LABORATORIO DE URGENCIAS

1. S Afr Med J. 2016 Mar;106(3):239-45.
Approach to chest pain and acute myocardial infarction.
Pandie S, Hellenberg D, Hellig F, Ntsekhe M.
Patient history, physical examination, 12-lead electrocardiogram (ECG) andcardiac biomarkers are key components of an effective chest pain assessment. The first priority is excluding serious chest pain syndromes, namely acute coronarysyndromes (ACSs), aortic dissection, pulmonary embolism, cardiac tamponade andtension pneumothorax. On history, the mnemonic SOCRATES (Site Onset CharacterRadiation Association Time Exacerbating/relieving factor and Severity) helpsdifferentiate cardiac from non-cardiac pain. On examination, evaluation of vital signs, evidence of murmurs, rubs, heart failure, tension pneumothoraces and chestinfections are important. A 12-lead ECG should be interpreted within 10 minutesof first medical contact, specifically to identify ST elevation myocardialinfarction (STEMI). High-sensitivity troponins improve the rapid rule-out ofmyocardial infarction (MI) and confirmation of non-ST elevation MI (NSTEMI). ACS (STEMI and NSTEMI/unstable anginapectoris (UAP)) result from acutedestabilisation of coronary atheroma with resultant complete (STEMI) or subtotal (NSTEMI/UAP) thrombotic coronary occlusion. The management of STEMI patientsincludes providing urgent reperfusion: primary percutaneous coronaryintervention(PPCI) if available, deliverable within 60 - 120 minutes, andfibrinolysis if PPCI is not available. Essential adjunctive therapies includeantiplatelet therapy (aspirin, P2Y12 inhibitors), anticoagulation (heparin orlow-molecular-weight heparin) and cardiac monitoring.

PMID: 27303759  [PubMed - indexed for MEDLINE]

2. Lancet. 2016 Jun 4;387(10035):2289. doi: 10.1016/S0140-6736(16)30686-9.
Measurement of cardiac troponin for exclusion of myocardial infarction.
Fujita T(1).
Author information: (1)Department of Surgery, Jikei University School of Medicine, Tokyo, Japan.Electronic address: tetsu@jg8.so-net.ne.jp.
Comment in    Lancet. 2016 Jun 4;387(10035):2289-91.
Comment on    Lancet. 2015 Dec 19;386(10012):2481-8.
DOI: 10.1016/S0140-6736(16)30686-9 PMID: 27302265  [PubMed - indexed for MEDLINE]

3. Lancet. 2016 Jun 4;387(10035):2289. doi: 10.1016/S0140-6736(16)30687-0.
Measurement of cardiac troponin for exclusion of myocardial infarction.
Ford C(1), Whitehead SJ(1), Gama R(2), Willmer KA(3).
Author information: (1)Department of Clinical Chemistry, Royal Wolverhampton NHS Trust,Wolverhampton, UK. (2)Department of Clinical Chemistry, Royal Wolverhampton NHSTrust, Wolverhampton, UK. Electronic address: rousseau.gama@nhs.net.(3)Department of Acute Medicine, Royal Wolverhampton NHS Trust, Wolverhampton,UK.
Comment in    Lancet. 2016 Jun 4;387(10035):2289-91.
Comment on    Lancet. 2015 Dec 19;386(10012):2481-8.
DOI: 10.1016/S0140-6736(16)30687-0 PMID: 27302264  [PubMed - indexed for MEDLINE]

4. Lancet. 2016 Jun 4;387(10035):2289-91. doi: 10.1016/S0140-6736(16)30517-7.
Measurement of cardiac troponin for exclusion of myocardial infarction - Authors'reply.
Shah AS(1), Anand A(2), Chapman AR(2), Newby DE(2), Mills NL(2); High-STEACSInvestigators.
Author information: (1)BHF Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.Electronic address: Anoop.Shah@ed.ac.uk. (2)BHF Centre for CardiovascularScience, University of Edinburgh, Edinburgh, UK.
Comment on    Lancet. 2016 Jun 4;387(10035):2289.    Lancet. 2016 Jun 4;387(10035):2288.    Lancet. 2016 Jun 4;387(10035):2289.    Lancet. 2016 Jun 4;387(10035):2288-9.    Lancet. 2015 Dec 19;386(10012):2481-8.
DOI: 10.1016/S0140-6736(16)30517-7 PMID: 27302263  [PubMed - indexed for MEDLINE]

5. Lancet. 2016 Jun 4;387(10035):2288. doi: 10.1016/S0140-6736(16)30684-5.
Measurement of cardiac troponin for exclusion of myocardial infarction.
Boeddinghaus J(1), Twerenbold R(1), Nestelberger T(1), Wildi K(1), Mueller C(2).
Author information: (1)Cardiovascular Research Institute Basel and Department of Cardiology,University Hospital Basel, Basel, Switzerland. (2)Cardiovascular ResearchInstitute Basel and Department of Cardiology, University Hospital Basel, Basel,Switzerland. Electronic address: christian.mueller@usb.ch.
Comment in    Lancet. 2016 Jun 4;387(10035):2289-91.
Comment on    Lancet. 2015 Dec 19;386(10012):2481-8.
DOI: 10.1016/S0140-6736(16)30684-5 PMID: 27302262  [PubMed - indexed for MEDLINE]

6. Lancet. 2016 Jun 4;387(10035):2288-9. doi: 10.1016/S0140-6736(16)30685-7.
Measurement of cardiac troponin for exclusion of myocardial infarction.
Mullen L(1), Chew PG(2), Frost F(2), Obafemi T(2), Khand A(3).
Author information: (1)University Hospital Aintree, Liverpool, UK. Electronic address:liammullen@nhs.net. (2)University Hospital Aintree, Liverpool, UK. (3)University Hospital Aintree, Liverpool, UK; Liverpool Heart and Chest Hospital, Liverpool,UK.
Comment in    Lancet. 2016 Jun 4;387(10035):2289-91.
Comment on    Lancet. 2015 Dec 19;386(10012):2481-8.
DOI: 10.1016/S0140-6736(16)30685-7 PMID: 27302261  [PubMed - indexed for MEDLINE]

7. Mymensingh Med J. 2016 Apr;25(2):226-31.
Correlation between Troponin-I and B-Type Natriuretic Peptide Level in AcuteMyocardial Infarction Patients with Heart Failure.
Islam MN(1), Alam MF, Debnath RC, Aditya GP, Ali MH, Hossain MA, Siddique SR.
Author information: (1)Dr Mirza Md Nazrul Islam, Associate Professor, Department of Cardiology,Mymensingh Medical College (MMC), Mymensingh, Bangladesh.
Troponins are regarded as markers of choice for the diagnosis of acute myocardialinfarction (AMI). But B-type natriuretic peptide (BNP) level is also elevated in AMI and is a quantitative biochemical marker related to the extent of infarction and the left ventricle systolic dysfunction. Thus, BNP has prognostic value. Inthis study, we investigate the correlation of Troponin-I with BNP levels inpatients presenting with AMI with or without Acute Heart Failure. Rationale ofthis study is to see, whether quantitative Troponin alone can serve for bothdiagnosis and prognosis of AMI Patients with heart failure or not. Thiscross-sectional analytical study was conducted in the Department of Cardiology inMymensingh Medical College Hospital from January 2014 to December 2014. Total 100patients were studied and divided into two groups - 50 patients in each group.Group I: Patients with first attack of acute myocardial infarction (without heartfailure) & Group II: Patients with first attack of acute myocardial infarctionwith acute heart failure. Mean Troponin-I of Group I and Group II were 3.10±2.68 and 62.93±32.75ng/ml respectively & mean BNP value of Group I and Group II were20.96±14.18 and 615.65±249.27pg/ml respectively. In this study, it was shown thatthe levels of BNP had positive correlation with Troponin-I levels, with mediumstrength of association (r=0.734, p<0.05). Echocardiography shows that patientswith high BNP level has low ejection fraction (LVEF) and patients with low BNPlevel has preserved ejection fraction (LVEF). Thus, the present study shows that the higher the Troponin-I levels, the higher the BNP levels in first attack ofAMI patients and the more severe the heart failure (more severe left ventricledysfunction). There is positive correlation between Troponin-I and BNP levels in first attack of AMI patients with acute heart failure.

