C a rdi a c Bi o m a r k e r s i n

E m e r g e n c y Ca re
Richard Body, MB ChB, PhDa,b,c,*, Cara Hendry, MDd

KEYWORDS
 Acute coronary syndromes  Biomarkers  Sensitivity and specificity  Troponin

KEY POINTS
 Cardiac troponin is the reference standard biomarker for diagnosing acute myocardial infarction
and has replaced creatine kinase-MB.
 High-sensitivity assays can rule in and rule out acute myocardial infarction for many patients with
just 1 blood test; with a second sample just 1 hour later, most patients can have the diagnosis either
ruled in or ruled out.
 Biomarkers such as copeptin and heart-type fatty acid-binding protein have shown great promise
as early markers of myocardial injury, although their use has yet to become established in wide-
spread clinical practice.

BACKGROUND for diagnosis of AMI.1 Since then, assays for cTn

Cardiac biomarkers have been used for the diag-
nosis of acute myocardial infarction (AMI) since
the 1950s. Identifying a characteristic release
pattern of creatine kinase (CK), alanine amino-
transferase, and lactate dehydrogenase could
take as long as several days but was neither sen-
sitive nor specific. Matters improved through the
subsequent use of CK-MB, a cardiac-specific iso-
form of CK. However, the subsequent develop-
ment of assays for cardiac troponin (cTn) types
cTnI and cTnT yielded substantial improvements
in diagnostic performance. In the year 2000, the
European Society of Cardiology and American
College of Cardiology jointly recommended that
cTn should be considered the preferred biomarker
have improved greatly. The third universal defini-
tion of myocardial infarction (Box 1) now defines
AMI as an increase and/or decrease of cTn with
at least 1 concentration above the 99th percentile
of values in a healthy reference population, in
conjunction with at least 1 supporting feature
from the patient’s history, electrocardiogram
(ECG), cardiac imaging, and coronary angiog-
raphy.2 The use of CK-MB is only recommended
when cTn assays are not available.
ANALYTICAL CONSIDERATIONS
Troponin is a structural protein contained within
the contractile apparatus of myofibrils. There are
3 troponins: I, T, and C. Commercially available

Disclosure Statement: R. Body’s institution has received research grants from Abbott Point of Care and Roche
Diagnostics, and has received donation of reagents for research from Alere, FABPulous BV, and Randox Labo-
ratories. C. Hendry has nothing to disclose.
a
Emergency Department, Central Manchester University Hospitals NHS Foundation Trust, Manchester Aca-
cardiology.theclinics.com

demic Health Science Centre, Oxford Road, Manchester M13 9WL, UK; b Cardiovascular Sciences Research
Group, Core Technology Facility, Grafton Street, Manchester M13 9PL, UK; c Healthcare Sciences Department,
Manchester Metropolitan University, Oxford Road, Manchester M1 5GD, UK; d Manchester Heart Centre, Cen-
tral Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Ox-
ford Road, Manchester M13 9WL, UK
* Corresponding author. Emergency Department, Central Manchester University Hospitals NHS Foundation
Trust, Manchester Academic Health Science Centre, Oxford Road, Manchester M13 9WL, UK.
E-mail address: Richard.body@manchester.ac.uk

