Laboratorio de Urgencias

Bibliografía

Buenos Aires 01 de Agosto del 2020

Búsqueda Bibliográfica: hsTroponina (2017-2018)

1. Int Heart J. 2018 Mar 30;59(2):256-262. doi: 10.1536/ihj.17-204. Epub 2018 Mar
20.

Diagnostic Approach to Cardiac Involvement in Idiopathic Inflammatory Myopathies.

Chen F(1), Peng Y(1), Chen M(1).

Author information:
(1)Department of Cardiology, West China Hospital, Sichuan University.

Cardiac involvement in idiopathic inflammatory myopathies (IIMs) attracts more
attention than it ever did because of its morbidity and impact on worse
prognosis, although the accurate information needs further epidemiological
studies. Early identification and intervention for the diseased heart may help
improve the clinical outcomes of IIMs with cardiac involvement. Cardiac troponin
assays, allowing for sensitive detection of minor myocardium injury, may provide
a new way for early detection for heart involvement in IIMs. While elevated
cardiac troponin I (cTnI) specifically indicates cardiomyocyte injury, the
elevation of cardiac troponin T (cTnT) levels may not only derive from damaged
heart but also diseased adult skeletal muscles in which cTnT could re-express in
patients with IIMs. cTnI is the biomarker of choice for diagnosis of cardiac
involvement and may also be a prognostic factor in IIMs. Meanwhile,
electrocardiography (ECG), cardiac imaging (e.g., echocardiography, cardiac
magnetic resonance) and histopathological techniques (e.g., endomyocardial
biopsy) take on different degrees of importance for the diagnosis of cardiac
involvement. We propose a diagnostic strategy combining the routine use of cTnI
assay with other techniques (routine ECG and echocardiography, cardiac magnetic
resonance, and or endomyocardial biopsy in necessity) and clinical investigation
for early detection of heart involvement in IIMs. Future researches are required
to validate the algorithm for performance.

DOI: 10.1536/ihj.17-204
PMID: 29563381 [Indexed for MEDLINE]

2. Vnitr Lek. Winter 2018;63(12):935-944.

[Diagnostic and prognostic biomarkers in acute coronary syndrome].

[Article in Czech]

Kuběna P, Špinar J, Dastych M, Lokaj P, Pařenica J.

Acute myocardial infarction (AMI) is an important cause of mortality and
morbidity worldwide. Early diagnostics of this disease helps in the appropriate
treatment of patients. Great attention is paid to the diagnostic and risk
stratification of patients according to circulating biomarkers. There are a lot
of scientific publications describing this topic. The aim of this article is to
provide a comprehensive overview of the most important and most examined
biomarkers in acute coronary syndrome. Meanwhile troponin takes a fundamental
place for AMI diagnostic (mostly the high-sensitive methods) in preference to
MB-fraction of creatine kinase and myoglobin. The connection to a higher sudden
death risk, reinfarcts and heart failure occurring was also proved by many other
biomarkers. The most important of them are the natriuretic peptides, the
C-reactive protein, the heart fatty acid binding protein, the
pregnancy-associated plasma protein-A, CD146, cystatin C, NGAL, copeptin,
MR-proadrenomedullin, and the growth differentiation factor-15. More prospective
randomized studies are needed for the further use of these other biomarkers in
clinical practice.Key words: acute coronary syndrome - biomarkers.

PMID: 29334742 [Indexed for MEDLINE]

3. Medicine (Baltimore). 2017 Dec;96(49):e8976. doi: 10.1097/MD.0000000000008976.

Volatile sedation in the intensive care unit: A systematic review and
meta-analysis.

Kim HY(1), Lee JE, Kim HY, Kim J.

Author information:
(1)aDepartment of Anesthesiology and Pain Medicine, Sungkyunkwan University
School of MedicinebBiostatistics Collaboration UnitcDepartment of Anesthesiology
and Pain Medicine, Anesthesia and Pain Research Institute, Yonsei University
College of Medicine, Seoul, Republic of Korea.

BACKGROUND: Volatile sedation in the intensive care unit (ICU) may reduce the
number of adverse events and improve patient outcomes compared with intravenous
(IV) sedation. We performed a systematic review and meta-analysis comparing the
effects of volatile and IV sedation in adult ICU patients.
METHODS: We searched the PubMed, Embase, Cochrane Central Register, and Web of
Science databases for all randomized trials comparing volatile sedation using an
anesthetic-conserving device (ACD) with IV sedation in terms of awakening and
extubation times, lengths of ICU and hospital stay, and pharmacologic end-organ
effects.
RESULTS: Thirteen trials with a total of 1027 patients were included. Volatile
sedation (sevoflurane or isoflurane) administered through an ACD shortened the
awakening time [mean difference (MD), -80.0 minutes; 95% confidence intervals
(95% CIs), -134.5 to -25.6; P = .004] and extubation time (MD, -196.0 minutes;
95% CIs, -305.2 to -86.8; P < .001) compared with IV sedation (midazolam or
propofol). No differences in the lengths of ICU and hospital stay were noted
between the 2 groups. In the analysis of cardiac effects of sedation from 5
studies, patients who received volatile sedation showed lower serum troponin
levels 6 hours after ICU admission than patients who received IV sedation
(P < .05). The effect size of troponin was largest between 12 and 24 hours after
ICU admission (MD, -0.27 μg/L; 95% CIs, -0.44 to -0.09; P = .003).
CONCLUSION: Compared with IV sedation, volatile sedation administered through an
ACD in the ICU shortened the awakening and extubation times. Considering the
difference in serum troponin levels between both arms, volatile anesthetics might
have a myocardial protective effect after cardiac surgery even at a subanesthetic
dose. Because the included studies used small sample sizes with high
heterogeneity, further large, high-quality prospective clinical trials are needed
to confirm our findings.

DOI: 10.1097/MD.0000000000008976
PMCID: PMC5728884
PMID: 29245269 [Indexed for MEDLINE]

4. Stroke. 2018 Jan;49(1):e10-e13. doi: 10.1161/STROKEAHA.117.019173. Epub 2017 Nov
22.

Symptomatic Intracranial Atherosclerosis With Impaired Distal Perfusion: A Case
Study.

Dakay K(1), Yaghi S(2).

Author information:
(1)From the Department of Neurology, Warren Alpert Medical School of Brown
University, Providence, RI.
(2)From the Department of Neurology, Warren Alpert Medical School of Brown
University, Providence, RI. shadiyaghi@yahoo.com.

DOI: 10.1161/STROKEAHA.117.019173
PMID: 29167389 [Indexed for MEDLINE]

5. Parasit Vectors. 2017 Nov 9;10(Suppl 2):534. doi: 10.1186/s13071-017-2448-2.

Cardiopulmonary and inflammatory biomarkers in heartworm disease.

Carretón E(1), Morchón R(2), Montoya-Alonso JA(3).

Author information:
(1)Faculty of Veterinary Medicine, Research Institute of Biomedical and Health
Sciences (IUIBS), University of Las Palmas de Gran Canaria, Trasmontaña s/n,
35413-Arucas, Las Palmas, Spain. elena.carreton@ulpgc.es.
(2)Laboratory of Parasitology, Faculty of Pharmacy, Institute of Biomedical
Research of Salamanca(IBSAL), University of Salamanca, Salamanca, Spain.
(3)Faculty of Veterinary Medicine, Research Institute of Biomedical and Health
Sciences (IUIBS), University of Las Palmas de Gran Canaria, Trasmontaña s/n,
35413-Arucas, Las Palmas, Spain.

