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Búsqueda Bibliográfica: hs-Troponina (2015-2016)
1. Bratisl Lek Listy. 2016;117(8):442-7.
Parathyroid hormone is associated with heart failure with preserved ejectionfraction.
Bezgin T, Elveran A, Karagoz A, Canga Y, Dogan C.
BACKGROUND: Parathyroid hormone (PTH) is a novel promising biomarker that canpredict hospitalization, functional status and mortality in patients who sufferedheart failure with preserved ejection fraction (HFpEF).OBJECTIVE: We aimed to investigate the association of serum PTH levels andmeasures of disease severity (NYHA functional class, NT-proBNP, CRP, EF, TroponinI) in patients with HFpEF.METHODS: A total of consecutive 58 outpatients with HFpEF and 30 controls wereprospectively studied. All patients underwent laboratory tests, includingNT-proBNP and PTH analyses.RESULTS: PTH, NT-proBNP, troponin I, and CRP levels were significantly higher in patients with HFpEF when compared with control group (54.61 ± 31.02 vs 40.40 ±14.22 pg/ml, p < 0.05; 126.05 ± 162.94 vs 44.57 ± 14.95 pg/ml, p < 0.01; 0.011 ± 0.013 vs 0.004 ± 0.001 ug/L, p < 0.01; 4.65 ± 4.24 vs 1.63 ± 0.97 mg/L, p < 0.01,respectively). Left atrium was found to be more enlarged in HFpEF patients (LAVI = 36 ± 18 vs 28 ± 11 ml/m², p < 0.01). Most indices of left ventricular diastolicfunction were more severely impaired compared to controls (p < 0.05). There wasno correlation between PTH and CRP, troponin I, LVMI, LV volumes, LV diameters,E/E', age, and BMI in both groups (p = NS). There was strong positive correlationbetween PTH and NT-proBNP levels in all study participants (r = 0.359; p < 0.01).CONCLUSION: PTH together with other markers of heart failure may provide valuableinformation both in the diagnosis and staging of heart failure syndromes (Tab. 4,Fig. 1, Ref. 40).
PMID: 27546695 [PubMed - indexed for MEDLINE]
2. Rev Fac Cien Med Univ Nac Cordoba. 2016;73(1):8-14.
[High sensitivity T troponin and CA-125 as prognostic biomarkers in patients withend stage renal disease in hemodialysis].
[Article in Spanish]
Moreno JS(1), Lépori AJ(1), Novoa P(2), De Elia R(3), Guglielmone R(3), BonoJP(1).
Author information: (1)Servicio de Cardiología, Sanatorio Allende Nueva Córdoba, Córdoba, Argentina. (2)Servicio de Nefrología, Sanatorio Allende Nueva Córdoba, Córdoba, Argentina.(3)Laboratorio central, Sanatorio Allende Nueva Córdoba, Córdoba, Argentina.
INTRODUCTION: The end stage renal disease confers a high morbidity and mortality risk, mainly due to cardiovascular disease. The cardiac T troponin andcarbohydrate antigen-125 (CA-125) are useful biomarkers to determinecardiovascular prognosis in order to start preventive treatment in the high risk patients.METHODS: We included patients with end stage renal disease in hemodialysistreatment. Plasma high sensitivity cardiac T troponin (hs-TNT) and CA-125 weremeasured at the beginning of follow up. The patients with clinical evidence of anacute myocardial infarction were excluded. Twelve month after the measurement of the biomarkers the patients were called to assess the occurrence of major adversecardiovascular events (MACE) and hospitalizations for any reason.RESULTS: Eighty seven patients were included. The mean age was 58ï‚±15 years, and76% were male. The hs-TNT was elevated in 95.4% of the patients and the medianvalue was 49 ng/l (15.3 - 214.1). CA-125 median value was 13.7 U/ml (6.1 - 52.7).The patients that presented a MACE had higher CA-125 (p< 0.03) and hs-TNT (p<0.001); and all of them had a troponin value ≥ 69.37 ng/l.CONCLUSIONS: The prevalence of high hs-TNT was 95.4% and of CA-125 10%. MACE weresignificantly higher in patients with elevated biomarkers, conferring themprognostic utility in this group of patients.
PMID: 27419890 [PubMed - indexed for MEDLINE]
3. Biochem Med (Zagreb). 2016;26(2):233-9. doi: 10.11613/BM.2016.025.
Recovery of spiked troponin I in four routine assays.
Loh TP(1), Lim XC(1), Kieu K(1), Sajiir H(1), Neo SF(1), Cheng WL(1), SethiSK(1).
Author information: (1)Department of Laboratory Medicine, National University Hospital, Singapore,Singapore.
INTRODUCTION: This study aimed to examine the recovery of spiked human cardiactroponin I (cTnI) results measured by four routine assays, and investigatepossible interference from microclots.MATERIALS AND METHODS: 457 consecutive samples with cTnI concentration belowlimit of quantitation (12 ng/L), declared by the Vitros TnI ES assay (referenceassay), were measured on Beckman Coulter Accu TnI+3, Siemens TnI-Ultra and Roche TnI STAT assays. These samples were enriched with native full-length cTnI to aconcentration of 100 ng/L and retested. A post-spiking result that exceeded thecritical difference at a predefined probability of 0.0005 of the targetconcentration (the median post-spiking result for each individual assay) wasconsidered as outlier. To determine whether microclots were a significant causeof critically discrepant outlier results, a separate 50 samples were centrifuged twice between two post-spiking measurements using the Vitros TnI ES assay.RESULTS: The median recovery of the enriched cTnI was highest with the Rocheassay (271 ng/L) and lowest with the Vitros assay (29 ng/L). The Vitros assay hadthe highest percentage of results that exceeded the critical difference (49%),followed by the Siemens (38%), Roche (18%) and Beckman Coulter (7%) assays. None of the 50 additional samples produced a critically lower cTnI result afterre-centrifugation.CONCLUSIONS: Our findings underscored the variability of cTnI assays in measuringnative cTnI. The lack of cTnI results that became significantly lower afterre-centrifugation suggested that microclots are unlikely to be a major cause ofthe outlier results.
DOI: 10.11613/BM.2016.025 PMCID: PMC4910266PMID: 27346968 [PubMed - indexed for MEDLINE]
4. 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]
5. Lancet. 2016 Jun 4;387(10035):2289. doi: 10.1016/S0140-6736(16)30686-9.
Measurement of cardiac troponin for exclusion of myocardial infarction.