Cardiol Clin 36 (2018) 27–36

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28 Body & Hendry

Box 1 of cTn. This includes an understanding of some

A summary of the requirements for a diagnosis
of acute myocardial infarction as specified in
the third universal definition of myocardial
infarction
This requires
 Detection of an increase and/or decrease of
cTn with at least 1 value above the 99th
percentile of a healthy reference population
Plus at least 1 of
 History compatible with myocardial ischemia
 New compatible ECG changes (eg, ST-segment
deviation, left bundle branch block, patho-
logic Q waves)
 Imaging evidence of new loss of viable
myocardium
 Intracoronary thrombus on coronary
angiography
AMI, evidence of myocardial necrosis plus evidence of
myocardial ischemia.
Data from Thygesen K, Alpert JS, Jaffe AS, et al.
Third universal definition of myocardial infarction. J
Am Coll Cardiol 2012;60(16):1581–98.
automated immunoassays are available for highly
cardiac-specific isoforms of cTnI and cTnT. To
comprehend recent advances in cTn assays
and their practical application, it is important for
clinicians to have a basic understanding of impor-
tant analytical issues relating to the measurement
key terminology, summarized in Box 2.
Importantly, clinicians must understand the
concept of precision. No cTn assay will return
exactly the same result when the same sample is
repeatedly measured. The precision of the assay
relates to the degree of scatter that is likely to be
obtained, and this is measured by the coefficient
of variation (CV). When measuring a sample with
a concentration equal to the 99th percentile upper
reference limit, the optimal CV for a cTn assay is
less than or equal to 10%. A CV greater than
20% has been described as unacceptable for clin-
ical use.3 As precision improves, it is possible to
have greater confidence that an observed increase
or decrease of cTn concentrations on serial sam-
pling is in fact genuine, rather than being a conse-
quence of assay imprecision.
Until recently, cTn assays have been limited by
the inability to detect cTn concentrations in appar-
ently healthy individuals. Thus, the 99th percentile
upper reference limit has been equal to the limit of
detection (LoD) of the assay. This may explain why
cTn remains an insensitive tool for diagnosis of
AMI in the first hours after the onset of AMI.
Because of this, with contemporary cTn assays
patients must usually remain in the hospital for se-
rial sampling over 6 to 9 hours before the diagnosis
of AMI can be confidently ruled out.
HIGH-SENSITIVITY TROPONIN ASSAYS
The clinical utility of the first high-sensitivity cTn
(hs-cTn) assay was first reported in 2009.4,5 There

Box 2
Key definitions relating to analytical performance of cardiac troponin T assays

99th percentile
Refers to the 99th percentile of cTn concentrations in a sample of apparently healthy individuals
By convention, this is used to define the upper reference limit of cTn assays
Limit of blank (LoB)
When analyzing a sample containing no cTn, assays will not always return a result of zero
The LoB is derived by repeatedly testing a sample that is known to contain no cTn and is equal to the
mean plus 1.645 multiplied by the standard deviation of the results obtained
Limit of detection (LoD)
The lowest concentration of analyte that can be distinguished from the LoB; the LoD will, therefore,
be higher than the LoB
Coefficient of variation (CV)
Measures the precision of an assay and expressed as a percentage
Equal to the standard deviation divided by the mean of repeated measurements on any given sample
Data from Armbruster D, Pry T. Limit of blank, limit of detection and limit of quantitation. Clin Biochem Rev
2008;29(Supplement 1):S49–52.

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 Cardiac Biomarkers in Emergency Care 29

are currently 2 commercially available hs-cTn as-
says available from Roche Diagnostics (Roche
Elecsys fifth generation, Basel, Switzerland)
and Abbott Laboratories (Abbott ARCHITECT,
Chicago, IL).6 The hs-cTnT assay recently
received US Food and Drug Administration
approval in the United States. To be labeled as
high sensitivity, cTn assays must fulfill 2 criteria:
 The CV must be less than 10% when
measuring cTn concentrations equal to the
99th percentile upper reference limit of the
assay (this relates to the precision of the assay)
 The assay must be able to detect cTn concen-
trations in at least 50% of apparently healthy
individuals (this relates to the analytical sensi-
tivity of the assay).
Thus, an assay is defined as high-sensitivity
based on analytical characteristics rather than
diagnostic performance. However, the favorable
analytical characteristics of hs-cTn assays do
lead to important tangible benefits for the early
diagnosis of AMI.
EARLY RULE-OUT STRATEGIES WITH HIGH-
SENSITIVITY TROPONIN ASSAYS
Accelerated Serial Sampling
The first advantage of hs-cTn assays for ruling out
AMI is that the period of so-called troponin
blindness, in which patients with AMI still have
troponin concentrations within the normal range,
is reduced. As such, it is now apparent that the
detection of hs-cTn concentrations within the
normal range, both on arrival in the emergency
department (ED) and 3 hours later, has a high sensi-
tivity and negative predictive value (NPV) for AMI.7
This strategy has been recommended for clinical
use by the European Society of Cardiology.8 There
is, however, a reason for caution with this
approach. Evidence emerging since publication of
that guidance does suggest that the 3-hour rule-
out strategy may actually have suboptimal sensi-
tivity.9 Therefore, if used, it would seem prudent
to use additional means of risk stratification (Fig. 1).
The enhanced precision of hs-cTn assays yields
another important benefit. Because there will be
less variation when repeatedly testing samples
known to contain the same concentration of
troponin, clinicians can be more confident that
any observed small change on serial sampling is
genuine, rather than being due to assay impreci-
sion. By this principle, AMI can be ruled out by se-
rial sampling over as little as 1 hour in the presence
of low initial hs-cTn concentrations and minimal
absolute change (Box 3). With the hs-cTnT assay,
this 1-hour algorithm has been shown to have a
sensitivity of 96.7% and a NPV of 99.1% in a multi-
center observational study of 1282 patients in 9
countries who presented to the ED within 6 hours