PMID: 27277352  [PubMed - indexed for MEDLINE]

8. Med Intensiva. 2016 Apr;40(3):200. doi: 10.1016/j.medin.2016.01.010. Epub 2016Mar 22.
[Methods can influence the value of copeptin to rule-out acute myocardialinfarction without ST segment elevation].
[Article in Spanish]
García de Guadiana-Romualdo L(1), Consuegra-Sánchez L(2), Esteban-Torrella P(3), Martínez-Díaz JJ(2), Albaladejo-Otón MD(3).
Author information: (1)Servicio de Análisis Clínicos, Hospital Universitario Santa Lucía, Cartagena, Murcia, España. Electronic address: guadianarom@yahoo.es. (2)Servicio deCardiología y Hemodinámica, Hospital Universitario Santa Lucía, Cartagena,Murcia, España. (3)Servicio de Análisis Clínicos, Hospital Universitario SantaLucía, Cartagena, Murcia, España.
Comment on    Med Intensiva. 2016 Apr;40(3):199.    Med Intensiva. 2015 Nov;39(8):477-82.
DOI: 10.1016/j.medin.2016.01.010 PMID: 27015787  [PubMed - indexed for MEDLINE]

9. J Am Heart Assoc. 2016 Mar 9;5(3):e002708. doi: 10.1161/JAHA.115.002708.
Sample Size in Clinical Cardioprotection Trials Using Myocardial Salvage Index,Infarct Size, or Biochemical Markers as Endpoint.
Engblom H(1), Heiberg E(2), Erlinge D(3), Jensen SE(4), Nordrehaug JE(5),Dubois-Randé JL(6), Halvorsen S(7), Hoffmann P(8), Koul S(3), Carlsson M(1), AtarD(7), Arheden H(9).
Author information: (1)Department of Clinical Sciences Lund, Clinical Physiology, Skane UniversityHospital, Lund University, Lund, Sweden. (2)Department of Clinical Sciences Lund,Clinical Physiology, Skane University Hospital, Lund University, Lund, SwedenDepartment of Biomedical Engineering, Faculty of Engineering, Lund University,Lund, Sweden. (3)Department of Cardiology, Skåne University Hospital and LundUniversity, Lund, Sweden. (4)Department of Cardiology, Aalborg UniversityHospital, Aalborg, Denmark. (5)Department of Clinical Science, University ofBergen, Norway. (6)Department of Cardiology, Henri Mondor Hospital, Creteil,France. (7)Department of Cardiology B, Oslo University Hospital Ullevål,University of Oslo, Norway Faculty of Medicine, University of Oslo, Norway.(8)Section for Interventional Cardiology, Department of Cardiology, OsloUniversity Hospital, Ullevål, Norway. (9)Department of Clinical Sciences Lund,Clinical Physiology, Skane University Hospital, Lund University, Lund, Swedenhakan.arheden@med.lu.se.
BACKGROUND: Cardiac magnetic resonance (CMR) can quantify myocardial infarct (MI)size and myocardium at risk (MaR), enabling assessment of myocardial salvageindex (MSI). We assessed how MSI impacts the number of patients needed to reachstatistical power in relation to MI size alone and levels of biochemical markers in clinical cardioprotection trials and how scan day affect sample size.METHODS AND RESULTS: Controls (n=90) from the recent CHILL-MI and MITOCARE trialswere included. MI size, MaR, and MSI were assessed from CMR. High-sensitivitytroponin T (hsTnT) and creatine kinase isoenzyme MB (CKMB) levels were assessedin CHILL-MI patients (n=50). Utilizing distribution of these variables, 100 000clinical trials were simulated for calculation of sample size required to reachsufficient power. For a treatment effect of 25% decrease in outcome variables, 50patients were required in each arm using MSI compared to 93, 98, 120, 141, and143 for MI size alone, hsTnT (area under the curve [AUC] and peak), and CKMB (AUCand peak) in order to reach a power of 90%. If average CMR scan day betweentreatment and control arms differed by 1 day, sample size needs to be increasedby 54% (77 vs 50) to avoid scan day bias masking a treatment effect of 25%.CONCLUSION: Sample size in cardioprotection trials can be reduced 46% to 65%without compromising statistical power when using MSI by CMR as an outcomevariable instead of MI size alone or biochemical markers. It is essential toensure lack of bias in scan day between treatment and control arms to avoidcompromising statistical power.
© 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.
DOI: 10.1161/JAHA.115.002708 PMCID: PMC4943247PMID: 26961520  [PubMed - indexed for MEDLINE]

10. Clin Chim Acta. 2016 May 1;456:42-8. doi: 10.1016/j.cca.2016.02.017. Epub 2016Feb 26.
Pilot study on harmonization of cardiac troponin I immunoassays using patientsand quality control plasma samples. On behalf of the Italian Section of theEuropean Ligand Assay Society (ELAS) and of the Study Group on CardiovascularBiomarkers of the Società Italiana di Biochimica Clinica (SIBioC).
Clerico A(1), Ripoli A(2), Masotti S(3), Prontera C(2), Storti S(2), FortunatoA(4), Buzzi P(5), Casagranda I(5), Franzini M(6), Ndreu R(7), Zucchelli GC(7),Zaninotto M(8), Plebani M(8).
Author information: (1)Fondazione CNR Regione Toscana G. Monasterio, Pisa, Italy; Scuola SuperioreSant'Anna, Pisa, Italy. (2)Fondazione CNR Regione Toscana G. Monasterio, Pisa,Italy. (3)Scuola Superiore Sant'Anna, Pisa, Italy. (4)Department of LaboratoryMedicine, San Bortolo Hospital, Vicenza, Italy. (5)Dipartimento di Emergenza,Ospedale Civile Santi Antonio e Biagio e Cesare Arrigo di Alessandria,Alessandria, Italy. (6)Dipartimento di Ricerca Traslazionale e delle NuoveTecnologie in Medicina e Chirurgia, Università di Pisa, Pisa, Italy.(7)QualiMedLab, Istituto di Fisiologia Clinica del CNR, Pisa, Italy.(8)Department of Laboratory Medicine, University of Padova, Italy.
BACKGROUND: The aim of this study is to evaluate whether it is possible to reducethe between-methods variability of troponin I (cTnI) immunoassays usingmathematical algorithms calculated from the results of both patients' samples andquality control materials distributed in an external quality assessment (EQA)scheme.METHODS: We collected 122 heparinized plasma samples of patients admitted to the emergency department with thoracic pain or supraventricular tachyarrhythmia.Moreover, we also analyzed 20 control samples distributed in an EQA and 26 plasmapools prepared from healthy subjects and patients with myocardial infarction. We evaluated 4 different methods for cTnI assay: STAT Architect High Sensitive TnI(Abbott Diagnostics), ADVIA Centaur Troponin I Ultra (Siemens HealthcareDiagnostics), ST AIA-Pack cTnI Third Generation (Tosoh Bioscience), and AccessAccuTnI+3 (Beckman Coulter Diagnostics).RESULTS: Systematic differences between cTnI methods were observed. However,correlation coefficients (R from 0.976 to 0.990) between the log-transformed cTnIvalues measured in all 168 samples were significantly better (p=0.0037) thanthose obtained considering only the 122 patients' samples. cTnI values measuredin EQA and pool samples were included within the 95% prediction intervals oflinear regressions calculated with those of patients' samples. After therecalibration of cTnI values based on the robust principal component analysisapproach the between-methods variability decreased significantly (about 40%around the cut off values).CONCLUSIONS: Our pilot study suggests that EQA schemes for cTnI immunoassaymethods, based on both quality control samples with tested commutability androbust statistical analyses, are able to evaluate between-methods variability as well as allow a reliable recalibration and harmonization of results.
Copyright © 2016 Elsevier B.V. All rights reserved.
DOI: 10.1016/j.cca.2016.02.017 PMID: 26923393  [PubMed - indexed for MEDLINE]