Author information: (1)Department of Surgery, Jikei University School of Medicine, Tokyo, Japan.Electronic address: email@example.com.
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]
6. 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: firstname.lastname@example.org.(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]
7. 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]
8. 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: email@example.com.
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]
9. 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:firstname.lastname@example.org. (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]
10. 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]
11. Clin Lab. 2016;62(4):743-8.
High-Sensitivity Cardiac Troponin T: a Preanalytical Evaluation.
Michel M, Mestari F, Alkouri R, Atlan Grégory, Dever S, Devilliers C,Imbert-Bismut F, Bonnefont-Rousselot D, Monneret D.
BACKGROUND: Little is known about the effects of preanalytical conditions onhigh-sensitivity cardiac troponin T (hs-cTnT) concentrations.METHODS: Variations of hs-cTnT concentrations were evaluated under the following preanalytical conditions: 1) serum vs. lithium-heparin (Li-Hep) plasma, with orwithout separator gel; 2) centrifugation time (15-minutes vs. 10-minutes) andspeed (1467 to 3756 g); 3) stability in Li-Hep plasma at room temperature and +4 degrees C for 4 days and at -80 degrees C for up to 12 months, for threeconcentrations; 4) four freeze-thaw cycles at -20 degrees C and -80 degrees C,for three concentrations.RESULTS: No significant changes were found regarding the type of blood collectiontube, the centrifugation, and storage conditions. Minor decreases were observedafter four freeze-thaw cycles at -20 degrees C (< 6.5%) and -80 degrees C (<3.4%).CONCLUSIONS: High-sensitivity cardiac troponin T may be considered as notimpacted by usual preanalytical conditions, thus strengthening its reliability inlaboratory practice and clinical research.
PMID: 27215098 [PubMed - indexed for MEDLINE]
12. Clin Lab. 2016;62(4):739-42.
Performance Evaluation of the FREND Cardiac Triple Cartridge on the FREND System.
Lee K, Han M, Song SH, Park KU, Song WH, Song J.
BACKGROUND: We evaluated the performance of the FREND Cardiac Triple cartridge onthe FREND system in the detection of cardiac markers-myoglobin, cardiac troponin I (cTnI), and creatine kinase-MB (CK-MB).METHODS: Quantitative immunoassays were performed using the FREND system(NanoEnTek, Seoul, Korea) and its cartridge. The precision, detection limits,linearity, and correlation with the Siemens Dimension Vista 500 (SiemensHealthcare Diagnostics, Deerfield, IL, USA) were evaluated. The cutoff value for each marker was calculated in healthy individuals (men and women, n = 138 each).RESULTS: The coefficients of variation for imprecision were less than 19.0% atlow and high serum concentrations. The lower limits of quantification formyoglobin, cTnI, and CK-MB were 3.11, 0.073, and 0.70 ng/mL, respectively.Acceptable linearity was achieved for each marker (R2 < 0.99). The results fromthe FREND system were in good agreement with those from the Siemens DimensionVista (correlation coefficients > 0.9). The cutoff values in male and femaleindividuals (n = 138 each) were 104.3 and 98.9 ng/mL, respectively, formyoglobin, and 4.35 and 5.37 ng/mL, respectively, for CK-MB. The cutoff value forcTnI was 0.073 ng/mL.CONCLUSIONS: The FREND Cardiac Triple cartridge exhibited good precision,clinically acceptable linearity, and reliable correlation with the DimensionVista.
PMID: 27215097 [PubMed - indexed for MEDLINE]
13. Clin Lab. 2016;62(4):705-9.
The Influence of Blood Collection Tubes on Measurement of Cardiac Biomarkers.
Lan H, Du W, Mo Z, Huang H.
BACKGROUND: The tube used to collect a blood specimen may have an effect on some test results. This study evaluated three different types of blood collectiontubes manufactured in China for use in testing three cardiac biomarkers.METHODS: Blood samples were drawn from 42 patients in the Intensive Care Unit andwere sampled into three different types of blood collection tubes at the sametime. All samples were subjected to analysis of myoglobin (MYO), creatine kinase MB (CK-MB), and high-sensitive cardiac troponin T (hs-cTnT) using the Roche Cobase411 chemistry analyzer.RESULTS: There was no statistically significant difference in the test resultsfor MYO and CK-MB among the three different types of blood collection tubes.However, there was a statistically significant difference in the measured levelof hs-cTnT. The hs-cTnT values in tubes with clot activator were significantlylower than the values from tubes with no additive (p = 0.000) or lithium heparin (p = 0.002).CONCLUSIONS: Three types of blood collection tubes are safe for myoglobin andCK-MB determination without altering the results. However, the hs-cTnT value was lower in clot activator tubes than in tubes with no additive or with heparinlithium. Thus, we conclude that using clot activator tubes can affect thedetermination of hs-cTnT concentration which should be noted in clinicalpractice.
PMID: 27215091 [PubMed - indexed for MEDLINE]
14. BMC Cardiovasc Disord. 2016 May 4;16:79. doi: 10.1186/s12872-016-0255-x.
Troponin I levels in permanent atrial fibrillation-impact of rate control andexercise testing.
Horjen AW(1,)(2), Ulimoen SR(3), Enger S(3), Norseth J(4), Seljeflot I(5,)(6),Arnesen H(5,)(6), Tveit A(3).
Author information: (1)Department of Medical Research, Baerum Hospital, Vestre Viken Hospital Trust, N-3004, Drammen, Norway. email@example.com. (2)Faculty of Medicine, Universityof Oslo, Oslo, Norway. firstname.lastname@example.org. (3)Department of Medical Research,Baerum Hospital, Vestre Viken Hospital Trust, N-3004, Drammen, Norway. (4)Clinic for Medical Diagnostics, Vestre Viken Hospital Trust, Drammen, Norway. (5)Facultyof Medicine, University of Oslo, Oslo, Norway. (6)Center for Clinical HeartResearch, Department of Cardiology, Oslo University Hospital Ullevål, Oslo,Norway.