In heartworm disease, several biomarkers of cardiopulmonary injury and
inflammatory activity have been studied during the recent years. D-dimer is a
fibrin degradation product present after a clot is degraded, which has been
reported to provide support for the diagnosis of pulmonary thromboembolism in
heartworm disease. Furthermore, concentrations increment with increased disease
severity and during the adulticide treatment. This increase in concentration has
proved to be valuable. Cardiac biomarkers troponin I, myoglobin and NT-proBNP
demonstrated presence of myocardial injury and heart failure, especially in
chronic infections, which in some cases, slightly improve after the adulticide
treatment. An acute phase response in dogs with Dirofilaria immitis,
characterized by variations of acute phase proteins (APP), has been reported,
indicating inflammatory processes that could contribute to disease progression.
Among them, C-reactive protein (CRP) increases according to the severity of the
disease; and a strong correlation between pulmonary hypertension and CRP has been
observed. In cats, little work has been done to ascertain the utility of these
biomarkers in feline heartworm; the only published study in D.
immitis-seropositive cats reported significantly higher concentrations in
positive APP serum amyloid A, haptoglobin and ceruloplasmin.

DOI: 10.1186/s13071-017-2448-2
PMCID: PMC5688449
PMID: 29143665 [Indexed for MEDLINE]

6. JAMA. 2017 Nov 21;318(19):1913-1924. doi: 10.1001/jama.2017.17488.

Association of High-Sensitivity Cardiac Troponin I Concentration With Cardiac
Outcomes in Patients With Suspected Acute Coronary Syndrome.

Chapman AR(1), Lee KK(1), McAllister DA(2), Cullen L(3)(4)(5), Greenslade
JH(3)(4)(5), Parsonage W(3)(4)(5), Worster A(6), Kavsak PA(7), Blankenberg S(8),
Neumann J(8), Sörensen NA(8), Westermann D(8), Buijs MM(9), Verdel GJE(10),
Pickering JW(11)(12), Than MP(12), Twerenbold R(13), Badertscher P(13), Sabti
Z(13), Mueller C(13), Anand A(1), Adamson P(1), Strachan FE(1), Ferry A(1),
Sandeman D(1), Gray A(1)(14), Body R(15), Keevil B(16), Carlton E(17), Greaves
K(18), Korley FK(19), Metkus TS(20), Sandoval Y(21), Apple FS(22), Newby DE(1),
Shah ASV(1), Mills NL(1).

Author information:
(1)BHF Centre for Cardiovascular Science, University of Edinburgh, Edinburgh,
Scotland.
(2)Institute of Health and Wellbeing, University of Glasgow, Glasgow, Scotland.
(3)Department of Emergency Medicine, Royal Brisbane and Women's Hospital,
Brisbane, Australia.
(4)School of Medicine, University of Queensland, Brisbane, Australia.
(5)Faculty of Health, Queensland University of Technology, Brisbane, Australia.
(6)Division of Emergency Medicine, McMaster University, Hamilton, Ontario,
Canada.
(7)Department of Pathology and Molecular Medicine, McMaster University, Hamilton,
Ontario, Canada.
(8)University Heart Center, Hamburg, Germany.
(9)Atalmedial Diagnostic Centers, Hoofddorp, the Netherlands.
(10)Department of Cardiology, Spaarne Gasthuis, Haarlem, the Netherlands.
(11)Department of Medicine, University of Otago, Christchurch, New Zealand.
(12)Emergency Department, Christchurch Hospital, Christchurch, New Zealand.
(13)Cardiovascular Research Institute Basel and Department of Cardiology,
University Hospital, Basel, Switzerland.
(14)Department of Emergency Medicine and EMERGE, Royal Infirmary of Edinburgh,
Edinburgh, Scotland.
(15)Central Manchester University Hospitals NHS Foundation Trust and the
University of Manchester, Manchester, England.
(16)University Hospital South Manchester NHS Foundation Trust, Manchester,
England.
(17)Department of Emergency Medicine, Southmead Hospital, Bristol, England.
(18)Department of Cardiology, Sunshine Coast University Hospital, University of
the Sunshine Coast, Birtinya, Australia.
(19)University of Michigan Medical School, Ann Arbor.
(20)John Hopkins School of Medicine, Baltimore, Maryland.
(21)Hennepin County Medical Center and Minneapolis Heart Institute, Abbott
Northwestern Hospital, Minneapolis, Minnesota.
(22)Department of Laboratory Medicine and Pathology, Hennepin County Medical
Center and University of Minnesota, Minneapolis.

Erratum in
JAMA. 2018 Mar 20;319(11):1168. Soerensen NA [corrected to Sorensen NA].

Importance: High-sensitivity cardiac troponin I testing is widely used to
evaluate patients with suspected acute coronary syndrome. A cardiac troponin
concentration of less than 5 ng/L identifies patients at presentation as low
risk, but the optimal threshold is uncertain.
Objective: To evaluate the performance of a cardiac troponin I threshold of 5
ng/L at presentation as a risk stratification tool in patients with suspected
acute coronary syndrome.
Data Sources: Systematic search of MEDLINE, EMBASE, Cochrane, and Web of Science
databases from January 1, 2006, to March 18, 2017.
Study Selection: Prospective studies measuring high-sensitivity cardiac troponin
I concentrations in patients with suspected acute coronary syndrome in which the
diagnosis was adjudicated according to the universal definition of myocardial
infarction.
Data Extraction and Synthesis: The systematic review identified 19 cohorts.
Individual patient-level data were obtained from the corresponding authors of 17
cohorts, with aggregate data from 2 cohorts. Meta-estimates for primary and
secondary outcomes were derived using a binomial-normal random-effects model.
Main Outcomes and Measures: The primary outcome was myocardial infarction or
cardiac death at 30 days. Performance was evaluated in subgroups and across a
range of troponin concentrations (2-16 ng/L) using individual patient data.
Results: Of 11 845 articles identified, 104 underwent full-text review, and 19
cohorts from 9 countries were included. Among 22 457 patients included in the
meta-analysis (mean age, 62 [SD, 15.5] years; n = 9329 women [41.5%]), the
primary outcome occurred in 2786 (12.4%). Cardiac troponin I concentrations were
less than 5 ng/L at presentation in 11 012 patients (49%), in whom there were 60
missed index or 30-day events (59 index myocardial infarctions, 1 myocardial
infarction at 30 days, and no cardiac deaths at 30 days). This resulted in a
negative predictive value of 99.5% (95% CI, 99.3%-99.6%) for the primary outcome.
There were no cardiac deaths at 30 days and 7 (0.1%) at 1 year, with a negative
predictive value of 99.9% (95% CI, 99.7%-99.9%) for cardiac death.
Conclusions and Relevance: Among patients with suspected acute coronary syndrome,
a high-sensitivity cardiac troponin I concentration of less than 5 ng/L
identified those at low risk of myocardial infarction or cardiac death within 30
days. Further research is needed to understand the clinical utility and
cost-effectiveness of this approach to risk stratification.