11. Nat Commun. 2016 Feb 24;7:10794. doi: 10.1038/ncomms10794.
Rationally engineered Troponin C modulates in vivo cardiac function andperformance in health and disease.
Shettigar V(1), Zhang B(1), Little SC(2), Salhi HE(1), Hansen BJ(1), Li N(1),Zhang J(1), Roof SR(3), Ho HT(1), Brunello L(1), Lerch JK(4), Weisleder N(1),Fedorov VV(1), Accornero F(1), Rafael-Fortney JA(1), Gyorke S(1), Janssen PM(1), Biesiadecki BJ(1), Ziolo MT(1), Davis JP(1).
Author information: (1)Davis Heart and Lung Research Institute and Department of Physiology and Cell Biology, Columbus, Ohio 43210, USA. (2)Bristol-Myers Squibb, Department ofDiscovery Biology, Wallingford, Connecticut 06492, USA. (3)Q-Test Labs, Columbus,Ohio 43235, USA. (4)Center for Brain and Spinal Cord Repair, Department ofNeuroscience, The Ohio State University College of Medicine, Columbus, Ohio43210, USA.
Treatment for heart disease, the leading cause of death in the world, hasprogressed little for several decades. Here we develop a protein engineeringapproach to directly tune in vivo cardiac contractility by tailoring the ability of the heart to respond to the Ca(2+) signal. Promisingly, our smartly formulatedCa(2+)-sensitizing TnC (L48Q) enhances heart function without any adverse effectsthat are commonly observed with positive inotropes. In a myocardial infarction(MI) model of heart failure, expression of TnC L48Q before the MI preservescardiac function and performance. Moreover, expression of TnC L48Q after the MItherapeutically enhances cardiac function and performance, without compromisingsurvival. We demonstrate engineering TnC can specifically and precisely modulate cardiac contractility that when combined with gene therapy can be employed as atherapeutic strategy for heart disease.
DOI: 10.1038/ncomms10794 PMCID: PMC4770086PMID: 26908229  [PubMed - indexed for MEDLINE]

12. Eur J Vasc Endovasc Surg. 2016 Apr;51(4):481. doi: 10.1016/j.ejvs.2015.12.041.Epub 2016 Feb 16.
Commentary on 'The Clinical Relevance of Cardiac Troponin Assessment in Patients Undergoing Carotid Endarterectomy'.
De Rango P(1).
Author information: (1)Vascular Surgery Unit, Hospital S. Maria Misericordia, Perugia, Italy.Electronic address: plderango@gmail.com.
Comment on    Eur J Vasc Endovasc Surg. 2016 Apr;51(4):473-80.
DOI: 10.1016/j.ejvs.2015.12.041 PMID: 26895945  [PubMed - indexed for MEDLINE]

13. Int J Cardiol. 2016 Apr 15;209:26-33. doi: 10.1016/j.ijcard.2016.01.213. Epub2016 Feb 3.
Diagnostic and prognostic implications using age- and gender-specific cut-offsfor high-sensitivity cardiac troponin T - Sub-analysis from the TRAPID-AMI study.
Mueller-Hennessen M(1), Lindahl B(2), Giannitsis E(3), Biener M(1), Vafaie M(1), deFilippi CR(4), Christ M(5), Santalo-Bel M(6), Panteghini M(7), Plebani M(8),Verschuren F(9), Jernberg T(10), French JK(11), Christenson RH(12), Body R(13),McCord J(14), Dilba P(15), Katus HA(1), Mueller C(16); TRAPID-AMI Investigators.
Author information: (1)Department of Internal Medicine III, Cardiology, Angiology & Pulmonology,Heidelberg University Hospital, Heidelberg, Germany. (2)Department of MedicalSciences, Uppsala University, Uppsala, Sweden; Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden. (3)Department of Internal Medicine III,Cardiology, Angiology & Pulmonology, Heidelberg University Hospital, Heidelberg, Germany. Electronic address: evangelos_giannitsis@med.uni-heidelberg.de.(4)Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, United States. (5)Department of Emergency and Critical Care Medicine,Community Hospital, Paracelsus Medical University, Nuremberg, Germany.(6)Semicritical Unit, Hospital de Sant Pau &, Institut d'InvestigacionsBiomèdiques Sant Pau, Barcelona, Spain. (7)Department of Biomedical and Clinical Sciences 'Luigi Sacco', University of Milan Medical School, Milano, Italy.(8)Department of Laboratory Medicine, University Hospital of Padova, Padua,Italy. (9)Department of Acute Medicine, Cliniques Universitaires St-Luc,Université Catholique de Louvain, Brussels, Belgium. (10)Department of Medicine, KarolinskaInstitutet, Huddinge, Sweden. (11)Liverpool Hospital, University of NewSouth Wales, Sydney, Australia. (12)Department of Pathology, University ofMaryland School of Medicine, Baltimore, MD, United States. (13)Central ManchesterUniversity Hospitals NHS Foundation Trust, United Kingdom. (14)Henry Ford Heartand Vascular Institute, Henry Ford Health System, Detroit, MI, United States.(15)Roche Diagnostics Germany, Penzberg, Germany. (16)Cardiology & CardiovascularResearch Institute Basel, University Hospital Basel, Switzerland.
OBJECTIVES: To evaluate the impact of age- and gender-specific cut-offs forhigh-sensitivity cardiac troponin T (hs-cTnT) compared to the general 99thpercentile hs-cTnT cut-off on diagnosis and prognosis of acute myocardialinfarction (AMI).METHODS: 1282 unselected patients presenting to the emergency department withsuspected AMI were enrolled as part of the TRAPID-AMI study. In the presentsub-analysis, reclassification of AMI diagnosis was performed by comparing thegeneral hs-cTnT cut-off of 14ng/L to previously proposed age- andgender-dependent hs-cTnT 99th percentile cut-offs (28ng/L for ≥65years, 9ng/L forfemale and 15.5ng/L for male patients). Patients were further clinicallyadjudicated into acute coronary syndrome (ACS) and non-ACS.RESULTS: For patients ≥65years, application of age-specified cut-offs resulted ina decrease of AMI from 29.8% to 18.3% in the entire cohort (n=557) and 54.7% to40.9% in the ACS subcohort (n=225). Using gender-specific cut-offs, AMI-rateincreased from 16.6% to 22.6% (entire cohort, n=477) and 62.6% to 71.7% (ACSsubcohort, n=99) in women, whereas in men, rates decreased from 23.1% to 21.1%(entire cohort, n=805) and 48.8% to 45.9% (ACS, n=281), respectively.Age-specified cut-offs significantly reclassified patients for outcomes of1-month and 3-month mortality in the entire and ACS cohort (14.2% netreclassification improvement, p<0.001, respectively). Contrary, no significantdifferences in outcomes could be found using gender-specific cut-offs.CONCLUSIONS: While influence of gender-specific hs-cTnT cut-offs on diagnosticand prognostic reclassification was only modest in patients with suspected AMI,age-specific cut-offs showed a significant impact and may be considered forfurther validation.
Copyright © 2016. Published by Elsevier Ireland Ltd.
DOI: 10.1016/j.ijcard.2016.01.213 PMID: 26878470  [PubMed - indexed for MEDLINE]

14. Clin Chim Acta. 2016 May 1;456:36-41. doi: 10.1016/j.cca.2016.01.022. Epub 2016Feb 11.
Diagnosis of acute myocardial infarction in hemodialysis patients may be feasibleby comparing variation of cardiac troponins during acute presentation to baselinevariation.
van Berkel M(1), Dekker MJ(1), Bogers H(1), Geerse DA(1), Konings CJ(1),Scharnhorst V(2).
Author information: (1)Clinical Laboratory and Department of Internal Medicine, Catharina Hospital,Eindhoven, The Netherlands. (2)Department of Biomedical Engineering, TechnicalUniversity of Eindhoven, The Netherlands.
Acute myocardial infarction (AMI) is defined as a dynamic change in cardiactroponin (cTn) with at least one cTn value exceeding the 99 th percentile of areference population in combination with typical clinical symptoms. Inhemodialysis (HD) patients, a broad range of cTn concentrations is found,partially due to patient-specific comorbidities. Therefore, the 99 th percentile cannot be used in HD patients and decision algorithms to diagnose AMI should bebased on temporal variations of troponin. In this study, relative and absolutevariations of cTn in a large population of asymptomatic hemodialysis patientswere established during a period of 15 months. Patients were stratified accordingto their history of coronary artery disease (CAD). An intra-individual long term variation of 23% for cTroponin I (cTnI) and 12% for cTroponin T (cTnT) was found for patients without a history of CAD. The corresponding reference change values (RCVs) were 69% and 39% respectively. For patients with a history of CAD thisvariation was 29% for cTnI and 10% for cTnT, with RCVs of 86% and 35%respectively. During follow up, 27 HD patients developed an acute myocardialinfarction (AMI). During these events, irrespective of CAD history, cTnIincreased>172% and cTnT increased>97% above baseline cTn as measured duringclinically stable periods three months separate to the event. Therefore, if a HD patient has symptoms of an acute event and a cTn increase that exceeds the RCVsdescribed here, AMI may be suspected. If the troponin increase exceeds 172% forcTnI or 97% for cTnT, AMI is likely.
Copyright © 2016. Published by Elsevier B.V.
DOI: 10.1016/j.cca.2016.01.022 PMID: 26874043  [PubMed - indexed for MEDLINE]