BACKGROUND: High-sensitivity troponin I (hs-TnI) and troponin T (hs-TnT) aremoderately correlated and independently related to outcome in atrial fibrillation(AF). Rate controlling therapy has been shown to reduce hs-TnT, however thepotential impact on hs-TnI levels, and whether this differs from the effects onhs-TnT, has not been investigated previously.METHODS: Sixty patients with stable, permanent AF without heart failure or known ischemic heart disease were included in a randomised crossover study (mean age 71± 9 years, 18 women). Diltiazem 360 mg, verapamil 240 mg, metoprolol 100 mg, and carvedilol 25 mg were administered once daily for three weeks, in a randomisedsequence. At baseline and on the last day of each treatment period, hs-TnI wasmeasured at rest and after a maximal exercise test and compared to hs-TnT.RESULTS: Hs-TnI and hs-TnT correlated moderately at baseline (rs = 0.582, p <0.001). All drugs reduced both the resting and the peak exercise levels of hs-TnIcompared with baseline (p < 0.001 for all). The decline in resting hs-TnI andhs-TnT values relative to baseline levels was similar for all drugs except forverapamil, which reduced hs-TnI more than hs-TnT (p = 0.017). Levels of hs-TnIincreased significantly in response to exercise testing at baseline and at alltreatment regimens (p < 0.001 for all). The relative exercise-induced increase inhs-TnI was significantly larger compared to hs-TnT at baseline (p < 0.001), ondiltiazem (p < 0.001) and on verapamil (p = 0.001).CONCLUSIONS: In our population of stable, permanent AF patients, all four ratecontrol drug regimens reduced hs-TnI significantly, both at rest and duringexercise. The decline in hs-TnI and hs-TnT levels associated with beta-blockerand calcium channel blocker treatment was similar, except for a larger relativedecrease in hs-TnI levels following verapamil treatment.TRIAL REGISTRATION: www.clinicaltrials.gov ( NCT00313157 ).
DOI: 10.1186/s12872-016-0255-x PMCID: PMC4855853PMID: 27142292 [PubMed - indexed for MEDLINE]
15. PLoS One. 2016 Apr 20;11(4):e0153300. doi: 10.1371/journal.pone.0153300.eCollection 2016.
High-Sensitivity Cardiac Troponin Concentrations in Patients with ChestDiscomfort: Is It the Heart or the Kidneys As Well?
Cardinaels EP(1), Altintas S(2), Versteylen MO(2), Joosen IA(2), Jellema LJ(3),Wildberger JE(4), Das M(4), Crijns HJ(2), Bekers O(1), van Dieijen-Visser MP(1), Kietselaer BL(2,)(4), Mingels AM(1).
Author information: (1)Central Diagnostic Laboratory, Department of Clinical Chemistry,Cardiovascular Research Institute Maastricht (CARIM), Maastricht UniversityMedical Center (MUMC+), Maastricht, the Netherlands. (2)Department of Cardiology,CARIM, MUMC+, Maastricht, the Netherlands. (3)Department of Clinical Chemistryand Hematology, Gelre Hospitals, Apeldoorn, the Netherlands. (4)Department ofRadiology, CARIM, MUMC+, Maastricht, the Netherlands.
BACKGROUND: High-sensitivity cardiac troponins (hs-cTn) are the preferredbiomarkers to detect myocardial injury, making them promising risk-stratifyingtools for patients with symptoms of chest pain. However, circulating hs-cTn arealso elevated in other conditions like renal dysfunction, complicatingappropriate interpretation of low-level hs-cTn concentrations.METHODS: A cross-sectional analysis was performed in 1864 patients with symptoms of chest discomfort from the cardiology outpatient department who underwentcardiac computed tomographic angiography (CCTA). Serum samples were analyzedusing hs-cTnT and hs-cTnI assays. Renal function was measured by the estimatedglomerular filtration rate (eGFR), established from serum creatinine and cystatinC. On follow-up, the incidence of adverse events was assessed.RESULTS: Median hs-cTnT and hs-cTnI concentrations were 7.2(5.8-9.2) ng/L and2.6(1.8-4.1) ng/L, respectively. Multivariable regression analysis revealed that both assay results were more strongly associated with eGFR(hs-cTnT:stβ:-0.290;hs-cTnI:stβ:-0.222) than with cardiac imaging parameters,such as coronary calcium score, CCTA plaque severity score and left ventricularmass (all p<0.01). Furthermore, survival analysis indicated lower relative risks in patients with normal compared to reduced renal function for hs-cTnT[HR(95%CI), 1.02(1.00-1.03) compared to 1.07(1.05-1.09)] and hs-cTnI[1.01(1.00-1.01) compared to 1.02(1.01-1.02)] (all p<0.001).CONCLUSION: In patients with chest discomfort, we identified an independentinfluence of renal function on hs-cTn concentrations besides CAD, that affectedthe association of hs-cTn concentrations with adverse events. Estimating renalfunction is therefore warranted when interpreting baseline hs-cTn concentrations.
DOI: 10.1371/journal.pone.0153300 PMCID: PMC4838230PMID: 27096420 [PubMed - indexed for MEDLINE]
16. PLoS One. 2016 Apr 14;11(4):e0153492. doi: 10.1371/journal.pone.0153492.eCollection 2016.
Cardiac Troponin Is a Predictor of Septic Shock Mortality in Cancer Patients inan Emergency Department: A Retrospective Cohort Study.
Yang Z(1,)(2), Qdaisat A(1), Hu Z(1,)(3), Wagar EA(4), Reyes-Gibby C(1), MengQH(4), Yeung SC(1,)(5).
Author information: (1)Department of Emergency Medicine, The University of Texas MD Anderson CancerCenter, 1515 Holcombe Blvd., Houston, Texas 77030, United States of America.(2)Department of Intensive Care, Guangzhou First People's Hospital, GuangzhouMedical University, 1 Panfu Road, Guangdong, People's Republic of China.(3)Department of Medical Oncology, Sun Yat-sen University Cancer Center, 651Dongfeng East Rd., West F16, Guangzhou, Guangdong 510060, People's Republic ofChina. (4)Laboratory Medicine, The University of Texas MD Anderson Cancer Center,1515 Holcombe Blvd., Houston, Texas 77030, United States of America.(5)Department of Endocrine Neoplasia and Hormonal Disorders, The University ofTexas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, Texas 77030,United States of America.
