Creatinine Diagnosis Fever Gender Heart Ventricle Hemoglobin High Blood Pressures Infection Inflammation Kidney Kidney Failure Leukocytosis Patients Physicians Precipitating Factors Pulmonary Edema Serum Shock, Cardiogenic Systolic Pressure Troponin Vision

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More about "Troponin"

Troponin, a key regulatory protein complex, plays a crucial role in the calcium-mediated control of muscle contraction in both skeletal and cardiac muscle.
This complex is composed of three subunits: troponin C, troponin I, and troponin T.
Troponin C is responsible for binding calcium, while troponin I inhibits the actin-myosin interaction, and troponin T anchors the troponin complex to the tropomyosin filament.
Measurement of troponin levels, particularly cardiac troponin T and I, is a widely used diagnostic tool for the detection of myocardial infarction (heart attack) and other cardiac injuries.
Elevated troponin levels indicate damage to the heart muscle, making it a reliable biomarker for cardiovascular diseases.
To enhance the reproducibility and accuracy of troponin analysis, researchers can leverage PubCompare.ai's AI-powered platform.
This tool provides access to relevant scientific protocols from literature, preprints, and patents, and enables intelligent comparisons to identify the optimal methods and products for troponin detection and quantification.
In addition to troponin, researchers may also utilize other related tools and reagents, such as DAPI (a DNA-binding fluorescent dye), Ab8295 (an anti-α-actinin antibody), Hoechst 33342 (a cell-permeable DNA stain), bovine serum albumin (a common blocking agent), Perm/Wash buffer (for cell permeabilization and washing), and anti-cardiac troponin T antibodies (including the mouse anti-cardiac troponin T).
These tools can be used in conjunction with troponin analysis to provide a more comprehensive understanding of cardiac muscle structure and function.
By incorporating these insights and leveraging the capabilities of PubCompare.ai, researchers can enhance the reproducibility and accuracy of their troponin analysis, leading to improved research outcomes and a deeper understanding of cardiovascular diseases.