15. Med Intensiva. 2016 Apr;40(3):199. doi: 10.1016/j.medin.2015.11.007. Epub 2016Feb 8.
[Methods can influence the value of copeptin to rule-out acute myocardialinfarction without ST segment elevation].
[Article in Spanish]
Alquézar-Arbé A(1), Rizzi M(2), Álvarez-Albarrán M(2), Lozano-Polo L(2).
Author information: (1)Servicio de Urgencias, Hospital de la Santa Creu i Sant Pau, Barcelona,España. Electronic address: aalquezar@santpau.cat. (2)Servicio de Urgencias,Hospital de la Santa Creu i Sant Pau, Barcelona, España.
Comment in    Med Intensiva. 2016 Apr;40(3):200.
Comment on    Med Intensiva. 2015 Nov;39(8):477-82.
DOI: 10.1016/j.medin.2015.11.007 PMID: 26868934  [PubMed - indexed for MEDLINE]

16. Sci Rep. 2016 Feb 11;6:20812. doi: 10.1038/srep20812.
Analyzing the Release of Copeptin from the Heart in Acute Myocardial InfarctionUsing a Transcoronary Gradient Model.
Boeckel JN(1,)(2,)(3), Oppermann J(1), Anadol R(1), Fichtlscherer S(1), ZeiherAM(1,)(3), Keller T(1,)(3).
Author information: (1)Department of Cardiology, Internal Medicine III, Goethe-University Hospital,Theodor Stern Kai 7 60590 Frankfurt; Germany. (2)Institute for CardiovascularRegeneration, Center of Molecular Medicine, Theodor Stern Kai 7, 60590 Frankfurt;Germany. (3)German Center of Cardiovascular Research (DZHK), RheinMain, 60590Frankfurt, Germany.
Copeptin is the C-terminal end of pre-provasopressin released equimolar tovasopressin into circulation and recently discussed as promising cardiovascularbiomarker amendatory to established markers such as troponins. Vasopressin is acytokine synthesized in the hypothalamus. A direct release of copeptin from theheart into the circulation is implied by data from a rat model showing a cardiac origin in hearts put under cardiovascular wall stress. Therefore, evaluation of apotential release of copeptin from the human heart in acute myocardial infarction(AMI) has been done.
DOI: 10.1038/srep20812 PMCID: PMC4749978PMID: 26864512  [PubMed - indexed for MEDLINE]

17. Eur J Vasc Endovasc Surg. 2016 Apr;51(4):607. doi: 10.1016/j.ejvs.2015.12.007.Epub 2016 Feb 6.
Response to 'Re: Clinical Relevance of Cardiac Troponin Assessment in PatientsUndergoing Carotid Endarterectomy'.
Grobben RB(1), Nathoe HM(2), van Klei WA(3), de Borst GJ(4).
Author information: (1)Department of Cardiology, University Medical Center Utrecht, The Netherlands. Electronic address: r.b.grobben@umcutrecht.nl. (2)Department of Cardiology,University Medical Center Utrecht, The Netherlands. (3)Department ofAnesthesiology, University Medical Center Utrecht, The Netherlands. (4)Departmentof Vascular Surgery, University Medical Center Utrecht, The Netherlands.
Comment on    Eur J Vasc Endovasc Surg. 2016 Apr;51(4):473-80.    Eur J Vasc Endovasc Surg. 2016 Apr;51(4):606-7.
DOI: 10.1016/j.ejvs.2015.12.007 PMID: 26860253  [PubMed - indexed for MEDLINE]

18. Acta Cardiol. 2016 Feb;71(1):47-54. doi: 10.2143/AC.71.1.3132097.
ST-segment elevation in lead aVR in the setting of acute coronary syndrome.
Nabati M, Emadi M, Mollaalipour M, Bagheri B, Nouraei M.
OBJECTIVES: The purpose of our study was to assess the value of aVR ST-segmentelevation (STE) during acute non ST-segment elevation myocardial infarction(NSTEMI) or unstable angina.BACKGROUND: STE in lead aVR has been associated with severe coronary lesions inpatients with acute coronary syndromes. However, there are conflicting dataregarding the prognostic significance of this finding.METHODS: We evaluated the initial electrocardiogram (ECG) in 129 patientsadmitted to our hospital with acute NSTEMI or unstable angina without STE inleads other than aVR or V1. STE in aVR lead was measured and echocardiography andcoronary angiography were performed within 48-72 hours after hospitalization.RESULTS: Overall, 40.3% (52 patients) had more than 0.05 mv STE in lead aVR.These patients had an increased prevalence of ST ≥ 1 mm in lead V1, a morefrequent and extensive ST-segment depression (STD) in other leads, a higherprevalence of anterior and lateral STD and a lower frequency of isolated negativeT waves. It was also strongly associated with cardiac enzyme rising and a trendtoward higher 3-month mortality. Furthermore, patients with STE in lead aVR were more likely to have three-vessel or multivessel disease, higher Gensini score of the coronary arteries, lower left ventricular ejection fraction (LVEF) and higherincidence of mitral regurgitation (MR).CONCLUSIONS: Our study showed that among ECG markers, the sole criterion STE inlead aVR was independently associated with atherosclerosis severity and decreasedLVEF. Also, it was significantly associated with the presence of MR.
DOI: 10.2143/AC.71.1.3132097 PMID: 26853253  [PubMed - indexed for MEDLINE]

19. Circulation. 2016 Feb 2;133(5):e375. doi: 10.1161/CIRCULATIONAHA.115.017572.
Letter by Yang and Xu Regarding Article, "Optimal Cutoff Levels of More SensitiveCardiac Troponin Assays for the Early Diagnosis of Myocardial Infarction inPatients With Renal Dysfunction".
Yang P(1), Xu G(2).
Author information: (1)Medical Center of the Graduate School, Nanchang University, Nanchang, Jiangxi,China. (2)Department of Nephrology, Second Affiliated Hospital, NanchangUniversity, Nanchang, Jiangxi, China.
Comment on    Circulation. 2015 Jun 9;131(23):2041-50.
DOI: 10.1161/CIRCULATIONAHA.115.017572 PMID: 26831440  [PubMed - indexed for MEDLINE]

20. Circulation. 2016 Feb 2;133(5):e374. doi: 10.1161/CIRCULATIONAHA.115.018157.
Letter by Lippi and Cervellin Regarding Article, "Optimal Cutoff Levels of MoreSensitive Cardiac Troponin Assays for the Early Diagnosis of MyocardialInfarction in Patients With Renal Dysfunction".
Lippi G(1), Cervellin G(2).
Author information: (1)Section of Clinical Biochemistry, University of Verona, Verona, Italy.(2)Emergency Department, Academic Hospital of Parma, Parma, Italy.
Comment on    Circulation. 2015 Jun 9;131(23):2041-50.
DOI: 10.1161/CIRCULATIONAHA.115.018157 PMID: 26831439  [PubMed - indexed for MEDLINE]

21. Clin Chim Acta. 2016 Apr 1;455:189-94. doi: 10.1016/j.cca.2016.01.029. Epub 2016 Jan 29.
Unrecognized myocardial infarctions detected by cardiac magnetic resonanceimaging are associated with cardiac troponin I levels.
Nordenskjöld AM(1), Hammar P(2), Ahlström H(3), Bjerner T(3), Duvernoy O(3),Eggers KM(4), Fröbert O(5), Hadziosmanovic N(6), Lindahl B(4).
Author information: (1)Department of Cardiology, Faculty of Health, Örebro University, Örebro,Sweden. Electronic address: anna.nordenskjold@regionorebrolan.se. (2)Departmentof Radiology, Västerås Hospital, Västerås, Sweden; Department of Radiology,Oncology and Radiation Science, Uppsala University, Uppsala, Sweden.(3)Department of Radiology, Oncology and Radiation Science, Uppsala University,Uppsala, Sweden. (4)Department of Medical Sciences, Cardiology, UppsalaUniversity, Uppsala, Sweden; Uppsala Clinical Research Centre, Uppsala, Sweden.(5)Department of Cardiology, Faculty of Health, Örebro University, Örebro,Sweden. (6)Uppsala Clinical Research Centre, Uppsala, Sweden.
BACKGROUND: Both unrecognized myocardial infarction (UMI) and elevated levels of biomarkers are common in patients with stable coronary artery disease (CAD). The objective of this study was to determine the association between levels ofcardiac biomarkers, UMI and extent of CAD in patients with stable CAD.METHODS: A total of 235 patients (median age: 65years; 34% women) with stable CADwithout previously known myocardial infarction were examined with late gadoliniumenhancement cardiovascular magnetic resonance imaging and coronary angiography.Blood samples were drawn at enrolment and high sensitivity cardiac troponin I(cTnI), NT-proBNP and Galectin-3 were analyzed.RESULTS: UMI was detected in 58 patients (25%). The median levels of cTnI,NT-proBNP and Galectin-3 were significantly higher in patients with UMI compared to those without, (p<0.001, p=0.006 and p=0.033, respectively). After adjustment for cardiovascular risk factors, left ventricular ejection fraction and renalfunction, cTnI remained independently associated with the presence of UMI(p=0.031) and the extent of CAD (p=0.047). Neither NT-proBNP, nor Galectin-3, wasindependently associated with UMI or extent of CAD.CONCLUSIONS: The independent association between levels of cTnI and UMI indicatesa common pathophysiological pathway for the cTnI elevation and development ofUMI.CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov (NCT01257282).
Copyright © 2016 Elsevier B.V. All rights reserved.
DOI: 10.1016/j.cca.2016.01.029 PMID: 26828531  [PubMed - indexed for MEDLINE]