DOI: 10.1001/jama.2017.17488
PMCID: PMC5710293 [Available on 2018-05-21]
PMID: 29127948 [Indexed for MEDLINE]

7. Tech Vasc Interv Radiol. 2017 Sep;20(3):162-174. doi: 10.1053/j.tvir.2017.07.005.
Epub 2017 Jul 5.

Systemic Thrombolysis for Pulmonary Embolism: Who and How.

Tapson VF(1), Friedman O(2).

Author information:
(1)Division of Pulmonary and Critical Care, Venous Thromboembolism and Pulmonary
Vascular Disease Research, Pulmonary and Critical Care Medicine, Cedars-Sinai
Medical Center, Los Angeles, CA. Electronic address: Victor.tapson@cshs.org.
(2)Division of Pulmonary and Critical Care, Pulmonary and Critical Care Medicine,
Cardiac Surgery Intensive Care Unit, Cedars-Sinai Medical Center, Los Angeles,
CA.

Anticoagulation has been shown to improve mortality in acute pulmonary embolism
(PE). Initiation of anticoagulation should be considered when PE is strongly
suspected and the bleeding risk is perceived to be low, even if acute PE has not
yet been proven. Low-risk patients with acute PE are simply continued on
anticoagulation. Severely ill patients with high-risk (massive) PE require
aggressive therapy, and if the bleeding risk is acceptable, systemic thrombolysis
should be considered. However, despite clear evidence that parenteral
thrombolytic therapy leads to more rapid clot resolution than anticoagulation
alone, the risk of major bleeding including intracranial bleeding is
significantly higher when systemic thrombolytic therapy is administered. It has
been demonstrated that right ventricular dysfunction, as well as abnormal
biomarkers (troponin and brain natriuretic peptide) are associated with increased
mortality in acute PE. In spite of this, intermediate-risk (submassive) PE
comprises a fairly broad clinical spectrum. For several decades, clinicians and
clinical trialists have worked toward a more aggressive, yet safe solution for
patients with intermediate-risk PE. Standard-dose thrombolysis, low-dose systemic
thrombolysis, and catheter-based therapy which includes a number of devices and
techniques, with or without low-dose thrombolytic therapy, have offered potential
solutions and this area has continued to evolve. On the basis of heterogeneity
within the category of intermediate-risk as well as within the high-risk group of
patients, we will focus on the use of systemic thrombolysis in carefully selected
high- and intermediate-risk patients. In certain circumstances when the need for
aggressive therapy is urgent and the bleeding risk is acceptable, this is an
appropriate approach, and often the best one.

DOI: 10.1053/j.tvir.2017.07.005
PMID: 29029710 [Indexed for MEDLINE]

8. Am J Clin Pathol. 2017 Oct 1;148(4):281-295. doi: 10.1093/ajcp/aqx066.

Variability and Error in Cardiac Troponin Testing: An ACLPS Critical Review.

Herman DS(1), Kavsak PA(2), Greene DN(3).

Author information:
(1)Department of Pathology and Laboratory Medicine, University of
Pennsylvania,Philadelphia.
(2)Department of Pathology and Molecular Medicine, McMaster University,Hamilton,
Canada.
(3)Department of Laboratory Medicine, University of Washington, Seattle.

Objectives: To provide a comprehensive overview of the complexities associated
with cardiac troponin (cTn) testing. An emphasis is placed on the sources of
error, organized into the preanalytical, analytical, and postanalytical phases of
the testing pathway. Controversial areas are also explored.
Methods: A case scenario and review of the relevant literature describing
laboratory considerations involving cTn testing are described.
Results: Advanced comprehension of the specific assay used in a given laboratory
is necessary for optimal reporting, utilization, and quality monitoring of cTn.
Conclusions: cTn assays are reliable diagnostic tests for acute myocardial
infarction, but understanding their limitations is required for appropriate
result interpretation.

DOI: 10.1093/ajcp/aqx066
PMID: 28967956 [Indexed for MEDLINE]

9. Lakartidningen. 2017 Sep 25;114. pii: ERAH.

Troponinnivåer ger nu bättre hjälp vid misstänkt hjärtinfarkt - Låga nivåer kan
med hög säkerhet utesluta hjärtinfarkt – nya analysmetoder ökar den medicinska
säkerheten.

[Article in Swedish]

Hammarsten O(1), Bjurman C(2), Holzmann M(3), Lindahl B(4).

Author information:
(1)Sahlgrenska Universitetssjukhuset - Avdelning för klinisk kemi och
transfusionsmedicin Göteborg, Sweden Sahlgrenska Universitetssjukhuset -
Avdelning för klinisk kemi och transfusionsmedicin Göteborg, Sweden.
(2)Medicinkliniken - Hallands Sjukhus Varberg, Sweden Medicinkliniken - Hallands
Sjukhus Varberg, Sweden.
(3)Institutionen för Medicin - Akutkliniken Karolinska universitetssjukhuset
Stockholm, Sweden Institutionen för Medicin - Akutkliniken Karolinska
universitetssjukhuset Stockholm, Sweden.
(4)Institutionen för medicinska vetenskaper - Uppsala, Sweden -.

Assessment of troponin levels on the emergency ward Patients with myocardial
infarction are at a high risk of sudden death and new cardiovascular events. For
this reason, it is important to identify these patients and device treatment to
reduce the risk. Patients who seek care with symptoms indicative of myocardial
infarction, mainly chest pain, constitute a large proportion of patients at our
emergency departments. However, only 5-10 % of these patients have myocardial
infarction, whereas the majority has benign causes of their symptoms. This means
that it is important not only to identify patients with myocardial infarction
quickly, but also to rule out myocardial infarction and other serious disease as
fast and safely as possible. With the aid of assays capable of measuring low
levels of the cardiac damage biomarker troponin, so-called high-sensitive
troponin assays, and several large high-quality clinical studies, myocardial
infarction can now be ruled out safely and quickly. If the patient presents with
a troponin T level below 5 ng/L and has a normal ECG, myocardial infarction can
normally be ruled out without the need for further investigation. In this way,
about 30 % of all patients who present with a suspected myocardial infarction can
leave the emergency room quickly with a high degree of medical security. On the
other hand, when patients present with troponin T levels above 40 ng/L, the
patient should normally be admitted to the hospital. These patients are a
high-risk group and constitute only 6 % of those who seek medical attention with
a suspected myocardial infarction.

PMID: 28949393 [Indexed for MEDLINE]

10. Curr Cardiol Rep. 2017 Aug 24;19(10):92. doi: 10.1007/s11886-017-0904-4.

High-Sensitivity Cardiac Troponin for the Diagnosis of Patients with Acute
Coronary Syndromes.

Vasile VC(1), Jaffe AS(2)(3).

Author information:
(1)Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic
College of Medicine, Gonda 5, Mayo Clinic, 200 First Street SW, Rochester, MN,
55905, USA.
(2)Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic
College of Medicine, Gonda 5, Mayo Clinic, 200 First Street SW, Rochester, MN,
55905, USA. Jaffe.Allan@Mayo.edu.
(3)Department of Laboratory Medicine and Pathology, Edmonton, AB, T6G 2R3,
Canada. Jaffe.Allan@Mayo.edu.