BACKGROUND: Septic shock may be associated with myocardial damage; however, theprognostic value of cardiac enzymes in cancer patients with septic shock isunknown. In this study, we evaluated the prognostic significance of cardiacenzymes in combination with established prognostic factors in predicting the7-day mortality rate of patients with septic shock, and we constructed a newscoring system, Septic Oncologic Patients in Emergency Department (SOPED), which includes cardiac enzymes, to predict 7-day mortality rates.METHODS AND FINDINGS: We performed a retrospective cohort study of 375 adultcancer patients with septic shock who visited the emergency department of acomprehensive cancer center between 01/01/2004 and 12/31/2013. The 7-day and28-day mortality rates were 19.7% and 37.6%, respectively. The creatine kinasemyocardial band fraction and troponin-I were significantly higher in patients whodied in ≤7 days and ≤28 days than in those who did not. In Cox regression models,troponin-I >0.05 ng/mL plus Predisposition, Infection, Response, and OrganFailure (PIRO2011) or Mortality in Emergency Department Sepsis (MEDS) score was asignificant predictor of survival for ≤7 days. With our new SOPED scoring system,the receiver operating characteristic area under the curve was 0.836, higher thanthose for PIRO2011 and MEDS.CONCLUSIONS: Troponin-I >0.05 ng/mL was an important predictor of short-termmortality (≤7 days). The SOPED scoring system, which incorporated troponin-I, wasmore prognostically accurate than were other scores for 7-day mortality. Largemulticenter studies are needed to verify our results and prospectively validatethe prognostic performance of the SOPED score.
DOI: 10.1371/journal.pone.0153492 PMCID: PMC4831781PMID: 27077648 [PubMed - indexed for MEDLINE]
17. Evid Based Med. 2016 Jun;21(3):100. doi: 10.1136/ebmed-2016-110405. Epub 2016 Apr13.
High-sensitivity troponin predicts coronary disease outcomes in type 2 diabetesbut yields no benefit in selecting patients for revascularisation.
Author information: (1)Medical Research Center Oulu, University of Oulu and Oulu University Hospital,Oulu, Finland.
Comment on N Engl J Med. 2015 Aug 13;373(7):610-20.
DOI: 10.1136/ebmed-2016-110405 PMID: 27075268 [PubMed - indexed for MEDLINE]
18. JACC Cardiovasc Interv. 2016 Apr 11;9(7):754. doi: 10.1016/j.jcin.2016.02.003.
Reply: Immediate Invasive Strategy for Patients With Both New IschemicElectrocardiographic Changes and Troponin Elevation.
Milosevic A, Vasiljevic-Pokrajcic Z, Milasinovic D, Vukcevic V, Asanin M,Stankovic G.
Comment on JACC Cardiovasc Interv. 2016 Mar 28;9(6):541-9. JACC Cardiovasc Interv. 2016 Apr 11;9(7):753.
DOI: 10.1016/j.jcin.2016.02.003 PMID: 27056318 [PubMed - indexed for MEDLINE]
19. JACC Cardiovasc Interv. 2016 Apr 11;9(7):753. doi: 10.1016/j.jcin.2016.01.019.
Immediate Invasive Strategy for Patients With Both New IschemicElectrocardiographic Changes and Troponin Elevation.
Sanchis J, Núñez J.
Comment in JACC Cardiovasc Interv. 2016 Apr 11;9(7):754.
Comment on JACC Cardiovasc Interv. 2016 Mar 28;9(6):541-9.
DOI: 10.1016/j.jcin.2016.01.019 PMID: 27056317 [PubMed - indexed for MEDLINE]
20. Ann Card Anaesth. 2016 Apr-Jun;19(2):321-7. doi: 10.4103/0971-9784.179638.
Troponin elevations in patients with chronic cardiovascular disease: An analysis of current evidence and significance.
Martin AK, Malhotra AK, Sullivan BL, Ramakrishna H(1).
Author information: (1)Division of Cardiovascular and Thoracic Anesthesiology, Mayo Clinic Arizona,AZ, USA.
Serum troponin elevation above the 99th percentile of the upper reference limitin healthy subjects (<0.01 ng/ml measured using currently availablehigh-sensitivity cardiac troponin laboratory assays) is required to establish thediagnosis the diagnosis of myocardial necrosis in acute cardiovascular syndromes,as well as guide prognosis and therapy. In the perioperative period, for patientswith cardiac disease undergoing noncardiac surgery, it is a particularly criticalbiomarker universally used to assess the myocardial damage. The value of troponintesting and elevation (as well as its significance) in patients with chroniccardiac valvular, vascular, and renal disease is relatively less well understood.This evidence-based review seeks to examine the currently available dataassessing the significance of troponin elevation in certain chronic valvular and other disease states.
DOI: 10.4103/0971-9784.179638 PMCID: PMC4900336PMID: 27052076 [PubMed - indexed for MEDLINE]
21. Tex Heart Inst J. 2016 Feb 1;43(1):38-42. doi: 10.14503/THIJ-14-4712. eCollection2016.
Predictors of Elevated Cardiac Enzyme Levels in Hospitalized Patients with AtrialFibrillation and No Known Coronary Artery Disease.
Vinales KL, Najib MQ, Marella PC, Katayama M, Chaliki HP.
We retrospectively studied the predictive capabilities of elevated cardiac enzymelevels in terms of the prognosis of patients who were hospitalized with atrialfibrillation and who had no known coronary artery disease. Among 321 patientswith atrial fibrillation, 60 without known coronary artery disease had theircardiac enzyme concentrations measured during hospitalization and underwentstress testing or cardiac catheterization within 12 months before or afterhospitalization. We then compared the clinical and electrocardiographiccharacteristics of the 20 patients who had elevated cardiac enzyme levels and the40 patients who had normal levels. Age, sex, and comorbidities did not differbetween the groups. In the patients with elevated cardiac enzyme levels, the meanconcentrations of troponin T and creatine kinase-MB isoenzymes were 0.08 ± 0.08ng/mL and 6.49 ± 4.94 ng/mL, respectively. In univariate analyses, only peakheart rate during atrial tachyarrhythmia was predictive of elevated enzyme levels(P <0.0001). Mean heart rate was higher in the elevated-level patients (146 ± 22 vs 117 ± 29 beats/min; P=0.0007). Upon multivariate analysis, heart rate was the only independent predictor of elevated levels. Coronary artery disease was found in only 2 patients who had elevated levels and in one patient who had normallevels (P=0.26). Increased myocardial demand is probably why the presenting heartrate was predictive of elevated cardiac enzyme levels. Most patients withelevated enzyme levels did not have coronary artery disease, and none died ofcardiac causes during the 6-month follow-up period. To validate our findings,larger studies are warranted.
DOI: 10.14503/THIJ-14-4712 PMCID: PMC4810582PMID: 27047283 [PubMed - indexed for MEDLINE]
22. 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: email@example.com. (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]
23. Swiss Med Wkly. 2016 Mar 21;146:w14285. doi: 10.4414/smw.2016.14285. eCollection 2016.
Elevated high-sensitivity troponin T levels are associated with adverse cardiacremodelling and myocardial fibrosis in hypertrophic cardiomyopathy.