Fig. 1. European Society of Cardiology proposed 0/1h diagnostic algorithm with high sensitivity cardiac troponin
assays. (From Roffi M, Patrono C, Collet J-P, et al. 2015 ESC Guidelines for the management of acute coronary syn-
dromes in patients presenting without persistent ST-segment elevation: task force for the management of acute
coronary syndromes in patients presenting without persistent ST-segment elevation of the European Society of
Cardiology (ESC). Eur Heart J 2016;37:276; with permission.)

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30 Body & Hendry

Box 3
Summary of the 0-hour/1-hour rule-out algorithm for high-sensitivity cardiac troponin T (Roche Elecsys
assay) and high-sensitivity cardiac troponin I (Abbott ARCHITECT assay)

Admission blood sample

 Rule out if hs-cTnT (Roche) is less than 5 ng/L or hs-cTnI (Abbott) is less than 2 ng/L
 Rule in if hs-cTnT or hs-cTnI is greater than 52 ng/L
 All other patients require a second sample in 1 hour
1-hour blood sample
 Rule out if hs-cTnT is less than 12 ng/L on arrival and less than 3 ng/L change at 1 hour, or hs-cTnI is less
than 5 ng/L on arrival and less than 2 ng/L change at 1 hour
 Rule in if change from baseline is greater than 5 ng/L (hs-cTnT) or greater than 6 ng/L (hs-cTnI)
 All other patients remain in the observation zone and require further serial sampling at later time
points
Data from Roffi M, Patrono C, Collet J-P, et al. 2015 ESC guidelines for the management of acute coronary syndromes
in patients presenting without persistent ST-segment elevation. Eur Heart J 2016;37(3):267–315; and Authors/Task
Force Members, Hamm CW, Bassand J-P, Agewall S, et al. ESC Guidelines for the management of acute coronary syn-
dromes in patients presenting without persistent ST-segment elevation: The Task Force for the management of acute
coronary syndromes (ACS) in patients presenting without persistent ST-segment elevation of the European Society of
Cardiology (ESC). Eur Heart J 2011;32(23):2999–3054.

of symptom onset.10 This strategy could rule out recommended for clinical adoption by the
AMI in more than 60% of patients’. European Society of Cardiology.8

Using Cardiac Troponin with Risk Scores

Single Test Rule-Out
These accelerated rule-out algorithms can clearly
help to unburden crowded EDs and hospitals by
reducing overall length of stay. However, they do
still rely on serial troponin sampling. In a busy
ED, an ideal diagnostic strategy would enable
AMI to be ruled out with a single blood test at
the time of arrival. With the enhanced analytical
sensitivity of hs-cTn assays and the ability to
detect smaller troponin concentrations, this can
now be achieved. In the absence of ECG ischemia,
a single hs-cTn concentration below the LoD of the
assay has consistently been shown to have a high
sensitivity and NPV for AMI with both the hs-
cTnT11–16 and hs-cTnI17,18 assays, especially if
more than 2 hours have elapsed since symptom
onset. This has been dubbed the LoD rule-out
strategy. Prospective studies, which are most
likely to best represent the population in which
this strategy is likely to be used in practice, sug-
gest that the proportion of patients ruled out will
vary between 17% and 40%.
Combining this LoD rule-out strategy with the
1-hour algorithm, such that patients who are not
ruled out by the former would undergo repeat
hs-cTn sampling 1 hour later, would mean that
all patients are ruled out at the earliest possible
opportunity with maximal sensitivity. This is
called the 0-hour/1-hour algorithm has also been
Troponin-based strategies such as the 0/1-hour
algorithm enable rapid exclusion of AMI but
cannot necessarily be used alone to guide deci-
sions to admit or discharge patients. With hs-cTn
assays, many patients who were previously diag-
nosed with unstable angina are now diagnosed
with non-ST-elevation myocardial infarction
(NSTEMI).19 However, the term unstable angina
cannot yet be completely eliminated. The inci-
dence of major adverse cardiac events (MACEs)
in patients who have AMI ruled out by troponin-
based strategies is far from negligible. For
example, the 1-hour algorithm with hs-cTnT has
been shown to have a sensitivity of only 87.5%
for MACE at 30 days.20 In total, 3.4% of patients
ruled out with the LoD strategy also develop
MACE within 30 days.14 Therefore, additional risk
stratification remains necessary before making a
decision to discharge patients and terminate
further investigation. Several approaches have
been validated and are summarized in Table 1.
USING CARDIAC TROPONIN TO RULE IN
ACUTE MYOCARDIAL INFARCTION
Although early rule-out of AMI is important to
unburden crowded hospitals and EDs, early
rule-in may also facilitate rapid treatment of those
who do have the condition. For example,

