Early rule-out and rule-in of myocardial infarction using sensitive cardiac Troponin I

Druey, Sophie; Wildi, Karin; Twerenbold, Raphael; Jaeger, Cédric; Reichlin, Tobias; Haaf, Philip; Giménez, María Rubini; Puelacher, Christian; Wagener, Max; Radosavac, Milos; Honegger, Ursina; Schumacher, Carmela; Delfine, Valentina; Kreutzinger, Philip; Herrmann, Thomas; Weidmann, Zoraida Moreno; Krivoshei, Lian; Freese, Michael; Stelzig, Claudia; Isenschmid, Cyril; Bassetti, Stefano; Rentsch, Katharina; Oßwald, Stefan

doi:10.1016/j.ijcard.2015.05.079

Cited by 33 publications

(19 citation statements)

References 40 publications

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“…An increased cTnI concentration is defined as a value exceeding the 99% of a normal reference population [13]. Blood samples were obtained after 1 h in the emergency department [14]. Plasma cTnI concentrations were determined by chemiluminescence immunoassays according to manufacturer’s protocol (Beckman Coulter, Fullerton, CA, U.S.A.).…”

Section: Methodsmentioning

confidence: 99%

Circulating endothelial microparticles and miR-92a in acute myocardial infarction

et al. 2017

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Microparticles (MPs) and miRNAs have been shown to play important roles in coronary artery disease (CAD) by monitoring endothelial dysfunction. The present study aims to investigate the diagnostic value of endothelial MPs (EMPs) and miRNAs (miR-92a or miR-23a) as biomarkers in distinguishing patients with acute myocardial infarction (AMI) from those with CAD. Plasma samples from 37 patients with AMI, 42 patients with stable CAD (SCAD), and 35 healthy adults were collected for investigation in the present study. The numbers of CD31+/CD42b− MPs, CD31+/CD42b+ MPs, and CD31−/CD42b− MPs were measured by flow cytometry and the levels of miR-92a and miR-23a were analyzed using reverse transcription-quantitative PCR. Moreover, cardiac troponin I (cTnI) expression was detected by ELISA to serve as a routine diagnostic parameter. The number of CD31+/CD42b− was higher in AMI group than those in SCAD and healthy groups. Besides, the expression of miR-92a was higher in AMI group compared with two other groups. Furthermore, evidence showed that there was a positive correlation between the levels of CD31+/CD42b− MPs and miR-92a. Finally, the receiver operating characteristic (ROC) curve revealed that the area value under the curve of CD31+/CD42b− MPs, miR-92a and cTnI was 0.893, 0.888, and 0.912 respectively. CD31+/CD42b− MPs and miR-92a might have great potential to provide diagnostic value for AMI and could probably regulate the endothelial dysfunction in AMI patients.

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Section: Methodsmentioning

confidence: 99%

Circulating endothelial microparticles and miR-92a in acute myocardial infarction

et al. 2017

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“…This approach to ruling out AMI appears to be safe for all hs-cTn assays and likely many sensitive cTn assays. 49 Assuming a 1-hour turn-around time for hs-cTn, this approach facilitates a disposition decision within ≈4 hours of presentation.…”

Section: -And 3-hour Esc Algorithmmentioning

confidence: 99%

State-of-the-Art Evaluation of Emergency Department Patients Presenting With Potential Acute Coronary Syndromes