22. Int J Cardiol. 2016 Mar 15;207:238-45. doi: 10.1016/j.ijcard.2016.01.112. Epub2016 Jan 11.
Characterization of the observe zone of the ESC 2015 high-sensitivity cardiactroponin 0h/1h-algorithm for the early diagnosis of acute myocardial infarction.
Nestelberger T(1), Wildi K(1), Boeddinghaus J(1), Twerenbold R(1), Reichlin T(1),Giménez MR(1), Puelacher C(1), Jaeger C(1), Grimm K(1), Sabti Z(2), HillingerP(2), Kozhuharov N(2), du Fay de Lavallaz J(1), Pinck F(2), Lopez B(3), SalgadoE(3), Miró Ò(3), Bingisser R(4), Lohrmann J(5), Osswald S(2), Mueller C(6).
Author information: (1)Department of Cardiology, University Hospital Basel, Switzerland;Cardiovascular Research Institute Basel (CRIB), University Hospital Basel,Switzerland; GREAT network. (2)Department of Cardiology, University HospitalBasel, Switzerland; Cardiovascular Research Institute Basel (CRIB), UniversityHospital Basel, Switzerland. (3)GREAT network; Emergency department, HospitalClinic, Barcelona, Catalonia, Spain. (4)Department of Emergency Medicine,University Hospital Basel, Switzerland. (5)Department of Cardiology, UniversityHospital Basel, Switzerland; Cardiovascular Research Institute Basel (CRIB),University Hospital Basel, Switzerland; Department of Emergency Medicine,University Hospital Basel, Switzerland. (6)Department of Cardiology, UniversityHospital Basel, Switzerland; Cardiovascular Research Institute Basel (CRIB),University Hospital Basel, Switzerland; GREAT network. Electronic address:christian.mueller@usb.ch.
OBJECTIVE: The novel high-sensitivity cardiac troponin (hs-cTn) 0h/1h-algorithmsubstantially improves the early triage of patient's assigned "rule-out" or"rule-in" of acute myocardial infarction (AMI), while diagnostic uncertaintyremains in that 25-30% of patients assigned to "observe". We aimed to bettercharacterize these patients.METHODS: In a prospective multicenter diagnostic study, we applied the hs-cTnT0h/1h-algorithm in 2213 unselected patients presenting with symptoms suggestiveof AMI to the emergency department. The final diagnosis was adjudicated by twoindependent cardiologists using all available information. Survival at 720-dayswas the prognostic endpoint. Findings were validated using a hs-cTnI0h/1h-algorithm.RESULTS: Twenty-four percent (n=523) of patients were assigned to "observe" bythe hs-cTnT 0h/1h-algorithm. These patients differed significantly in multiplecharacteristics from "rule-out" and "rule-in" patients: they were older, in 75%male, and very often (57%) had pre-existing coronary artery disease (CAD).Diagnostic uncertainty for the presence of an AMI/UA was high. Only 39% ofpatients were suitable for coronary computed tomography angiography (CCTA). Themost common final adjudicated diagnoses were non-cardiac disease (38%),non-coronary cardiac disease (24%), unstable angina (UA, 21%), and AMI (15%).Absolute hs-cTnT-changes within 3h had the highest diagnostic accuracy for AMI(AUC 0.86). Cumulative 720-day survival rate was 86%, which was significantlylower as compared to "rule-out" (p<0.001) and comparable to "rule-in" (p=ns).Findings were similar for the hs-cTnI "observe" zone.CONCLUSION: "Observe" patients are typically elderly men with pre-existing CADand high long-term mortality. Absolute hs-cTn-changes within 3h, functionalstress imaging and coronary angiography are the key diagnostic modalities.
Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
DOI: 10.1016/j.ijcard.2016.01.112 PMID: 26808985  [PubMed - indexed for MEDLINE]

23. Clin Chem. 2016 Mar;62(3):494-504. doi: 10.1373/clinchem.2015.249508. Epub 2016Jan 21.
Two-Hour Algorithm for Triage toward Rule-Out and Rule-In of Acute MyocardialInfarction by Use of High-Sensitivity Cardiac Troponin I.
Boeddinghaus J(1), Reichlin T(2), Cullen L(3), Greenslade JH(3), Parsonage WA(4),Hammett C(5), Pickering JW(6), Hawkins T(3), Aldous S(7), Twerenbold R(2), Wildi K(8), Nestelberger T(1), Grimm K(1), Rubini-Gimenez M(2), Puelacher C(8), KernV(8), Rentsch K(9), Than M(7), Mueller C(10).
Author information: (1)Cardiovascular Research Institute Basel (CRIB), Department of Cardiology, and Department of Internal Medicine, University Hospital Basel, Basel, Switzerland;(2)Cardiovascular Research Institute Basel (CRIB), Department of Cardiology, and.(3)Department of Emergency Medicine, Royal Brisbane and Women's Hospital,Brisbane, Australia; School of Public Health, The Queensland University ofTechnology, Brisbane, Australia; (4)School of Public Health, The QueenslandUniversity of Technology, Brisbane, Australia; School of Medicine, The Universityof Queensland, Brisbane, Australia; (5)School of Medicine, The University ofQueensland, Brisbane, Australia; (6)Department of Medicine, University of Otago, Christchurch, New Zealand; Emergency Department, Christchurch Hospital,Christchurch, New Zealand; (7)Emergency Department, Christchurch Hospital,Christchurch, New Zealand; (8)Cardiovascular Research Institute Basel (CRIB).(9)Laboratory Medicine, University Hospital Basel, Basel, Switzerland.(10)Cardiovascular Research Institute Basel (CRIB), Department of Cardiology, andchristian.mueller@usb.ch.
BACKGROUND: The early triage of patients toward rule-out and rule-in of acutemyocardial infarction (AMI) is challenging. Therefore, we aimed to develop a 2-h algorithm that uses high-sensitivity cardiac troponin I (hs-cTnI).METHODS: We prospectively enrolled 1435 (derivation cohort) and 1194 (externalvalidation cohort) patients presenting with suspected AMI to the emergencydepartment. The final diagnosis was adjudicated by 2 independent cardiologists.hs-cTnI was measured at presentation and after 2 h in a blinded fashion. Wederived and validated a diagnostic algorithm incorporating hs-cTnI values atpresentation and absolute changes within the first 2 h.RESULTS: AMI was the final diagnosis in 17% of patients in the derivation and 13%in the validation cohort. The 2-h algorithm developed in the derivation cohortclassified 56% of patients as rule-out, 17% as rule-in, and 27% as observation.Resulting diagnostic sensitivity and negative predictive value (NPV) were 99.2%and 99.8% for rule-out; specificity and positive predictive value (PPV) were95.2% and 75.8% for rule-in. Applying the 2-h algorithm in the externalvalidation cohort, 60% of patients were classified as rule-out, 13% as rule-in,and 27% as observation. Diagnostic sensitivity and NPV were 98.7% and 99.7% forrule-out; specificity and PPV were 97.4% and 82.2% for rule-in. Thirty-daysurvival was 100% for rule-out patients in both cohorts.CONCLUSIONS: A simple algorithm incorporating hs-cTnI baseline values andabsolute 2-h changes allowed a triage toward safe rule-out or accurate rule-in ofAMI in the majority of patients.
© 2015 American Association for Clinical Chemistry.
DOI: 10.1373/clinchem.2015.249508 PMID: 26797687  [PubMed - indexed for MEDLINE]