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 Cardiac Biomarkers in Emergency Care 31

Table 1
A summary of some of the contemporary methods for risk stratification in the high-sensitivity troponin
era

Troponin
Timing Details of Risk Score Summary of Evidence Base
HEART score On arrival 0–2 points for each of the Derivation
(original following N/A (intuition)
version)  history (highly suspicious, External validation35
moderately suspicious, slightly Systematic review and meta-analysis
suspicious) of 9 studies, including 11,217
 ECG (ST depression; T wave subjects, showed a pooled
inversion, normal) sensitivity and specificity of the
 Age (>65 y, 45–65 y, <45 y) HEART score for predicting MACE of
 Risk factors (3, 1–2, 0) 96.7% (95% CI 94.0%–98.2%) and
 Troponin (>3 times upper 47.0% (95% CI 41.0%–53.5%),
reference limit, respectively
1–3 times upper reference Pooled incidence of MACE in low risk
limit, normal) subjects was 1.6%.
<3 points 5 low risk (suitable for Interventional trial36
early discharge) Stepped wedge noninferiority RCT
comparing HEART score to usual
care (not further specified) in 3648
subjects
HEART score had a noninferior
incidence of MACE at 6 wk ( 1.3%
difference in favor of the HEART
score, with a 1-sided 95%
CI of 2.1%)
The HEART score did not increase early
discharges (adjusted difference
0.7%, 95% CI 5.6%–7.0%) or
length of stay
Troponin-only On arrival Computer algorithm, accounting Derivation37
Manchester for n 5 703, derived by logistic
Acute  troponin regression 37.7% subjects ruled
Coronary  ECG ischemia out with sensitivity 98.7%
Syndromes  sweating observed (95% CI 97.3%–99.9%) and NPV
(MACS)  pain associated with vomiting 99.3% (95% CI 97.3%–99.9%)
decision aid  pain radiation to right arm or Rule in for 10.1% with 100%
right shoulder specificity
 worsening (crescendo) angina External validation37
 systolic blood pressure n 5 1459 from 3 centers
<100 mm Hg 40.4% subjects ruled out with
T-MACS calculates the sensitivity 98.1% (95% CI
probability of ACS 95.2%–99.5%), NPV 99.3%
Rule out if probability <2% (98.3%–99.8%)
Rule in if probability >95% 4.7% subjects ruled in with 91.3% PPV
Interventional trial38 (original version of
the rule, MACS)
131 subjects randomized to MACS or
standard care (12h troponin) MACS
increased successful discharges
(26% vs 8%, adjusted odds ratio 5.5,
95% CI 1.7–17.1, P 5 .004)
No MACE among early discharges
(continued on next page)

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32
Table 1
(continued )