Hasler S(1), Manka R(1), Greutmann M(1), Gämperli O(1), Schmied C, Tanner FC(1), Biaggi P(2), Lüscher TF(1), Keller DI(3), Gruner C(1).
Author information: (1)University Heart Centre, Department of Cardiology, University Hospital Zurich,Switzerland. (2)Heart Clinic, Hirslanden, Zurich, Switzerland. (3)EmergencyDepartment, University Hospital Zurich, Switzerland.
INTRODUCTION: Clinical manifestations of hypertrophic cardiomyopathy (HCM) range from asymptomatic disease to early-onset heart failure and sudden cardiac death(SCD). Risk stratification for SCD remains imperfect and novel risk markers areneeded. The aim of our study was to evaluate the association of elevatedhigh-sensitivity cardiac troponin T levels (hs-cTnT) with the severity of diseaseexpression and adverse events in patients with HCM.METHODS: All patients followed-up at a dedicated HCM clinic at a tertiary carecentre between April 2012 and March 2014 were analysed. The clinical care trackfor these patients includes 12-lead ECG, blood work-up, echocardiography, Holter ECG, exercise stress testing and cardiovascular magnetic resonance imaging (CMR).Clinical data were obtained from medical records.RESULTS: Of 91 HCM patients (77% males, mean age at follow up 51 ± 16 years), 46 (51%) had elevated hs-cTnT levels (>0.014 ng/ml). Patients with elevated hs-cTnT levels had greater maximum wall thickness (23 ± 7 mm vs 19 ± 3 mm, p = 0.001),more often had myocardial fibrosis (96% vs 54%, p <0.001), and lower exercisecapacity (90% predicted vs 76% predicted, p = 0.002). There was a trend towardslower event-free survival estimates (Kaplan-Meier method, 15% vs 7%, p = 0.16).CONCLUSIONS: Elevated hs-cTnT levels in HCM patients are associated with disease severity and, potentially, with more adverse cardiac events. Future studiesshould test whether integration of hs-cTnT in clinical decision algorithms willimprove risk stratification.
DOI: 10.4414/smw.2016.14285 PMID: 26999566 [PubMed - indexed for MEDLINE]
24. Am Heart J. 2016 Apr;174:43-50. doi: 10.1016/j.ahj.2015.12.015. Epub 2015 Dec 31.
High-sensitive troponin T is associated with all-cause and cardiovascularmortality in stable outpatients with type 2 diabetes (ZODIAC-37).
Hendriks SH(1), van Dijk PR(2), van Hateren KJ(2), van Pelt JL(3), GroenierKH(4), Bilo HJ(5), Bakker SJ(6), Landman GW(7), Kleefstra N(8).
Author information: (1)Diabetes Centre, Isala, Zwolle, the Netherlands. Electronic address:firstname.lastname@example.org. (2)Diabetes Centre, Isala, Zwolle, the Netherlands.(3)Department of Clinical Chemistry, University Medical Center Groningen andUniversity of Groningen, Groningen, The Netherlands. (4)Diabetes Centre, Isala,Zwolle, the Netherlands; Department of General Practice, University MedicalCenter Groningen and University of Groningen, Groningen, the Netherlands.(5)Diabetes Centre, Isala, Zwolle, the Netherlands; Department of InternalMedicine, University Medical Center Groningen and University of Groningen,Groningen, the Netherlands; Department of Internal Medicine, Isala, Zwolle, theNetherlands. (6)Department of Internal Medicine, University Medical CenterGroningen and University of Groningen, Groningen, the Netherlands. (7)DiabetesCentre, Isala, Zwolle, the Netherlands; Department of Internal Medicine, Gelrehospital, Apeldoorn, the Netherlands. (8)Diabetes Centre, Isala, Zwolle, theNetherlands; Department of Internal Medicine, University Medical Center Groningenand University of Groningen, Groningen, the Netherlands; Langerhans MedicalResearch Group, Zwolle, the Netherlands.
BACKGROUND: We aimed to investigate whether high-sensitive cardiac troponin T(hs-cTnT) is associated with all-cause and cardiovascular mortality in stabletype 2 diabetes (T2D) outpatients treated in primary care.METHODS: Cardiac troponin T was measured with a high-sensitive assay at baseline in patients with T2D participating in the observational ZODIAC study. Coxproportional hazards models were used to investigate the relationship betweenhs-cTnT and mortality with adjustment for selected confounders. Risk predictioncapabilities of hs-cTnT were assessed with Harrell C statistics.RESULTS: Complete baseline data were available for 1,133 patients. During median follow-up of 11 (7-14) years, 513 (45%) patients died, of which 218 (42%) died ofcardiovascular causes. Of the patients with undetectable hs-cTnT levels (<3ng/L), only 23% died, compared with 58% with low detectable levels (3-14 ng/L)and 84% with raised levels (≥14 ng/L). Natural log hs-cTnT was significantlyassociated with all-cause mortality (hazard ratio 1.30, 95% CI 1.19-1.42) andcardiovascular mortality (hazard ratio 1.33, 95% CI 1.15-1.53), independent ofpotential confounders. The Harrell C statistic for the crude model of hs-cTnT was0.72 (95% CI 0.70-0.75) for all-cause mortality and 0.74 (95% CI 0.71-0.77) forcardiovascular mortality.CONCLUSIONS: Higher levels of hs-cTnT are associated with mortality in stableoutpatients with T2D. The high crude Harrell C values and the excellent prognosisof patients with undetectable levels illustrate the strength of hs-cTnT as apotential marker for mortality.
Copyright © 2015 Elsevier Inc. All rights reserved.
DOI: 10.1016/j.ahj.2015.12.015 PMID: 26995369 [PubMed - indexed for MEDLINE]
25. Eur J Med Res. 2016 Mar 17;21:11. doi: 10.1186/s40001-016-0206-0.
How rapid is rapid? Exemplary results of real-life rapid rule-out troponin timingin troponin-positive acute coronary syndromes without persistent ST-segmentelevation in two contrasting German chest pain unit facilities.
Fischer D(1), Remberg F(2), Böse D(2), Lichtenberg M(3), Kümpers P(4), LebiedzP(5), Pavenstädt HJ(4), Waltenberger J(5), Breuckmann F(2).
Author information: (1)Department of Cardiology and Angiology, University Hospital Münster,Albert-Schweitzer-Campus 1, A1, 48149, Münster, Germany.email@example.com. (2)Department of Cardiology, Arnsberg MedicalCenter, Arnsberg, Germany. (3)Department of Angiology, Arnsberg Medical Center,Arnsberg, Germany. (4)Department of General Internal Medicine, Nephrology andRheumatology, University Hospital Münster, Münster, Germany. (5)Department ofCardiology and Angiology, University Hospital Münster, Albert-Schweitzer-Campus1, A1, 48149, Münster, Germany.