24. Heart. 2016 Apr;102(8):610-6. doi: 10.1136/heartjnl-2015-308917. Epub 2016 Jan21.
Direct comparison of clinical decision limits for cardiac troponin T and I.
Kimenai DM(1), Henry RM(2), van der Kallen CJ(2), Dagnelie PC(3), Schram MT(2),Stehouwer CD(4), van Suijlen JD(5), Niens M(5), Bekers O(1), Sep SJ(2), SchaperNC(4), van Dieijen-Visser MP(1), Meex SJ(1).
Author information: (1)Department of Clinical Chemistry, Maastricht University Medical Centre (MUMC),Maastricht, The Netherlands Cardiovascular Research Institute Maastricht (CARIM),Maastricht University, Maastricht, The Netherlands. (2)Cardiovascular ResearchInstitute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands Department of Medicine, MUMC, Maastricht, The Netherlands. (3)CardiovascularResearch Institute Maastricht (CARIM), Maastricht University, Maastricht, TheNetherlands Department of Epidemiology, MUMC, Maastricht, The Netherlands School for Public Health and Primary Care (CAPHRI), Maastricht University, Maastricht,The Netherlands. (4)Cardiovascular Research Institute Maastricht (CARIM),Maastricht University, Maastricht, The Netherlands Department of Medicine, MUMC, Maastricht, The Netherlands School for Public Health and Primary Care (CAPHRI),Maastricht University, Maastricht, The Netherlands. (5)Department of ClinicalChemistry, Gelre Hospital, Apeldoorn, The Netherlands.
OBJECTIVE: The 99th percentile upper reference limit of high-sensitivity cardiac troponin (hs-cTn) from a healthy reference population is used for diagnosingacute myocardial infarction (AMI). Accepted current thresholds of hs-cTnT (Roche)and hs-cTnI (Abbott) are 14 and 26 ng/L, respectively. Since thresholds forhs-cTnT and hs-cTnI were derived from different reference cohorts it is unclearwhether they are biologically equivalent. We directly assessed sex-specific andage-specific 99th percentile upper reference limits of hs-cTnT and hs-cTnI in asingle reference cohort, to investigate whether current divergent thresholds ofhs-cTnT and hs-cTnI stem from intrinsic assay differences or reflect cohortvariation.METHODS: A healthy reference population was derived from a population-basedcohort (the Maastricht Study: n=3451; age: 40-75 years). Individuals withdiabetes mellitus, a history of cardiovascular disease, cardiac ischaemia on ECG,N-terminal pro-brain natriuretic peptide >125 ng/L or estimated glomerularfiltration rate <60 mL/min/1.73 m(2) were excluded. Non-parametric analyses were performed to assess 99th percentile upper reference limits.RESULTS: 1540 individuals were included in the healthy reference population (age 57±8 years, 52.4% women). Overall 99th percentile upper reference limits ofhs-cTnT and hs-cTnI were 15 and 13 ng/L, respectively. Upper reference limitswere higher in men than women (hs-cTnT: 16 vs 12 ng/L), (hs-cTnI: 20 vs 11 ng/L) and increased with age.CONCLUSIONS: Direct comparison reveals numerically similar thresholds for hs-cTnTand hs-cTnI assays. This finding is in line with recently reported underdiagnosisof AMI with the current decision limit of 26 ng/L for hs-cTnI, especially amongwomen. Downwards adjustment of the hs-cTnI threshold, differentiated for sex,would equalise clinical decision limits for both assays, and may prevent further underdiagnosis of AMI.
Published by the BMJ Publishing Group Limited. For permission to use (where notalready granted under a licence) please go tohttp://www.bmj.com/company/products-services/rights-and-licensing/
DOI: 10.1136/heartjnl-2015-308917 PMID: 26794233  [PubMed - indexed for MEDLINE]

25. Genet Mol Res. 2015 Dec 22;14(4):17959-65. doi: 10.4238/2015.December.22.21.
Clinical application of high-sensitivity cardiac troponin T test in acutemyocardial infarction diagnosis.
Wang JA(1), Qin Y(1), Lv J(1), Tian YF(1), Dong YJ(1).
Author information: (1)Department of Laboratory Medicine, Shandong Rizhao People's Hospital, Rizhao, China.
The aim of this study was to investigate the clinical application of ahigh-sensitivity cardiac troponin T (hs-cTnT) test in the diagnosis of acutemyocardial infarction (AMI). Serum levels of hs-cTnT and cardiac troponin I(cTnI) were detected in 240 AMI patients and 200 healthy donors and used to plot receiver operating characteristic (ROC) curves. A clinically applicablediagnostic cut-off value of hs-cTnT was determined from the ROC curve and thediagnostic accuracy of hs-cTnT and cTnI levels in AMI were compared.The serumhs-cTnT levels in the AMI group were higher than 0.014 ng/mL (the 99th percentileof the healthy population), among which hs-cTnT levels in patients withST-segment elevation myocardial infarction (STEMI) were higher than in patientswith non-STEMI (NSTEMI). The area under the ROC curve (AUC) for hs-cTnT wassignificantly higher than for cTnI, and the detection combining hs-cTnT andcreatine kinase isoenzyme (CK-MB) further increased the AUC. When 0.014 ng/mL wasset as the cut-off value for hs-cTnT, the diagnostic sensitivity for AMI reached 100% but the specificity was only 45.5%. The diagnostic ability of hs-cTnT forAMI peaked at a cut-off value of 0.035 ng/mL, resulting in the highest Youdenindex (0.654) and sensitivity and specificity values of 91.8 and 74.9%,respectively. The diagnostic utility of the hs-cTnT test for AMI is superior tothe traditional cTnI method. However, since hs-cTnT levels of non-AMI patientscan be over the diagnostic cut-off value, further studies are necessary to defineclinically applicable cut-off values of hs-cTnT.
DOI: 10.4238/2015.December.22.21 PMID: 26782442  [PubMed - indexed for MEDLINE]

26. Am J Med. 2016 Feb;129(2):e45. doi: 10.1016/j.amjmed.2015.10.005.
The Reply.
Mickley H(1).
Author information: (1)Odense University Hospital, Denmark.
Comment on    Am J Med. 2016 Feb;129(2):e43.    Am J Med. 2015 Aug;128(8):852-60.
DOI: 10.1016/j.amjmed.2015.10.005 PMID: 26777619  [PubMed - indexed for MEDLINE]

27. Am J Med. 2016 Feb;129(2):e43. doi: 10.1016/j.amjmed.2015.08.042.
Troponinemia: An Area That Still Needs to Be Explored.
Arunachalam K(1).
Author information: (1)Alpert Medical School of Brown University, Providence, RI.
Comment in    Am J Med. 2016 Feb;129(2):e45.
Comment on    Am J Med. 2015 Aug;128(8):852-60.
DOI: 10.1016/j.amjmed.2015.08.042 PMID: 26777618  [PubMed - indexed for MEDLINE]

28. Eur J Vasc Endovasc Surg. 2016 Apr;51(4):606-7. doi: 10.1016/j.ejvs.2015.11.018. Epub 2016 Jan 8.
Re: 'Clinical Relevance of Cardiac Troponin Assessment in Patients UndergoingCarotid Endarterectomy'.
Filis K(1), Vavuranakis M(2), Galyfos G(3).
Author information: (1)First Department of Propaedeutic Surgery, University of Athens Medical School,Hippocration Hospital, Athens, Greece. (2)First Department of Cardiology,University of Athens Medical School, Hippocration Hospital, Athens, Greece.(3)First Department of Propaedeutic Surgery, University of Athens Medical School,Hippocration Hospital, Athens, Greece. Electronic address:georgegalyfos@hotmail.com.
Comment in    Eur J Vasc Endovasc Surg. 2016 Apr;51(4):607.
Comment on    Eur J Vasc Endovasc Surg. 2016 Apr;51(4):473-80.
DOI: 10.1016/j.ejvs.2015.11.018 PMID: 26776707  [PubMed - indexed for MEDLINE]