Troponin
Timing Details of Risk Score Summary of Evidence Base
ADAPT ADP 0 and 2 h TIMI risk score criteria: 1 point Derivation
for each of N/A
 Aspirin use in past 7 d External validation39
 Age 65 y n 5 1975
 Severe anginal symptoms 20.0% ruled out, sensitivity 99.7%
(>2 episodes in 24 h) (95% CI 98.1%–99.9%); NPV 99.7%
 Known coronary stenosis of (95% CI 98.6%–100.0%)
50% or more (or history of Interventional trial40
coronary artery disease) Individually randomized 542 subjects
 At least 3 risk factors for to TIMI protocol or standard care
coronary artery disease (6h troponin testing)
 ST deviation >0.5 mm Successful discharge within 6 h for
 Troponin elevation (>99th 19.3% vs 11.0%, P 5 .08, odds ratio
percentile) 1.92 (95% CI 1.18–3.13)
Subjects discharged if TIMI 1 MACE in intervention group (0.4%)
score 5 0 and serial troponins
normal
ED-ACS score On arrival Score calculated using the Derivation41
and 2 h following n 5 1974
later  Age 42.2% ruled out with sensitivity 99.0%
 Known coronary artery disease External validation42,43
 At least 3 risk factors for 1. n 5 763, 41.6% ruled out with 100%
coronary artery disease (95% CI 94.2%–100.0%) sensitivity
 Diaphoresis 2. N 5 282, 66.7% ruled out with
 Pain radiation to neck, arm, sensitivity 88.2% (95% CI
or jaw 63.6%–98.5%) for MACE
 Pain worse on inspiration Interventional trial44
 Palpation reproduces pain N 5 558
Subjects with normal ECG, ED-ACS vs TIMI No different in early
normal troponins, and score discharge (32.2% vs 34.4%, P 5 .65)
<16 can be ruled out No MACE at 30 d
HEART On arrival As for the HEART score but Derivation (retrospective)45
pathway and 3 h requires a second troponin test 1070 subjects with nondiagnostic ECG
later after 3 h Incidence of MACE in subjects with
(original) HEART score <3 was 0.6%
but sensitivity for MACE only 58%
(95% CI 32%–81%).
Adding a second troponin at 4-6 h
gave 100% sensitivity (95%
CI 72%–100%)
External validation46
Secondary analysis from prospective
cohort, n 5 1050. 20% subjects
identified as low-risk
Sensitivity 99% (95% CI 97%–100%)
for MACE
Intervention trial
282 subjects randomized to HEART
pathway or standard care (serial
biomarkers plus subsequent
objective cardiac testing)
More subjects discharged without
objective cardiac testing in the
HEART pathway arm (39.7% vs
18.3%, P<.001) with no MACEs
at 30 d

Abbreviations: ADAPT ADP, A 2hr Accelerated Diagnostic Protocol to Assess patients with chest Pain symptoms using
contemporary Troponins as the only biomarker; ED-ACS, emergency department assessment of chest pain score; HEART,
history, electrocardiogram, age, risk factors and troponin; PPV, positive predictive value; RCT, randomized controlled trial;
T-MACS, Troponin-only Manchester Acute Coronary Syndromes; TIMI, thrombolysis in myocardial infarction.