AIM: To analyse the timing of cardiac troponin (cTn) measurements in high-riskand cTn-positive acute coronary syndromes without persistent ST-segment elevation(NSTE-ACS) in two structurally different German chest pain units (CPUs),contrasting an urban university maximum care and a rural regional primary carefacility.METHODS: All patients encoded as NSTEMI during the year 2013 were retrospectivelyenrolled in two centres: site (I)--centre of maximum care in an urban university setting and site (II)--centre of primary care in a rural regional care setting.Data acquisition included time intervals from admission to baseline cTn and firstand second cTn control as well as type and timing of invasive management.RESULTS: The median times (site I vs. site II) from admission to cTn resultannouncement were 26.5 vs. 33.0 min (p = 0.02) for baseline, 4 vs. 4 h (p = 0.43)for the first and 11.0 vs. 16.5 h (p = 0.03) for the second control. Timelyannouncement, as recommended by guidelines, was available in 86.9% at baseline,59.4% for the first or 41.1% for the second cTn control. Rates and timing ofinvasive management were independent from the time point of positive cTnannouncement (p = 0.51 and p = 0.68, respectively).CONCLUSIONS: German CPUs provide timely identification of cTn-positive patientsin a narrow and guideline-adherent time frame using a rapid rule-out protocol.Especially, baseline and early cTn timing was comparable between the urbanuniversity maximum care and the rural regional primary care facility withoutrelevant impact on guideline-conforming invasive management, underlining the highstandard of care in those highly professional institutions.
DOI: 10.1186/s40001-016-0206-0 PMCID: PMC4794842PMID: 26984277 [PubMed - indexed for MEDLINE]
26. Am J Cardiol. 2016 May 1;117(9):1397-404. doi: 10.1016/j.amjcard.2016.02.002.Epub 2016 Feb 17.
Usefulness of High-Sensitivity Cardiac Troponin T for the Identification ofOutlier Patients With Diffuse Coronary Atherosclerosis and Low-Risk Factors.
Magnoni M(1), Masson S(2), Andreini D(3), Moccetti T(4), Modena MG(5), CanestrariM(6), Berti S(7), Casolo G(8), Gabrielli D(9), Marraccini P(10), Pontone G(3),Latini R(2), Maggioni AP(11), Maseri A(12); CAPIRE Study Group.
Collaborators: Maseri A, Andreini D, Berti S, Canestrari M, Casolo G, GabrielliD, Latini R, Magnoni M, Marraccini P, Masson S, Moccetti T, Modena MG, AndreiniD, Pontone G, Masson S, Gaspari F, Ferrari S, Cannata A, Stucchi N, Fois M,Bernasconi R, Balconi G, Vago T, Letizia T, Bottazzi B, Leone R, Suliman I,Sommaruga M, Gremigni P, Olivieri R, Pennacchietti L, Magnacca M, Rossi MG,Pasotti E, Moccetti T, Susini C, Andreini D, Pontone G, Mushtaq S, Spadafora G,Rossi R, Faggioni L, Ciardetti M, Piccoli G.
Author information: (1)Heart Care Foundation Onlus, Florence, Italy. Electronic address:firstname.lastname@example.org. (2)Department of Cardiovascular Research, Istituto diRicovero e Cura a Carattere Scientifico, Istituto di Ricerche FarmacologicheMario Negri, Milan, Italy. (3)Centro Cardiologico Monzino, Milan, Italy.(4)Servizio di Ricerca Cardiovascolare, Cardiocentro Ticino, Lugano, Switzerland.(5)Department of Cardiology, Ospedale Policlinico, Modena, Italy. (6)Departmentof Cardiology, Santa Croce Hospital, Fano, Italy. (7)Fondazione Toscana Gabriele Monasterio, Stabilimento di Massa, Unità Operativa Adult Cardiology, Massa,Italy. (8)Department of Cardiology, Nuovo Ospedale Versilia, Lido di Camaiore,Italy. (9)Department of Cardiology, Ospedale Civile A. Murri, Fermo, Italy.(10)Istituto di Fisiologia Clinica-Consiglio Nazionale delle Ricerche, FondazioneToscana G. Monasterio, S.A. Emodinamica, Pisa, Italy. (11)Associazione Nazionale Medici Cardiologi Ospedalieri Research Center, Florence, Italy. (12)Heart CareFoundation Onlus, Florence, Italy.
Novel high-sensitivity assay can detect very low levels of circulating cardiactroponin (hs-cTnT) in apparently healthy subjects. Within normal range, higherlevels are associated with coronary artery disease (CAD) and cardiacabnormalities commonly associated to traditional risk factors (RFs) for CAD.Therefore, we investigated the relation between circulating hs-cTnT and CAD inpatients with a spectrum of RF burden aiming to assess the added value of hs-cTnTto identify "outlier" patients with CAD despite a low RF burden. Hs-cTnT wasmeasured in 525 stable patients without previous diagnosis of ischemic heartdisease with 0 to 1 RF, excluded diabetes, (low-RF group, n = 263) or ≥2 RFs(multiple-RF group, n = 262) and without CAD (segment involvement score = 0) ordiffuse CAD (segment involvement score >5) at coronary computed tomographyangiography. Outlier patients with diffuse CAD despite low-RF burden had similar extent, severity, and plaque composition than patients with multiple RFs.Overall, hs-cTnT was measurable in 81% of patients with median value of 6.0 ng/L.In both groups, hs-cTnT concentration was higher in patients with CAD than inpatients with normal coronary arteries (p <0.0001). Hs-cTnT was more accurate to detect patients with CAD in the low-RF group than in the multiple-RF group (p =0.04). In multivariate analysis, higher level of hs-cTnT (>6 ng/L) wasindependently associated with CAD in low-RF group only. Despite very lowcirculating concentrations, hs-cTnT may identify with a good accuracy the outlierpatients with diffuse CAD despite low-RF burden.
Copyright © 2016 Elsevier Inc. All rights reserved.
DOI: 10.1016/j.amjcard.2016.02.002 PMID: 26976791 [PubMed - indexed for MEDLINE]
27. Clin Biochem. 2016 Apr;49(6):419-20. doi: 10.1016/j.clinbiochem.2016.03.001. Epub2016 Mar 10.
Use of high sensitivity cardiac troponin assays as an adjunct to cardiac stresstesting.