29. Biosens Bioelectron. 2016 May 15;79:495-9. doi: 10.1016/j.bios.2015.12.083. Epub 2015 Dec 25.
Graphene quantum dots FRET based sensor for early detection of heart attack inhuman.
Bhatnagar D(1), Kumar V(2), Kumar A(3), Kaur I(4).
Author information: (1)CSIR-Central Scientific Instruments Organization, Sector 30-C, Chandigarh160030, India; CSIR-Institute of Genomics and Integrative Biology, Mall Road,Delhi 110007, India; Academy of Scientific and Innovative Research (AcSIR), NewDelhi, India. (2)CSIR-Central Scientific Instruments Organization, Sector 30-C,Chandigarh 160030, India; Academy of Scientific and Innovative Research (AcSIR), New Delhi, India. (3)CSIR-Institute of Genomics and Integrative Biology, MallRoad, Delhi 110007, India; Academy of Scientific and Innovative Research (AcSIR),New Delhi, India. Electronic address: ashokigib@rediffmail.com. (4)CSIR-CentralScientific Instruments Organization, Sector 30-C, Chandigarh 160030, India;Academy of Scientific and Innovative Research (AcSIR), New Delhi, India.Electronic address: inderpreety@yahoo.co.in.
Cardiac immunosensor for early detection of heart attack (myocardial infarction) was developed using amine functionalized graphene quantum dots (afGQDs)conjugated with antibody anti-cardiac Troponin I (anti-cTnI) to detect cardiacmarker antigen Troponin I (cTnI) in blood based on fluorescence resonance energy transfer (FRET) between conjugate and graphene (quencher) only in 10 min. Theanti-cTnI was covalently conjugated to afGQDs through carbodiimide couplingreaction. The conjugate was characterized by zeta potential UV-vis spectroscopyand field emission scanning electron microscopy (FESEM). The sensing performance of the sensor was studied with respect to changes in the photon count andphotoluminescence of GQDs based on interaction of target cTnI with its specificanti-cTnI antibody. The sensor is highly specific and shows negligible responseto non-specific antigens. The sensor displayed a linear response to cTnI from0.001 to 1000 ng mL(-1) with a limit of detection of 0.192 pg mL(-1).
Copyright © 2015 Elsevier B.V. All rights reserved.
DOI: 10.1016/j.bios.2015.12.083 PMID: 26748366  [PubMed - indexed for MEDLINE]

30. Microvasc Res. 2016 May;105:34-9. doi: 10.1016/j.mvr.2015.12.010. Epub 2015 Dec22.
Endothelial dysfunction evaluated by peripheral arterial tonometry is relatedwith peak TnI values in patients with ST elevation myocardial infarction treated with primary angioplasty.
Baptista SB(1), Faustino M(2), Simões J(3), Nédio M(3), Monteiro C(3), LourençoE(3), Leal P(3), Farto eAbreu P(3), Gil V(3).
Author information: (1)Cardiology Department, Hospital Fernando Fonseca, Amadora, Portugal.Electronic address: sergio.b.baptista@gmail.com. (2)Cardiology Department,Hospital Fernando Fonseca, Amadora, Portugal. Electronic address:marianafaustino85@gmail.com. (3)Cardiology Department, Hospital Fernando Fonseca,Amadora, Portugal.
PURPOSE: The role of endothelial-dependent function in patients with acute STelevation myocardial infarction (STEMI) is not clear. Endothelial dysfunction maycontribute to the pathophysiological processes occurring after STEMI andinfluence the extension of myocardial necrosis. Endothelial-dependent dysfunctionevaluated by peripheral arterial tonometry (PAT) has already showed to becorrelated with microvascular coronary endothelial dysfunction. Our purpose wasto evaluate the impact of endothelial dysfunction on peak Troponin I (TnI)values, as a surrogate for the extension of myocardial infarction, in patientswith STEMI treated with primary angioplasty (P-PCI).METHODS: 58 patients with STEMI treated with P-PCI (mean age 59.0 ± 14.0 years,46 males) were included. Endothelial function was assessed by reactive hyperaemiaindex (RHI) determined by PAT. Patients were divided in two groups according tothe previously reported RHI threshold for high risk (1.67). The extension ofmyocardial necrosis was evaluated by peak TnI levels.RESULTS: RHI median value was 1.78 (IQR0.74);25 patients had endothelialdysfunction (RHI b 1.67). The two groups had no significant differences in age,gender, main risk factors and pain-to-balloon time. Patients with an RHI b 1.67had significant larger infarcts: TnI 73.5 ng/mL (IQR 114.42 ng/mL) versus TnI33.2 ng/mL (IQR 65.2 ng/mL); p = 0.028. On multivariate analysis, the presence ofan RHI b 1.67 kept significant impact on TnI peak values (p=0.02).CONCLUSIONS: The presence of endothelial-dependent dysfunction, assessed by PAT, is related with higher peak TnI values in STEMI patients treated with P-PCI.These results strength the possibility that endothelial-dependent dysfunction maybe a marker of poor prognosis and eventually a therapeutic target in patientswith STEMI.
DOI: 10.1016/j.mvr.2015.12.010 PMID: 26721522  [PubMed - indexed for MEDLINE]

31. Arch Pathol Lab Med. 2016 Jan;140(1):75-80. doi: 10.5858/arpa.2014-0580-OA.
Diagnosis of Acute Myocardial Infarction in Hemodialysis Patients WithHigh-Sensitivity Cardiac Troponin T Assay.
Huang HL(1), Zhu S, Wang WQ, Nie X, Shi YY, He Y, Song HL, Miao Q, Fu P, Wang LL,Li GX.
Author information: (1)From the Departments of Laboratory Medicine (Drs Li and Wang L-L; Mss Huang,Wang W-Q, Nie, He, and Song; and Messrs Zhu and Miao) and Nephrology (Drs Shi andFu), West China Hospital, Sichuan University, Chengdu, China.
CONTEXT: Cardiac troponins have become the gold standard for diagnosing acutemyocardial infarction (AMI) in the general population; however, their diagnostic accuracy for hemodialysis (HD) patients presenting with chest pain or dyspnea is uncertain.OBJECTIVE: To examine the diagnostic accuracy of high-sensitivity cardiactroponin T (hs-cTnT) assay for AMI in HD patients.DESIGN: In this prospective study, we enrolled 670 consecutive stable HD patientspresenting with chest pain or dyspnea on routine predialysis therapy in thenephrology department. Receiver operating characteristic (ROC) curves were usedto examine the diagnostic accuracy of hs-cTnT levels at enrollment in HD patientspresenting with chest pain or dyspnea, and the dynamic change in these levelsafter 3 hours.RESULTS: Acute myocardial infarction was the adjudicated final diagnosis in 12%of HD patients. Among patients with a final diagnosis other than AMI, 97% had aplasma hs-cTnT concentration above the 99th percentile. At the time ofenrollment, the area under the ROC curve of hs-cTnT levels for diagnosis of AMIwas 0.68 (95% confidence interval [CI], 0.62-0.74; P < .001) with a cutoff value of 107.7 ng/L; the relative change after 3 hours was 0.90 (95% CI, 0.82-0.96, P <.001) with a cutoff value of 24%, and the absolute change was 0.88 (95% CI,0.82-0.94, P < .001) with a cutoff value of 32.6 ng/L. The prognostic value for40-day mortality varied with the magnitude of elevation in hs-cTnT levels.CONCLUSIONS: Tracking the dynamic change in hs-cTnT levels during the short term significantly increased this measure's diagnostic accuracy for AMI in HDpatients.
DOI: 10.5858/arpa.2014-0580-OA PMID: 26717058  [PubMed - indexed for MEDLINE]