PURPOSE OF REVIEW: High-sensitivity cardiac troponin (hscTn) assays are replacing
the older-generation assays used to detect myocardial injury because they have
improved analytical sensitivity and lead to a more rapid diagnosis of acute
myocardial infarction (AMI) and enhanced risk stratification in patients with
non-ST elevation acute coronary syndromes (NSTE-ACS). This review focuses on
advantages and difficulties of using hscTn as diagnostic and prognostic tools in
acute coronary syndromes (ACS).
RECENT FINDINGS: The newer assays have a lower specificity for AMI as compared to
conventional assays, potentially leading to an increased number of unwarranted
hospitalizations and amplified cost unless how to use these assays appropriately
is appreciated. Several approaches can increase the specificity of the high
sensitivity assays. This review will present the current literature data
regarding the use of hscTn assays and will focus on modalities used to increase
the specificity, as well as the advantages and pitfalls of using the high
sensitivity approach in clinical practice.

DOI: 10.1007/s11886-017-0904-4
PMID: 28840515 [Indexed for MEDLINE]

11. Expert Rev Cardiovasc Ther. 2017 Oct;15(10):729-741. doi:
10.1080/14779072.2017.1366312. Epub 2017 Aug 22.

Using biomarkers to guide heart failure management.

Chang KW(1)(2), Fox S(1)(2), Mojaver S(1)(2), Maisel AS(1)(2).

Author information:
(1)a Division of Cardiology, Department of Medicine , University of California ,
San Diego , CA , USA.
(2)b Veterans Affair San Diego Healthcare System , San Diego , CA , USA.

INTRODUCTION: Biomarkers have revolutionized the diagnosis of heart failure (HF),
but it remains unclear how to use biomarkers to guide management of HF. Areas
covered: An exhaustive literature search on using biomarkers to guide HF
management was performed. HF guidelines were carefully scrutinized for references
pertaining to this topic, and Medline was employed to identify further
references. This review focused on natriuretic peptides, troponin, and ST2 as
biomarkers used to guide HF management. Most trials have examined secondary
prevention of chronic HF patients, and data on primary prevention of HF and
therapy of acute HF are emerging. Expert commentary: While the current data on
using biomarkers to guide HF management remain mixed, more research is necessary
to better understand how to utilize biomarkers to improve HF management.

DOI: 10.1080/14779072.2017.1366312
PMID: 28830266 [Indexed for MEDLINE]

12. Am J Med. 2017 Dec;130(12):1351-1357. doi: 10.1016/j.amjmed.2017.08.003. Epub
2017 Aug 16.

Clinical Applications of Biomarkers in Atrial Fibrillation.

Chang KW(1), Hsu JC(1), Toomu A(1), Fox S(1), Maisel AS(2).

Author information:
(1)Division of Cardiology, Department of Medicine, Veterans Affair San Diego
Healthcare System, University of California, San Diego.
(2)Division of Cardiology, Department of Medicine, Veterans Affair San Diego
Healthcare System, University of California, San Diego. Electronic address:
amaisel@ucsd.edu.

While biomarkers have greatly impacted the diagnosis and management of myocardial
infarction and heart failure, the use of biomarkers has been slow to permeate
management of atrial fibrillation. Guideline recommendations on the use of
biomarkers in atrial fibrillation were virtually nonexistent until the 2016
European Society of Cardiology guidelines on atrial fibrillation offered a class
IIb recommendation to consider using biomarkers such as high-sensitivity troponin
and natriuretic peptide to further refine stroke and bleeding risk in atrial
fibrillation patients. Biomarker levels have been associated with incident atrial
fibrillation, postoperative atrial fibrillation, acute atrial fibrillation,
diagnosis of myocardial infarction and heart failure in atrial fibrillation, and
prognosis in atrial fibrillation. This review will offer an in-depth survey of
current evidence on the use of biomarkers in atrial fibrillation and propose
clinical algorithms to aid the internist in using biomarkers in atrial
fibrillation management.

Published by Elsevier Inc.

DOI: 10.1016/j.amjmed.2017.08.003
PMID: 28822701 [Indexed for MEDLINE]

13. J Am Coll Cardiol. 2017 Aug 22;70(8):996-1012. doi: 10.1016/j.jacc.2017.07.718.

Clinical Use of High-Sensitivity Cardiac Troponin in Patients With Suspected
Myocardial Infarction.

Twerenbold R(1), Boeddinghaus J(2), Nestelberger T(1), Wildi K(1), Rubini Gimenez
M(1), Badertscher P(1), Mueller C(3).

Author information:
(1)Cardiovascular Research Institute Basel (CRIB) and Department of Cardiology,
University Hospital Basel, University of Basel, Basel, Switzerland.
(2)Cardiovascular Research Institute Basel (CRIB) and Department of Cardiology,
University Hospital Basel, University of Basel, Basel, Switzerland; Department of
Internal Medicine, University Hospital Basel, University of Basel, Basel,
Switzerland.
(3)Cardiovascular Research Institute Basel (CRIB) and Department of Cardiology,
University Hospital Basel, University of Basel, Basel, Switzerland. Electronic
address: christian.mueller@usb.ch.

High-sensitivity cardiac troponin (hs-cTn) assays have been used clinically by
thousands of physicians in many countries throughout the world since their
clinical introduction 7 years ago. In the early diagnosis of myocardial
infarction (MI), beyond doubt, the most important indication of hs-cTn assays,
these simple, inexpensive, and highly reproducible tools complement detailed
clinical assessment including chest pain characteristics and the
electrocardiogram. Hs-cTn assays for the first time allowed the precise
quantification of cardiomyocyte injury around the 99th percentile and thereby
substantially increased the accuracy of MI detection from blood obtained at
presentation to the emergency department (ED). Higher accuracy at ED presentation
enabled the development and extensive validation of early hs-cTn-based diagnostic
algorithms, which substantially reduced the time required for the safe rule-out
or rule-in of MI. This review summarizes key principles underlying the safe and
effective use of hs-cTn in the ED in patients with suspected MI.

DOI: 10.1016/j.jacc.2017.07.718
PMID: 28818210 [Indexed for MEDLINE]

14. JAMA Intern Med. 2017 Oct 1;177(10):1508-1512. doi:
10.1001/jamainternmed.2017.3597.

Eliminating Creatine Kinase-Myocardial Band Testing in Suspected Acute Coronary
Syndrome: A Value-Based Quality Improvement.

Alvin MD(1), Jaffe AS(2), Ziegelstein RC(3), Trost JC(3).

Author information:
(1)Department of Radiology and Radiological Sciences, Johns Hopkins Hospital,
Baltimore, Maryland.
(2)Division of Cardiology, Department of Medicine, Mayo Clinic, Rochester,
Minnesota.
(3)Division of Cardiology, Department of Medicine, Johns Hopkins Bayview Medical
Center, Baltimore, Maryland.

Cardiac biomarker testing is estimated to occur in nearly 30 million emergency
department visits nationwide each year in the United States. The American College
of Cardiology/European Society of Cardiology indicate that cardiac troponin is
the biomarker of choice owing to its nearly absolute myocardial tissue
specificity and high clinical sensitivity for myocardial injury. Multiple
academic medical centers have implemented interventions to eliminate the routine
ordering of creatine kinase-myocardial band tests, with published patient safety
outcomes data; however, creatine kinase-myocardial band testing is still ordered
in many hospitals and emergency departments. Eliminating a simple laboratory test
that provides no incremental value to patient care can lead to millions of health
care dollars saved without adversely affecting patient care quality, and in this
case potentially improving patient care.