2016

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ABSTRACT:It is well established that clinicians cannot use clinical judgment alone to determine whether an individual patient who presents to the emergency department has an acute coronary syndrome. The history and physical examination do not distinguish sufficiently between the many conditions that can cause acute chest pain syndromes. Cardiac risk factors do not have sufficient discriminatory ability in symptomatic patients presenting to the emergency department. Most patients with non-ST-segment-elevation myocardial infarction do not present with electrocardiographic evidence of active ischemia. The improvement in cardiac troponin assays, especially in conjunction with well-validated clinical decision algorithms, now enables the clinician to rapidly exclude myocardial infarction. In patients in whom unstable angina remains a concern or there is a desire to evaluate for underlying coronary artery disease, coronary computed tomography angiography can be used in the emergency department. Once a process that took ≥24 hours, computed tomography angiography now can rapidly exclude myocardial infarction and coronary artery disease in patients in the emergency department.A bout 20 million patients present with symptoms possibly suggestive of acute coronary syndrome (ACS) to emergency departments (ED) in North America and Europe each year.1-3 Patients with ACS and acute myocardial infarction (AMI) present with a wide variety of symptoms such as chest pain, shortness of breath, weakness, nausea, vomiting, and even fatigue, making the diagnosis difficult. Demographics, cardiac risk factors, chest pain characteristics, and physical examination can assist disposition decisions but are insufficient to identify who does and does not have an ACS.4-7 Some patients may have objective evidence of a clearcut diagnosis, but the majority do not. 8 The majority ultimately will be found not to have ACS, but symptoms caused by noncardiac and often benign disorders such as musculoskeletal pain, pleuritis, or gastroesophageal reflux make the rapid rule-out of ACS more difficult and result in huge medical expenses. Safe and early rule-out of ACS contributes to more efficient and high-value healthcare delivery. History And PHysicAl ExAminAtionClinical features, alone or in combination with an ECG, are poorly predictive for AMI (Table 1). 9,10 In addition, they have variable reliability. Features classically associated with a lower probability of AMI such as pleuritic, positional, and sharp chest pain have poor to fair interphysician reliability (κ=0.27-0.44), 11 whereas high-risk features (radiation to left arm, substernal location, and history of AMI) are more reliable (κ=0.74-0.89). 11Traditional cardiac risk factors, derived from population-based longitudinal cohort studies of asymptomatic patients, are poor predictors of risk for AMI or ACS in symptomatic patients in the ED. 6,7 Similarly, the physical examination seldom is useful for distinguishing patients with ACS from patients with noncardiac chest pain.Trials of medications, onc...

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“…However, CK-MB also exists in skeletal muscle and brain, thus is non-specific. In contrast to CK-MB, cTnI has a higher specificity [1][2][3][4]. As a regulatory protein in healthy human, cTnI level is lower than 0.3 mg/ L in serum.…”

Section: Introductionmentioning

confidence: 99%

A New Molecularly Imprinted Polymer (MIP)‐based Electrochemical Sensor for Monitoring Cardiac Troponin I (cTnI) in the Serum

Zuo

Zhao

et al. 2016

Electroanalysis

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A novel molecularly imprinted polymer (MIP) sensor for rapid determination of cardiac troponin (cTnI) was established. Since it can bind to the template molecule cTnI specifically, it can be used to detect concentration of cTnI in serum without much sample pretreatment. What's more, the electrochemical signals depend on the concentration of template molecules. The synthetic sensor possesses advantages including simplicity, high specificity, low cost of preparation, good chemical and mechanical properties, sensitive and label‐free determination. The synthetic sensor shows good dynamic linearity at concentration range from 0.05 to 5.00 nM. The limit of detection (LOD) was found to be 0.027 nM. The detection time of whole process was within 5 minutes.

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Early rule-out and rule-in of myocardial infarction using sensitive cardiac Troponin I

Abstract: When used in conjunction with other clinical information including the ECG, a simple algorithm incorporating s-cTnI values at presentation and after 1h (or 2h) will allow safe rule-out and accurate rule-in of AMI in the majority of patients.

Cited by 33 publications

References 40 publications

Circulating endothelial microparticles and miR-92a in acute myocardial infarction

Circulating endothelial microparticles and miR-92a in acute myocardial infarction

State-of-the-Art Evaluation of Emergency Department Patients Presenting With Potential Acute Coronary Syndromes

A New Molecularly Imprinted Polymer (MIP)‐based Electrochemical Sensor for Monitoring Cardiac Troponin I (cTnI) in the Serum

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