Jarolim P(1), Morrow DA(2).
Author information: (1)Department of Pathology, Brigham and Women's Hospital, Harvard Medical School,Boston, MA, USA. Electronic address: email@example.com. (2)Department ofMedicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
DOI: 10.1016/j.clinbiochem.2016.03.001 PMID: 26969798 [PubMed - indexed for MEDLINE]
28. 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.firstname.lastname@example.org.
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]
29. Proc Natl Acad Sci U S A. 2016 Mar 22;113(12):3257-62. doi:10.1073/pnas.1519541113. Epub 2016 Mar 8.
Atomic resolution probe for allostery in the regulatory thin filament.
Williams MR(1), Lehman SJ(2), Tardiff JC(3), Schwartz SD(4).
Author information: (1)Department of Chemistry and Biochemistry, The University of Arizona, Tucson,AZ 85721; (2)Physiological Sciences, The University of Arizona, Tucson, AZ 85724;(3)Department of Medicine, The University of Arizona, Tucson, AZ 85724;Department of Cellular and Molecular Medicine, The University of Arizona, Tucson,AZ 85724. (4)Department of Chemistry and Biochemistry, The University of Arizona,Tucson, AZ 85721; email@example.com.
Calcium binding and dissociation within the cardiac thin filament (CTF) is afundamental regulator of normal contraction and relaxation. Although thedisruption of this complex, allosterically mediated process has long beenimplicated in human disease, the precise atomic-level mechanisms remain opaque,greatly hampering the development of novel targeted therapies. To address thisquestion, we used a fully atomistic CTF model to test both Ca(2+) bindingstrength and the energy required to remove Ca(2+) from the N-lobe binding site inWT and mutant troponin complexes that have been linked to geneticcardiomyopathies. This computational approach is combined with measurements of invitro Ca(2+) dissociation rates in fully reconstituted WT and cardiac troponin T R92L and R92W thin filaments. These human disease mutations represent knownsubstitutions at the same residue, reside at a significant distance from thecalcium binding site in cardiac troponin C, and do not affect either the binding pocket affinity or EF-hand structure of the binding domain. Both have been shown to have significantly different effects on cardiac function in vivo. We now show that these mutations independently alter the interaction between the Ca(2+) ionand cardiac troponin I subunit. This interaction is a previously unidentifiedmechanism, in which mutations in one protein of a complex indirectly affect athird via structural and dynamic changes in a second to yield a pathogenic changein thin filament function that results in mutation-specific disease states. Wecan now provide atom-level insight that is potentially highly actionable in drug design.
DOI: 10.1073/pnas.1519541113 PMCID: PMC4812746PMID: 26957598 [PubMed - indexed for MEDLINE]
30. Clin Chem. 2016 Apr;62(4):623-30. doi: 10.1373/clinchem.2015.250811. Epub 2016Mar 2.
High-Sensitivity Cardiac Troponin I Is a Strong Predictor of CardiovascularEvents and Mortality in the AGES-Reykjavik Community-Based Cohort of OlderIndividuals.
Thorsteinsdottir I(1), Aspelund T(2), Gudmundsson E(3), Eiriksdottir G(3), HarrisTB(4), Launer LJ(4), Gudnason V(2), Venge P(5).
Author information: (1)Icelandic Heart Association Research Institute, Kopavogur, Iceland; Departmentof Clinical Biochemistry, Landspitali University Hospital, Reykjavik, Iceland;(2)Icelandic Heart Association Research Institute, Kopavogur, Iceland; Faculty ofMedicine, University of Iceland, Reykjavik, Iceland; (3)Icelandic HeartAssociation Research Institute, Kopavogur, Iceland; (4)Laboratory ofEpidemiology, Demography and Biometry, Intramural Research Program, NationalInstitute on Aging Bethesda, MD; (5)Department of Medical Sciences, UppsalaUniversity, Uppsala, Sweden. firstname.lastname@example.org.
BACKGROUND: The objective of this study was to investigate the predictive powerof a high-sensitivity cardiac troponin I (hs-cTnI) assay for cardiovascularevents and mortality in a large population of older community dwellers.METHODS: Blood was collected from 5764 individuals (age 66-98 years) during theperiod of 2002-2006 and the outcome as to all-cause death and incidence ofcardiovascular disease (CVD) and coronary heart disease (CHD) followed up to 10years. hs-cTnI (Abbott) was measured in serum to assess the association of thismarker with CVD, CHD and death, and finally, to compare the results withconventional risk factors by multivariable statistical analysis.RESULTS: The median (interquartile range) concentrations of hs-cTnI were 8.4 ng/L(5.6-14.2 ng/L) and 5.3 ng/L (3.8-8.1 ng/L) in men (2416) and women (3275),respectively, and the concentrations increased linearly with age. Outcomes as to all-cause death and incidence of CVD and CHD were significantly associated withincreasing concentrations of hs-cTnI beginning well below the 99th percentileconcentrations. The associations with outcome remained after adjustments forconventional risk factors and were similar in men and women.CONCLUSIONS: Our findings suggest that hs-cTnI reflects the status of themyocardium even in seemingly healthy individuals and that the measurements ofhs-cTnI may be useful for primary prediction of heart disease; this should formthe basis for future prospective clinical trials for determining whethermeasuring hs-cTnI can be used in the prevention of CVD/CHD.
© 2016 American Association for Clinical Chemistry.
DOI: 10.1373/clinchem.2015.250811 PMID: 26936931 [PubMed - indexed for MEDLINE]
31. Circulation. 2016 Mar 29;133(13):1228-9. doi: 10.1161/CIRCULATIONAHA.116.021795. Epub 2016 Mar 1.
Relative Lack of Culprit and Obstructive Coronary Lesions in Patients With Acute Ischemic Stroke and Elevated Cardiac Troponin.
Hofmann Bowman MA(1), Liao JK(2).
Author information: (1)From Section of Cardiology, Department of Medicine, University of Chicago, IL.(2)From Section of Cardiology, Department of Medicine, University of Chicago, IL.email@example.com.
Comment on Circulation. 2016 Mar 29;133(13):1264-71.
DOI: 10.1161/CIRCULATIONAHA.116.021795 PMCID: PMC4891305PMID: 26933084 [PubMed - indexed for MEDLINE]
32. Circulation. 2016 Mar 29;133(13):1264-71. doi: 10.1161/CIRCULATIONAHA.115.018547.Epub 2016 Mar 1.
Coronary Angiographic Findings in Acute Ischemic Stroke Patients With ElevatedCardiac Troponin: The Troponin Elevation in Acute Ischemic Stroke (TRELAS) Study.