DOI: 10.1001/jamainternmed.2017.3597
PMID: 28806444 [Indexed for MEDLINE]

15. Curr Heart Fail Rep. 2017 Oct;14(5):434-443. doi: 10.1007/s11897-017-0358-4.

Novel Biomarkers for the Risk Stratification of Heart Failure with Preserved
Ejection Fraction.

Cypen J(1), Ahmad T(2), Testani JM(2), DeVore AD(3)(4).

Author information:
(1)Department of Medicine, Duke University School of Medicine, Durham, NC, USA.
(2)Section of Cardiovascular Medicine, Yale University School of Medicine, New
Haven, CT, USA.
(3)Department of Medicine, Duke University School of Medicine, Durham, NC, USA.
adam.devore@duke.edu.
(4)Duke Clinical Research Institute, Duke University School of Medicine, 2400
Pratt Street, NP-8064, Durham, NC, 27705, USA. adam.devore@duke.edu.

PURPOSE OF REVIEW: The use of biomarkers in heart failure (HF) is a rapidly
changing field. The purpose of this review is to assess the current evidence of
the use of biomarkers for risk stratification in patients with HF with preserved
ejection fraction (HFpEF).
RECENT FINDINGS: Despite differences in pathophysiology between HF with reduced
ejection fraction and HFpEF, traditional HF biomarkers such as brain natriuretic
peptide and troponin retain prognostic value in most HFpEF-specific populations.
Biomarkers of key pathophysiologic components of HFpEF, such as myocardial
fibrosis, remodeling, and systemic inflammation are also valuable prognostic
markers. Further investigation into HF biomarkers may identify significant
therapeutic targets for the treatment of HFpEF.

DOI: 10.1007/s11897-017-0358-4
PMID: 28803400 [Indexed for MEDLINE]

16. Curr Probl Cardiol. 2017 Sep;42(9):266-305. doi: 10.1016/j.cpcardiol.2017.04.006.
Epub 2017 Apr 12.

Non-ST Elevation Acute Coronary Syndromes: A Comprehensive Review.

Bob-Manuel T, Ifedili I, Reed G, Ibebuogu UN, Khouzam RN.

Non-ST elevation-acute coronary syndrome (NSTE-ACS) includes NSTE myocardial
infarction and unstable angina. This patient population forms approximately
two-thirds of all hospital admissions for ACS in the United States each year and
is associated with an in-hospital mortality of 5%. NSTE-ACS is primarily due to
an acute change in the supply and demand balance of coronary perfusion and
myocardial oxygen consumption, because of the significant coronary artery
obstruction presenting as plaque rupture or erosion. Nevertheless, nonobstructive
causes may lead to that same phenomenon by excessive myocardial oxygen demand or
reduced coronary supply from hypotension, anemia, or sepsis, including transient
coronary vasospasm and endocardial dysfunction. The recent clinical application
of high-sensitivity troponin biomarker assays and computer tomography angiography
shows promise for improving the diagnosis and the risk stratification of patients
with angina symptoms. Implementation of recent updates to the American College of
Cardiology/American Heart Association (ACC/AHA) guidelines on NSTE-ACS,
especially regarding the selection and duration of antiplatelet therapy, have led
to improvement in management and outcomes of this disease. Additionally, new
adjunctive therapies and approaches to diagnosis and treatment are discussed.
Despite the progress made in recent years in the diagnosis and management of
NSTE-ACS, morbidity remains high and mortality is significant. Such a fact
suggests that future research targeting prevention, early diagnosis, and
intervention in these patients is warranted. This article provides a detailed
overview of the most recent information on the pathophysiology, diagnosis,
treatment, and prognosis of NSTE-ACS.

DOI: 10.1016/j.cpcardiol.2017.04.006
PMID: 28764841 [Indexed for MEDLINE]

17. J Am Coll Cardiol. 2017 Aug 1;70(5):558-568. doi: 10.1016/j.jacc.2017.05.062.

High-Sensitivity Cardiac Troponin Concentration and Risk of
First-Ever Cardiovascular Outcomes in 154,052 Participants.

Willeit P(1), Welsh P(2), Evans JDW(3), Tschiderer L(4), Boachie C(2), Jukema
JW(5), Ford I(6), Trompet S(7), Stott DJ(2), Kearney PM(8), Mooijaart SP(7),
Kiechl S(4), Di Angelantonio E(9), Sattar N(2).

Author information:
(1)Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria;
Department of Public Health and Primary Care, University of Cambridge, Cambridge,
United Kingdom. Electronic address: peter.willeit@i-med.ac.at.
(2)Institute of Cardiovascular and Medical Sciences, University of Glasgow,
Glasgow, United Kingdom.
(3)Department of Public Health and Primary Care, University of Cambridge,
Cambridge, United Kingdom; Transplant Unit, Papworth Hospital NHS Foundation
Trust, Papworth Everard, Cambridge, United Kingdom.
(4)Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
(5)Department of Cardiology, Leiden University Medical Center, Leiden, the
Netherlands.
(6)Robertson Centre for Biostatistics, University of Glasgow, Glasgow, United
Kingdom.
(7)Department of Gerontology and Geriatrics, Leiden University Medical Center,
Leiden, the Netherlands.
(8)Department of Epidemiology and Public Health, University College Cork, Cork,
Ireland.
(9)Department of Public Health and Primary Care, University of Cambridge,
Cambridge, United Kingdom; National Institute for Health Research Blood and
Transplant Research Unit in Donor Health and Genomics, University of Cambridge,
Cambridge, United Kingdom; NHS Blood and Transplant, Cambridge, United Kingdom;
British Heart Foundation Cambridge Centre of Excellence, University of Cambridge,
Cambridge, United Kingdom.

BACKGROUND: High-sensitivity assays can quantify cardiac troponins I and T
(hs-cTnI, hs-cTnT) in individuals with no clinically manifest myocardial injury.
OBJECTIVES: The goal of this study was to assess associations of cardiac troponin
concentration with cardiovascular disease (CVD) outcomes in primary prevention
studies.
METHODS: A search was conducted of PubMed, Web of Science, and EMBASE for
prospective studies published up to September 2016, reporting on associations of
cardiac troponin concentration with first-ever CVD outcomes (i.e., coronary heart
disease [CHD], stroke, or the combination of both). Study-specific estimates,
adjusted for conventional risk factors, were extracted by 2 independent
reviewers, supplemented with de novo data from PROSPER (Pravastatin in Elderly
Individuals at Risk of Vascular Disease Study), then pooled by using random
effects meta-analysis.
RESULTS: A total of 28 relevant studies were identified involving 154,052
participants. Cardiac troponin was detectable in 80.0% (hs-cTnI: 82.6%; hs-cTnT:
69.7%). In PROSPER, positive associations of log-linear shape were observed
between hs-cTnT and CVD outcomes. In the meta-analysis, the relative risks
comparing the top versus the bottom troponin third were 1.43 (95% confidence
interval [CI]: 1.31 to 1.56) for CVD (11,763 events), 1.67 (95% CI: 1.50 to 1.86)
for fatal CVD (7,775 events), 1.59 (95% CI: 1.38 to 1.83) for CHD (7,061 events),
and 1.35 (95% CI: 1.23 to 1.48) for stroke (2,526 events). For fatal CVD,
associations were stronger in North American studies (p = 0.010) and those
measuring hs-cTnT rather than hs-cTnI (p = 0.027).
CONCLUSIONS: In the general population, high cardiac troponin concentration
within the normal range is associated with increased CVD risk. This association
is independent of conventional risk factors, strongest for fatal CVD, and applies
to both CHD and stroke.