32. Am Heart J. 2016 Jan;171(1):92-102.e1-5. doi: 10.1016/j.ahj.2015.07.022. Epub2015 Jul 26.
One-hour rule-in and rule-out of acute myocardial infarction usinghigh-sensitivity cardiac troponin I.
Jaeger C(1), Wildi K(1), Twerenbold R(1), Reichlin T(1), Rubini Gimenez M(2),Neuhaus JD(1), Grimm K(1), Boeddinghaus J(1), Hillinger P(1), Nestelberger T(1), Singeisen H(1), Gugala M(1), Pretre G(1), Puelacher C(1), Wagener M(1), Honegger U(3), Schumacher C(3), Moreno Weidmann Z(1), Kreutzinger P(1), Krivoshei L(1),Freese M(1), Stelzig C(1), Dietsche S(3), Ernst S(4), Rentsch K(5), Osswald S(6),Mueller C(7).
Author information: (1)Department of Cardiology, University Hospital, Basel, Switzerland;Cardiovascular Research Institute Basel (CRIB), University Hospital, Basel,Switzerland. (2)Department of Cardiology, University Hospital, Basel,Switzerland; Cardiovascular Research Institute Basel (CRIB), University Hospital,Basel, Switzerland; Servicio de Urgencias y Pneumologia, CIBERES ISC III,Hospital del Mar-Institut Municipal d'Investigació Mèdica, Barcelona, Spain.(3)Cardiovascular Research Institute Basel (CRIB), University Hospital, Basel,Switzerland. (4)Department of Internal Medicine, Kantonsspital, Olten,Switzerland. (5)Laboratory Medicine, University Hospital, Basel, Switzerland.(6)Department of Cardiology, University Hospital, Basel, Switzerland.(7)Department of Cardiology, University Hospital, Basel, Switzerland;Cardiovascular Research Institute Basel (CRIB), University Hospital, Basel,Switzerland. Electronic address: Christian.Mueller@usb.ch.
We aimed to prospectively derive and validate a novel 0-/1-hour algorithm usinghigh-sensitivity cardiac troponin I (hs-cTnI) for the early "rule-out" and"rule-in" of acute myocardial infarction (AMI).METHODS: In a prospectivemulticenter diagnostic study, we enrolled 1,500 patients presenting withsuspected AMI to the emergency department. The final diagnosis was centrallyadjudicated by 2 independent cardiologists blinded to hs-cTnI concentrations. Thehs-cTnI (Siemens Vista) 0-/1-hour algorithm incorporated measurements performedat baseline and absolute changes within 1 hour, was derived in the first 750patients (derivation cohort), and then validated in the second 750 (validationcohort).RESULTS: Overall, AMI was the final diagnosis in 16% of patients. Applying thehs-cTnI 0-/1-hour algorithm developed in the derivation cohort to the validation cohort, 57% of patients could be classified as "rule-out"; 10%, as "rule-in"; and33%, as "observe." In the validation cohort, the sensitivity and the negativepredictive value for AMI in the "rule-out" zone were 100% (95% CI 96%-100%) and100% (95% CI 99%-100%), respectively. The specificity and the positive predictivevalue (PPV) for AMI in the "rule-in" zone were 96% (95% CI 94%-97%) and 70% (95% CI 60%-79%), respectively. Negative predictive value and positive predictivevalue of the 0-/1-hour algorithm were higher compared to the standard of carecombining hs-cTnI with the electrocardiogram (both P < .001).CONCLUSION: The hs-cTnI 0-/1-hour algorithm performs very well for early rule-outas well as rule-in of AMI. The clinical implications are that used in conjunctionwith all other clinical information, the 0-/1-hour algorithm will be a safe andeffective approach to substantially reduce time to diagnosis.
Copyright © 2015 Elsevier Inc. All rights reserved.
DOI: 10.1016/j.ahj.2015.07.022 PMID: 26699605  [PubMed - indexed for MEDLINE]

33. Talanta. 2016 Jan 1;146:823-30. doi: 10.1016/j.talanta.2015.06.006. Epub 2015 Jun7.
SPR detection of cardiac troponin T for acute myocardial infarction.
Pawula M(1), Altintas Z(1), Tothill IE(2).
Author information: (1)Cranfield University, Cranfield, Bedfordshire, MK43 0AL England, UK.(2)Cranfield University, Cranfield, Bedfordshire, MK43 0AL England, UK.Electronic address: i.tothill@cranfield.ac.uk.
A surface plasmon resonance (SPR) sensor developed for the rapid, sensitive andspecific detection of cardiac troponin T (cTnT) in serum samples is reported inthis work. An extensive optimisation of assay parameters was conducted to achieveoptimal detection strategy. Both direct and sandwich immunoassay formats wereinvestigated and optimised. The response obtained was enhanced further by the useof gold nanoparticles (AuNPs) conjugated to the anti-cTnT detection antibody. Aregeneration method was developed to enable the reuse of the SPR sensor formultiple sample application. The SPR immunosensor showed good reproducibility forcTnT detection in the concentration range of 25-1000 ng mL(-1) and 5-400 ngmL(-1) for the direct and sandwich assays in buffer, respectively. The linearregression analysis was performed and R(2) value was found as 0.99 for bothassays. In order to optimise the sensor for serum analysis, nonspecific bindingof serum proteins was reduced through the use of additives in the dilutionbuffer. To achieve greater sensitivity, the performance of the cTnT immunosensor sandwich assay in human serum was evaluated using non-modified and AuNP modified detector antibodies. A detection limit (LOD) for the immunosensor in 50% serumwas assessed as 5 ng mL(-1) cTnT for the standard sandwich assay and 0.5 ngmL(-1) cTnT when using AuNP conjugated detector antibodies with a linear dynamic range of 0.5-40 ng mL(-1). The dissociation constant was found as 3.28 × 10(-9) Musing Langmuir binding model which indicates high affinity between cTnT and itsantibody. The proposed SPR immunosensor has a promising potential to be developedfor point-of-care testing for the early diagnosis of acute myocardial infarction (AMI). This method can also be used for the rapid detection of biomarkers incentral nervous system diseases.
Copyright © 2015 Elsevier B.V. All rights reserved.
DOI: 10.1016/j.talanta.2015.06.006 PMID: 26695335  [PubMed - indexed for MEDLINE]

34. J Med Assoc Thai. 2015 Oct;98(10):935-41.
CK-MB Activity, Any Additional Benefit to Negative Troponin in EvaluatingPatients with Suspected Acute Myocardial Infarction in the Emergency Department.
Jaruvongvanich V, Rattanadech W, Damkerngsuntorn W, Jaruvongvanich S,Vorasettakarnkij Y.
BACKGROUND: Coronary heart disease is now the leading cause of death. Diagnosing myocardial infraction (MI) needs cardiac marker in case of equivocal clinicalpresentations and EKG interpretations. Troponin yields high sensitivity andspecificity and could be used as a single screening assay. However, in actualpractice, clinicians send CK-MB activity (CKMBa) as a combined marker with anexpectation of providing additional diagnostic value due to large historicaldata. Discordant results from both markers lead to unclear management. Our study was to determine whether CKMBa has potential benefit for initial screening of MI in addition to cardiac troponin T (cTpT) in the Emergency Department (ED), andcan this marker be safely removed from the routine laboratory panel in theemergency setting in Thailand.MATERIAL AND METHOD: We conducted a retrospective cohort single-center study toexamine the usefulness of CKMBa in the ED from 907 patients who presented withclinically suspected acute M, and investigated with both biomarkers (CKMBa andcTpT). In these patients, 97 patients were included in the final analysis as theyhad negative cTpT associated with positive CKMBa or CKMBa turned to be positivewithin 24 hours after serial biomarkers measurements. The outcome was assessed bythe final diagnosis, the cause of death if patients died during admission, andthe 180-day mortality from medical chart review. In patients highly suspectedfor MI, further investigations were done including echocardiogram, exercise stresstest, and coronay angiogram by experienced cardiologists.RESULTS: During the studyperiod, cTpTwere sent 1,772 times and most (95.2%) ofthesamples were associated with CKMBa results. The outcome showed that no one withnegative cTpT was diagnosed as MI on a discharge diagnosis. Fourteen patientsdied during admission. The definitive cause was not defined as MI. The 180-daymortality was zero. During the follow-up, there was no MI suspected issues thatneeded further cardiac evaluations. The positive predictive value of CKMBa withnegative cTpT was 0% (95% CI, 0-0.047).CONCLUSION: CKMBa added no benefit to cTpT in diagnosing acute MI in ED. RemovingCKMBa from emergency panel could be considered.

PMID: 26638584  [PubMed - indexed for MEDLINE]

35. Can J Anaesth. 2016 Feb;63(2):227-32. doi: 10.1007/s12630-015-0539-0. Epub 2015Dec 3.
Chasing myocardial outcomes: perioperative myocardial infarction and cardiactroponin.
Royo MB(1), Fleisher LA(2,)(3).
Author information: (1)Department of Anesthesiology and Critical Care, Perelman School of Medicine,University of Pennsylvania, 310 Blockley Hall, 423 Guardian Drive, Philadelphia, PA, 19104-4865, USA. Marc.Royo@uphs.upenn.edu. (2)Department of Anesthesiologyand Critical Care, Perelman School of Medicine, University of Pennsylvania, 310Blockley Hall, 423 Guardian Drive, Philadelphia, PA, 19104-4865, USA. (3)SeniorScholar Leonard Davis Institute, University of Pennsylvania, Philadelphia, PA,USA.
Perioperative myocardial infarction represents the most common cardiovascularcomplication following non-cardiac surgery, but frequently presents without theusual clinical signs and