Mochmann HC(1), Scheitz JF(1), Petzold GC(1), Haeusler KG(1), Audebert HJ(1),Laufs U(1), Schneider C(1), Landmesser U(1), Werner N(1), Endres M(1),Witzenbichler B(1), Nolte CH(2); TRELAS Study Group.
Author information: (1)From Klinik für Kardiologie (H.-C.M., U.L.) and Klinik für Neurologie (J.F.S.,K.G.H., H.J.A., M.E., C.H.N.), Charité-Universitätsmedizin Berlin, CampusBenjamin Franklin, Germany; Center for Stroke Research Berlin (J.F.S., K.G.H.,H.J.A., M.E., C.H.N.) and ExcellenceCluster NeuroCure (M.E.),Charité-Universitätsmedizin Berlin, Germany; German Center for Neurodegenerative Diseases and Department of Neurology(G.C.P., C.S.) and Department of InternalMedicine II (N.W.), University of Bonn, Germany; Klinik für Innere Medizin III,Kardiologie, Angiologie undInternistische Intensivmedizin, Universitätsklinikumdes Saarlandes, Homburg, Germany (U.L.); German Center for NeurodegenerativeDiseases, Berlin,Germany (M.E.); Berlin Institute of Health, Germany (M.E.); and Klinik für Kardiologie und Pneumologie, Helios Amper-Klinikum Dachau, Germany(B.W.). (2)From Klinik für Kardiologie (H.-C.M., U.L.) and Klinik für Neurologie (J.F.S., K.G.H., H.J.A., M.E., C.H.N.), Charité-Universitätsmedizin Berlin,Campus Benjamin Franklin, Germany; Center for Stroke Research Berlin (J.F.S.,K.G.H., H.J.A., M.E., C.H.N.) and ExcellenceCluster NeuroCure (M.E.),Charité-Universitätsmedizin Berlin, Germany; German Center for Neurodegenerative Diseases and Department of Neurology(G.C.P., C.S.) and Department of InternalMedicine II (N.W.), University of Bonn, Germany; Klinik für Innere Medizin III,Kardiologie, Angiologie undInternistische Intensivmedizin, Universitätsklinikumdes Saarlandes, Homburg, Germany (U.L.); German Center for NeurodegenerativeDiseases, Berlin,Germany (M.E.); Berlin Institute of Health, Germany (M.E.); and Klinik für Kardiologie und Pneumologie, Helios Amper-Klinikum Dachau, Germany(B.W.). firstname.lastname@example.org.
Comment in Circulation. 2016 Mar 29;133(13):1228-9.
BACKGROUND: A relevant proportion of patients with acute ischemic stroke (AIS)have elevated levels of cardiac troponins (cTn). However, the frequency ofcoronary ischemia as the cause of elevated cTn is unknown. The aim of our studywas to analyze coronary vessel status in AIS patients with elevated cTn compared with patients presenting with non-ST-segment-elevation acute coronary syndrome(NSTE-ACS).METHODS AND RESULTS: Among 2123 consecutive patients with AIS prospectivelyscreened at 2 tertiary hospitals, 13.7% had cTn elevation (>50 ng/L). Accordingto a prespecified sample size estimation, 29 patients with AIS (median age, 76years [first-third quartiles, 70-82 years]; 52% male) underwent conventionalcoronary angiography and were compared with age- and sex-matched patients withNSTE-ACS. The primary end point was presence of coronary culprit lesions oncoronary angiograms as analyzed by independent interventional cardiologistsblinded for clinical data. Median cTn on presentation did not differ betweenpatients with AIS or NSTE-ACS (95 versus 94 ng/L; P=0.70). Compared with patientswith NSTE-ACS, patients with AIS were less likely to have coronary culpritlesions (7 of 29 versus 23 of 29; P<0.001) or any obstructive coronary arterydisease (15 of 29 versus 25 of 29; P=0.02; median number of vessels with >50%stenosis, 1 [first-third quartiles, 0-2] versus 2 [first-third quartiles, 1-3];P<0.01).CONCLUSIONS: Coronary culprit lesions are significantly less frequent in AISpatients compared with age- and sex-matched patients with NSTE-ACS despitesimilar baseline cTn levels. Half of all AIS patients had no angiographicevidence of coronary artery disease. Further studies are needed to clinicallyidentify the minority of patients with AIS and angiographic evidence of a culpritlesion.CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Uniqueidentifier: NCT01263964.
© 2016 American Heart Association, Inc.
DOI: 10.1161/CIRCULATIONAHA.115.018547 PMID: 26933082 [PubMed - indexed for MEDLINE]
33. Rev Port Cardiol. 2016 Mar;35(3):195. doi: 10.1016/j.repc.2015.09.005. Epub 2016 Feb 28.
We need more data to determine the significance of NT-proBNP and troponin Ilevels in high-risk patients.
Author information: (1)Department of Cardiology, Dinar State Hospital Dinar, Afyonkarahisar, Turkey. Electronic address: email@example.com.
Comment on Rev Port Cardiol. 2015 Apr;34(4):255-61.
DOI: 10.1016/j.repc.2015.09.005 PMID: 26928015 [PubMed - indexed for MEDLINE]
34. 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]
35. Clin Chim Acta. 2016 May 1;456:19-23. doi: 10.1016/j.cca.2016.02.014. Epub 2016Feb 24.
Reference values of galectin-3 and cardiac troponins derived from a single cohortof healthy blood donors.
Mueller T(1), Egger M(2), Leitner I(2), Gabriel C(3), Haltmayer M(2), Dieplinger B(2).
Author information: (1)Department of Laboratory Medicine, Konventhospital Barmherzige Brueder Linz,Linz, Austria. Electronic address: firstname.lastname@example.org. (2)Department ofLaboratory Medicine, Konventhospital Barmherzige Brueder Linz, Linz, Austria.(3)Red Cross Transfusion Service of Upper Austria, Linz, Austria.
BACKGROUND: Here we describe the determination of upper reference limits (URL)for galectin-3, high-sensitivity cardiac troponin I (hs-cTnI) andhigh-sensitivity cardiac troponin T (hs-cTnT) in a single cohort of healthy blooddonors using routine assays.METHODS: For this reference value study, we used a cohort of 402 consecutiveblood donors (64% were male and 36% were female). The median individuals' age was35.0 years (range, 18.0-64.4). Individuals of this reference population were free<