DOI: 10.1016/j.jacc.2017.05.062
PMCID: PMC5527070
PMID: 28750699 [Indexed for MEDLINE]

18. Medicine (Baltimore). 2017 Jul;96(27):e7030. doi: 10.1097/MD.0000000000007030.

Evidence of direct cardiac damage following high-intensity exercise in chronic
energy restriction: A case report and literature review.

Baird MF(1), Grace F, Sculthorpe N, Graham SM, Fleming A, Baker JS.

Author information:
(1)aInstitute of Clinical Exercise and Health Science, University of the West of
Scotland, Hamilton, UK bFaculty of Health, Federation University, Ballarat,
Victoria, Australia cSchool of Applied Sciences, Edinburgh Napier University,
Edinburgh dFaculty of Humanities and Social Sciences, Strathclyde University,
Glasgow, UK.

RATIONALE: Following prolonged endurance events such as marathons, elevated
levels of cardiospecific biomarkers are commonly reported. Although transiently
raised levels are generally not considered to indicate clinical myocardial
damage, comprehension of this phenomenon remains incomplete. The popularity of
high-intensity interval training highlights a paucity of research measuring
cardiac biomarker response to this type of exercise. This a posteriori case
report discusses the elevation of cardiac troponins (cTn) associated with short
interval, high-intensity exercise.
PATIENT CONCERNS: In this case report, an apparently healthy 29-year-old
recreationally active female presented clinically raised cardiac troponin I
(cTnI) levels (>0.04 ng/mL), after performing high-intensity cycle ergometer
sprints. As creatine kinase (CK) is expressed by multiple organs (e.g., skeletal
muscle, brain, and myocardium), cTnI assays were performed to determine any
changes in total serum CK levels not originating from skeletal muscle damage.
DIAGNOSIS: A posteriori the individual's daily energy expenditure indicated
chronically low-energy availability. Psychometric testing suggested that the
individual scored positive for disordered eating, highly for fatigue levels, and
low in mental health components.
OUTCOMES: The current case report provides novel evidence of elevated cTnI
occurring as a result of performing short duration, high intensity, cycle
ergometer exercise in an individual with self-reported chronically depleted
energy balance. A schematic to identify potentially "at risk" individuals is
presented.
LESSONS: Considering this as a case report, results cannot be generalized;
however, the main findings suggest that individuals who habitually restrict their
calorie intake below their bodies' daily energy requirements, may have elevated
biomarkers of exercise induced myocardial stress from performing high-intensity
exercise.

DOI: 10.1097/MD.0000000000007030
PMCID: PMC5502135
PMID: 28682862 [Indexed for MEDLINE]

19. Curr Pharm Biotechnol. 2017;18(6):456-471. doi:
10.2174/1389201018666170630120805.

Biomarkers in Stable Coronary Artery Disease.

Rusnak J(1), Fastner C(1), Behnes M(1), Mashayekhi K(2), Borggrefe M(1), Akin
I(1).

Author information:
(1)First Department of Medicine, University Medical Centre Mannheim (UMM),
Faculty of Medicine Mannheim, University of Heidelberg, Mannheim. Germany.
(2)Division of Cardiology and Angiology II, University Heart Center Freiburg -
Bad Krozingen, Bad Krozingen. Germany.

BACKGROUND: Coronary Artery Disease (CAD) is the most common reason for death in
the western hemisphere. Therefore, a well-functioning risk-management has been
established over the past decades with uprising interest in 'novel' biomarkers to
predict adverse coronary events and detect patients with subclinical CAD. This
review will focus on selected biomarkers belonging to the family of inflammatory
markers (fibrinogen or hs-CRP) or to the family of lipid-associated markers
(Lipoprotein associated PA2 or Lipoprotein a) and organ-specific biomarkers
(hs-troponin, Cystatin C or NTproBNP).
METHODS: This review is based on a pubmed search focusing on the biomarkers
fibrinogen, hs-CRP, Lipoprotein associated PA2, Lipoprotein a, hs-troponin,
NT-proBNP and Cystatin C.
RESULTS: The search retrieved 149 references containing meta-analysis,
prospective and retrospective studies concerning the usage of the selected
biomarkers in risk prediction and detection of CAD. Despite clinical studies,
current guidelines of the European Society of Cardiology (ESC), the American
Heart Association (AHA) and the Canadian Cardiovascular Society (CCS) were
analyzed regarding their recommendation of the implementation of biomarkers in
clinical routine. The review identified promising stand-alone biomarkers and
multi-marker risk models for CAD patients.
CONCLUSION: Novel biomarkers detect patients at risk beyond established risk
scores. However, an ideal biomarker fulfilling all necessary criteria does still
not exist.

DOI: 10.2174/1389201018666170630120805
PMID: 28669333 [Indexed for MEDLINE]

20. Curr Heart Fail Rep. 2017 Aug;14(4):284-300. doi: 10.1007/s11897-017-0339-7.

Biomarkers in Sleep Apnea and Heart Failure.

Zhao YY(1), Mehra R(2).

Author information:
(1)Sleep Care Solutions, 1835 Yonge Street, Suite 303, Toronto, Ontario, M4S 1X8,
Canada. yingzhao@mail.harvard.edu.
(2)Cleveland Clinic Lerner College of Medicine, Case Western Reserve University,
Cleveland, OH, USA.

PURPOSE OF REVIEW: Sleep-disordered breathing (SDB) is highly prevalent in heart
failure (HF) and may confer significant stress to the cardiovascular system and
increases the risk for future cardiovascular events. The present review will
provide updates on the current understanding of the relationship of SDB and
common HF biomarkers and the effect of positive airway pressure therapy on these
biomarkers, with particular emphasis in patients with coexisting SDB and HF.
RECENT FINDINGS: Prior studies have examined the relationship between HF
biomarkers and SDB, and the effect of SDB treatment on these biomarkers, with
less data available in the context of coexisting SDB and HF. Overall, however,
the association of SDB and circulating biomarkers has been inconsistent. Further
research is needed to elucidate the relationship between biomarkers and SDB in
HF, to evaluate the clinical utility of biomarkers over standard methods in
large, prospective studies and also to assess the impact of treatment of SDB on
these biomarkers in HF via interventional studies.

DOI: 10.1007/s11897-017-0339-7
PMID: 28667490 [Indexed for MEDLINE]

21. Curr Cardiol Rep. 2017 Aug;19(8):69. doi: 10.1007/s11886-017-0880-8.

Novel Risk Stratification Assays for Acute Coronary Syndrome.

Ahmed HM(1), Hazen SL(2)(3).

Author information:
(1)Preventive Cardiology and Rehabilitation, Cleveland Clinic, Heart and Vascular
Institute, 9500 Euclid Ave, Desk JB1, Cleveland, OH, 44195, USA. ahmedh3@ccf.org.
(2)Preventive Cardiology and Rehabilitation, Cleveland Clinic, Heart and Vascular
Institute, 9500 Euclid Ave, Desk JB1, Cleveland, OH, 44195, USA.
(3)Department of Cellular and Molecular Medicine, Cleveland Clinic, Lerner
Research Institute, Cleveland, OH, USA.

PURPOSE OF REVIEW: Since identification of aspartate aminotransferase as the
first cardiac biomarker in the 1950s, there have been a number of new markers
used for myocardial damage detection over the decades. There have also been
several generations of troponin assays, each with progressively increasing
sensitivity for troponin detection. Accordingly, the "standard of care" for
myocardial damage detection continues to change. The purpose of this paper is to
review the clinical utility, biological mechanisms, and predictive value of these
various biomarkers in contemporary clinical studies.
RECENT FINDINGS: As of this writing, a fifth "next" generation troponin assay has
now been cleared by the US Food and Drug Administration for clinical use in the
USA for subjects presenting with suspected acute coronary syndromes. Use of these
high-sensitivity assays has allowed for earlier detection of myocardial damage as
well as greater negative predictive value for infarction after only one or two
serial measurements. Recent algorithms utilizing these assays have allowed for
more rapid rule-out of myocardial infarction in emergency department settings. In
this review, we discuss novel assays available for the risk assessment of
subjects presenting with chest pain, including both the "next generation" cardiac
troponin assays as well as other novel biomarkers. We review the biological
mechanisms for these markers, and explore the positive and negative predictive
value of the assays in clinical studies, where reported. We also discuss the
potential use of these new markers within the context of future clinical care in
the modern era of higher sensitivity troponin testing. Finally, we discuss
advances in new platforms (e.g., mass spectrometry) that historically have not
been considered for rapid in vitro diagnostic capabilities, but that are taking a
larger role in clinical diagnostics, and whose prognostic value and power promise
to usher in new markers with potential for future clinical utility in acute
coronary syndrome.

DOI: 10.1007/s11886-017-0880-8
PMID: 28653131 [Indexed for MEDLINE]

22. Curr Pharm Biotechnol. 2017;18(6):482-490. doi:
10.2174/1389201018666170623090817.

Clinically Relevant Biomarkers in Acute Heart Failure: An Update.

Mukherji A(1), Ansari U(1), Borggrefe M(1), Akin I(1), Behnes M(1).

Author information:
(1)First Department of Medicine, University Medical Centre Mannheim (UMM),
Faculty of Medicine Mannheim, University of Heidelberg, Mannheim. Germany.

BACKGROUND: Acute Heart Failure (AHF), owing to the difficulties in diagnosis,
prognostic stratification and patient-related management, is still associated
with unusually high morbidity and mortality. The advent of novel biomarkers apart
from natriuretic peptides involved in myocardial injury, neuro-hormonal
activation, and ventricular remodeling augurs immense hope in redefining the
biomarker-based approach towards AHF.
METHODS: A thorough review of the available literature including latest review
articles from distinguished experts, textbook references and guidelines from
leading cardiological societies worldwide as well as the latest trials,
encompassing various biomarkers known in AHF was conducted. The most relevant
ones were chosen as references for the current review article.
RESULTS: Biomarkers such as midregional proatrial natriuretic peptide, soluble
ST2, highly-sensitive troponin, and midregional proadrenomedullin are some such
examples that have passed various stages of substantiation while there is an
array of potential biomarkers innascent stages like osteopontin, CTGF, GDF-15 and
TGF beta-1 awaiting further reiteration. Not only the diagnosis of AHF itself but
the evaluation of co-morbidities using markers like PCT, hematologic markers or
acute kidney injury markers like NGAL present a new perspective to the management
of AHF.
CONCLUSION: This review article outlines the current status of the most relevant
cardiac biomarkers related to AHF.

DOI: 10.2174/1389201018666170623090817
PMID: 28641514 [Indexed for MEDLINE]

23. Curr Heart Fail Rep. 2017 Aug;14(4):301-310. doi: 10.1007/s11897-017-0342-z.

Novel Biomarkers of Subclinical Cardiac Dysfunction in the General Population.

Shemisa K(1), Bhatt A(1), Cheeran D(1), Neeland IJ(2).

Author information:
(1)Department of Internal Medicine, Division of Cardiology, University of Texas
Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX, 75390-8830, USA.
(2)Department of Internal Medicine, Division of Cardiology, University of Texas
Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX, 75390-8830, USA.
ian.neeland@utsouthwestern.edu.

PURPOSE OF REVIEW: Recognition of subclinical myocardial dysfunction offers
clinicians and patients an opportunity for early intervention and prevention of
symptomatic cardiovascular disease. We review the data on novel biomarkers in
subclinical heart disease in the general population with a focus on
pathophysiology, recent observational or trial data, and potential applicability
and pitfalls for clinical use.
RECENT FINDINGS: High-sensitivity cardiac troponin and natriuretic peptide assays
are powerful markers of subclinical cardiac disease. Elevated levels of these
biomarkers signify subclinical cardiac injury and hemodynamic stress and portend
an adverse prognosis. Novel biomarkers of myocardial inflammation, fibrosis, and
abnormal contraction are gaining momentum as predictors for incident heart
failure, providing new insight into pathophysiologic mechanisms of cardiac
disease. There has been exciting growth in both traditional and novel biomarkers
of subclinical cardiac injury in recent years. Many biomarkers have demonstrated
associations with relevant cardiovascular outcomes and may enhance the diagnostic
and prognostic power of more conventional biomarkers. However, their use in
"prime time" to identify patients with or at risk for subclinical cardiac
dysfunction in the general population remains an open question. Strategic
investigation into their clinical applicability in the context of clinical trials
remains an area of ongoing investigation.

DOI: 10.1007/s11897-017-0342-z
PMCID: PMC5558204 [Available on 2018-08-01]
PMID: 28639234 [Indexed for MEDLINE]

24. Clin Chem. 2017 Sep;63(9):1457-1464. doi: 10.1373/clinchem.2017.271684. Epub 2017
Jun 19.

Impact of Sex on Cardiac Troponin Concentrations-A Critical Appraisal.

Eggers KM(1), Lindahl B(2).

Author information:
(1)Department of Medical Sciences and Uppsala Clinical Research Center, Uppsala
University, Uppsala, Sweden. kai.eggers@ucr.uu.se.
(2)Department of Medical Sciences and Uppsala Clinical Research Center, Uppsala
University, Uppsala, Sweden.

BACKGROUND: The use of sex-specific cutoffs for cardiac troponin (cTn) is
currently debated. Although endorsed by scientific working groups, concerns have
been raised that sex-specific cutoffs may have only a small clinical effect at
the cost of increased complexity in decision-making.
METHODS: We reviewed studies investigating the interrelations between
high-sensitivity (hs) cTn results and sex, diagnoses, and outcome. Investigated
populations included community-dwelling subjects and patients with stable angina,
congestive heart failure, or acute chest pain including those with acute coronary
syndromes.
RESULTS: Men usually have higher hs-cTn concentrations compared with women,
regardless of the assessed population or the applied assay. The distribution and
prognostic implications of hs-cTn concentrations indicate that women have a
broader cardiovascular risk panorama compared with men, particularly at lower
hs-cTn concentrations. At higher concentrations, particularly above the 99th
percentile, this variation is often attenuated. Sex-specific hs-cTn 99th
percentiles have so far shown clinical net benefit in only 1 study assessing
patients with chest pain. However, several methodological aspects need to be
considered when interpreting study results, e.g., issues related to the
determination of the 99th percentiles, the selection bias, and the lack of
prospective and sufficiently powered analyses.
CONCLUSIONS: Available studies do not show a consistent clinical superiority of
sex-specific hs-cTn 99th percentiles. This may reflect methodological aspects.
However, from a pathobiological perspective, the use of sex-specific hs-cTn 99th
percentiles makes sense for the ruling in of myocardial infarction. We propose a
new approach to hs-cTn 99th cutoffs taking into account the analytical properties
of the used assays.

DOI: 10.1373/clinchem.2017.271684
PMID: 28630238 [Indexed for MEDLINE]

25. West J Emerg Med. 2017 Jun;18(4):752-760. doi: 10.5811/westjem.2017.3.32666. Epub
2017 May 3.

Utility of the History and Physical Examination in the Detection of Acute
Coronary Syndromes in Emergency Department Patients.

Dezman ZD(1), Mattu A(1), Body R(2).

Author information:
(1)University of Maryland School of Medicine, Department of Emergency Medicine,
Baltimore, Maryland.
(2)Manchester Royal Infirmary, Department of Emergency Medicine, Manchester,
United Kingdom.

Chest pain accounts for approximately 6% of all emergency department (ED) visits
and is the most common reason for emergency hospital admission. One of the most
serious diagnoses emergency physicians must consider is acute coronary syndrome
(ACS). This is both common and serious, as ischemic heart disease remains the
single biggest cause of death in the western world. The history and physical
examination are cornerstones of our diagnostic approach in this patient group.
Their importance is emphasized in guidelines, but there is little evidence to
support their supposed association. The purpose of this article was to summarize
the findings of recent investigations regarding the ability of various components
of the history and physical examination to identify which patients presenting to
the ED with chest pain require further investigation for possible ACS. Previous
studies have consistently identified a number of factors that increase the
probability of ACS. These include radiation of the pain, aggravation of the pain
by exertion, vomiting, and diaphoresis. Traditional cardiac risk factors
identified by the Framingham Heart Study are of limited diagnostic utility in the
ED. Clinician gestalt has very low predictive ability, even in patients with a
non-diagnostic electrocardiogram (ECG), and gestalt does not seem to be enhanced
appreciably by clinical experience. The history and physical alone are unable to
reduce a patient's risk of ACS to a generally acceptable level (<1%). Ultimately,
our review of the evidence clearly demonstrates that "atypical" symptoms cannot
rule out ACS, while "typical" symptoms cannot rule it in. Therefore, if a patient
has symptoms that are compatible with ACS and an alternative cause cannot be
identified, clinicians must strongly consider the need for further investigation
with ECG and troponin measurement.

DOI: 10.5811/westjem.2017.3.32666
PMCID: PMC5468083
PMID: 28611898 [Indexed for MEDLINE]

Conflict of interest statement: Conflicts of Interest: By the WestJEM article
submission agreement, all authors are required to disclose all affiliations,
funding sources and financial or management relationships that could be perceived
as potential sources of bias. No author has professional or financial
relationships with any companies that are relevant to this study. There are no
conflicts of interest or sources of funding to declare.

26. BMJ Open. 2017 Jun 9;7(6):e013653. doi: 10.1136/bmjopen-2016-013653.

The organisational value of diagnostic strategies using high-sensitivity troponin
for patients with possible acute coronary syndromes: a trial-based
cost-effectiveness analysis.

Jülicher P(1), Greenslade JH(2), Parsonage WA(3), Cullen L(2).

Author information:
(1)Health Economics and Outcomes Research, Medical Affairs, Abbott Laboratories,
Wiesbaden, Germany.
(2)Department of Emergency Medicine, Royal Brisbane and Women's Hospital,
Herston, Australia.
(3)Department of Cardiology, Royal Brisbane and Women's Hospital, Herston,
Australia.

OBJECTIVES: To evaluate hospital-specific health economic implications of
different protocols using high-sensitivity troponin I for the assessment of
patients with chest pain.
DESIGN: A cost prediction model and an economic microsimulation were developed
using a cohort from a single centre recruited as part of the (ADAPT) trial, a
prospective observational trial conducted from 2008 to 2011. The model was
populated with 40 000 bootstrapped samples in five high-sensitivity troponin
I-enabled algorithms versus standard care.
SETTING: Adult emergency department (ED) of a tertiary referral hospital.
PARTICIPANTS: Data were available for 938 patients who presented to the ED with
at least 5 min of symptoms suggestive of acute coronary syndrome. The analyses
included 719 patients with complete data.
MAIN OUTCOMES/MEASURES: This study examined direct hospital costs, number of
false-negative and false-positive cases in the assessment of acute coronary
syndrome.
RESULTS: High-sensitivity troponin I-supported algorithms increased diagnostic
accuracy from 90.0% to 94.0% with an average cost reduction per patient compared
with standard care of $490. The inclusion of additional criteria for accelerated
rule-out (limit of detection and the modified 2-hour ADAPT trial rules) avoided
7.5% of short-stay unit admissions or 25% of admissions to a cardiac ward.
Protocols using high-sensitivity troponin I alone or high-sensitivity troponin I
within accelerated diagnostic algorithms reduced length of stay by 6.2 and
13.6 hours, respectively. Overnight stays decreased up to 43%. Results were seen
for patients with non-acute coronary syndrome; no difference was found for
patients with acute coronary syndrome.
CONCLUSIONS: High-sensitivity troponin I algorithms are likely to be
cost-effective on a hospital level compared with sensitive troponin protocols.
The positive effect is conferred by patients not diagnosed with acute coronary
syndrome. Implementation could improve referral accuracy or facilitate safe
discharge. It would decrease costs and provide significant hospital benefits.
TRIAL REGISTRATION: The original ADAPT trial was registered with the
Australia-New Zealand Clinical trials Registry, ACTRN12611001069943.

DOI: 10.1136/bmjopen-2016-013653
PMCID: PMC5577894
PMID: 28601817 [Indexed for MEDLINE]

Conflict of interest statement: Competing interests: All authors completed and
submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. PJ is
a full-time employee of Abbott Diagnostics. JHG has received funding from the
Queensland Emergency Medicine Research Foundation. WAP has received funding from
the Queensland Emergency Medicine Research Foundation, Abbott Diagnostics, Roche,
Alere and Beckmann Coulter for research on diagnostic protocols; and honoraria,
travel expenses and consultancy fees from Abbott, AstraZeneca, Hospira and
Sanofi-Aventis. LC has received funding from the Queensland Emergency Medical
Research Foundation for chest pain clinical trials from Abbott Diagnostics,
Roche, Alere, Siemens and Radiometer Pacific for clinical trials; and from Alere,
Boehringer-Ingelheim, Pfizer, AstraZeneca, Abbott Diagnostics and Radiometer
Pacific for speaking and education

27. Clin Chem Lab Med. 2017 Oct 26;55(11):1634-1651. doi: 10.1515/cclm-2016-0933.

The 99th percentile of reference population for cTnI and cTnT assay: methodology,
pathophysiology and clinical implications.

Clerico A(1), Zaninotto M(1), Ripoli A(1), Masotti S(1), Prontera C(1), Passino
C(1), Plebani M(1); on the behalf of the Study Group on Cardiovascular Risk
Biomarkers of the Italian Society of Clinical Biochemistry (SIBioC).

Author information:
(1).

According to recent international guidelines, including the 2012 Third Universal
Definiton of Myocardial Infarction by the Joint ESC/ACCF/AHA/WHF Task Force, an
increase in