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meta-analysis has demonstrated that early inter-
vention reduces recurrent ischemia (relative risk
0.59, 95% CI 0.38–0.92, P 5 .02) and hospital
stay (by 28%, 95% CI 22%–35%, P<.001) with a
trend toward reduced major bleeding.21 In the
Troponin-only Manchester Acute Coronary Syn-
dromes (T-MACS) trial, selection of an early inva-
sive strategy in high-risk patients resulted in a
28% reduction in the endpoint of death, myocar-
dial injury, stroke, or refractory ischemia.22 In
conjunction with risk-scoring, hs-cTn may aid in
streamlining of pathways to intervention and sup-
port clinicians in reducing risk and length of hospi-
tal stay.
However, with increasingly sensitive assays, the
prevalence of positive cTn results has increased.19
Although many of these patients have small AMIs
that could not previously be detected, there has
also been an increase in positive results in patients
who do not have AMI. This presents new chal-
lenges for practicing clinicians.
It is important to note that cTn is highly cardiac-
specific. Detection of an elevated concentration is,
therefore, a reliable indication of myocardial injury.
However, there are many causes of myocardial
injury, of which AMI is just 1. To differentiate AMI
from other causes of myocardial injury, clinicians
must consider 2 key points, as follows.
Clinical Context
Considering the clinical context is arguably the
most crucial step in determining the cause of
myocardial injury. Patients with type 1 AMI (pri-
marily caused by complications of coronary artery
disease, including plaque rupture) are likely to pre-
sent with symptoms that are compatible with
myocardial ischemia. Those symptoms may, of
course, be atypical.23 Type 2 AMI is caused by
an imbalance in the supply and demand of oxygen
to the myocardium. In this case, consideration of
the clinical context will reveal systemic distur-
bance (eg, arrhythmia, shock). Differentiation be-
tween these is important because patients with
type 2 AMI should focus on addressing the under-
lying condition. Although it is clear that an inter-
ventional strategy and antiplatelet agents are
beneficial for patients with type 1 AMI, this is not
clear for those with type 2 AMI. Detection of the
type 2 AMI is, however, important because the
mortality is approximately double that of type 1
AMI.24
Detection of an Increase and/or Decrease
of Troponin Concentrations
Many patients have a chronic elevation of cTn at
baseline, in which case serial sampling will not
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Cardiac Biomarkers in Emergency Care 33
demonstrate a significant change in the concen-
tration over time. There are many causes of
chronic cTn elevation, including chronic kidney
disease, left ventricular systolic impairment, car-
diovascular disease, a heavy burden of risk factors
for coronary artery disease, and advancing age.25
Understanding that such patients may have
chronic cTn elevations may help to avoid over-
diagnosis and over-treatment while the outcome
of serial sampling is awaited.
In contrast, in patients with acute myocardial
injury clinicians would expect to detect an increase
and/or decrease in cTn concentration over time.
Serial sampling is, therefore, required to rule in
the diagnosis of AMI. With the improved precision
of modern cTn assays, it is possible to be confi-
dent that smaller changes in cTn concentration
over time are genuine, rather than being the result
of assay imprecision. Perhaps as a result, it has
been demonstrated that absolute changes in cTn
concentration (maximum cTn concentration minus
minimum cTn concentration) have greater diag-
nostic accuracy than relative changes. The degree
of change required will vary by assay but is
approximately equal to half the 99th percentile.26
Possible Exceptions to the Requirement
for Serial Sampling
The third universal definition of myocardial infarc-
tion clearly states the requirement to detect an in-
crease and/or decrease of cTn, implying that serial
sampling is always necessary to rule in the diag-
nosis of AMI. There may, however, be exceptions.
First, detection of an intracoronary thrombus at
invasive angiography before the outcome of serial
cTn sampling could be considered diagnostic.
Second, serial sampling may not increase positive
predictive value in patients with very high cTn con-
centrations on arrival. For example, a recent anal-
ysis demonstrated that serial sampling offers no
additional diagnostic value when initial hs-cTnT
concentrations are greater than 80 ng/L.27
OTHER BIOMARKERS TO ENHANCE THE
DIAGNOSIS OF ACUTE CORONARY
SYNDROME
A decade ago there was substantial interest in
identifying additional biomarkers of acute coro-
nary syndrome, particularly those that may identify
early presenters in the period of so-called troponin
blindness before cTn concentrations begin to in-
crease. Unfortunately, these biomarkers failed to
live up to early promise and none could be shown
to add value when used in addition to sensitive cTn
assays. There does, however, remain interest in 2
biomarkers.
34 Body & Hendry
Copeptin is the prohormone of vasopressin.
Circulating levels increase very early after the
onset of AMI. Two meta-analyses have demon-
strated that the combination of copeptin and cTn
has greater diagnostic accuracy than cTn
alone.28,29 However, the sensitivity for the combi-
nation of a contemporary (ie, not high-sensitivity)
cTn assay plus copeptin is probably suboptimal
for rule-out (pooled sensitivity 95%; 95% CI
89%–98%).29 The combination of hs-cTnT and
copeptin yields a higher pooled sensitivity (98%;
95% CI 96%–100%) but the added value of
copeptin, over and above cTn-based rule-out stra-
tegies, remains to be proven. Promisingly, howev-
er, a 7-center randomized controlled trial of 902
subjects has shown that copeptin can be used to
reduce length of stay and yields noninferior clinical
outcomes. In that trial, subjects were randomized
to receive care guided by a copeptin-based algo-
rithm or standard care. Those in the copeptin arm
showed modest reductions in length of stay
(7 hours vs 4 hours, P<.001), whereas the inci-
dence of MACE was not statistically significantly
different between groups.30
Another biomarker that has shown promise is
heart-type fatty acid-binding protein (H-FABP).
Concentrations of this small, highly cardiac-
specific protein have been shown to increase early
after the onset of AMI.31 Interestingly, H-FABP
seems to provide diagnostic and prognostic infor-
mation that is independent of cTn and ECG abnor-
malities.32,33 However, systematic review has
suggested that sensitivity and NPV may be subop-
timal for early rule-out.34 More evidence is still
required for routine use of this promising
biomarker to be recommended.
SUMMARY
Cardiac biomarkers are central to the diagnosis of
AMI. CTn is the reference standard biomarker.
With the availability of hs-cTn assays, it is now
possible to immediately rule out AMI in the ED
following a single blood test in many patients.
Although sensitivity is not perfect, up to two-
thirds of patients could have AMI ruled out with 2
samples drawn an hour apart. The use of validated
risk scores may help to increase the safety of early
discharge. Although cTn is highly cardiac specific,
it is important to remember that it is a marker of
myocardial injury. AMI is only 1 cause of myocar-
dial injury. Clinicians must remember to interpret
cTn concentrations in conjunction with the clinical
context. Except in patients with very high initial
cTn elevations, serial sampling remains a neces-
sity to differentiate chronic cTn elevations from
acute myocardial injury. More evidence is required
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before routine use of additional biomarkers can be
recommended.
REFERENCES
1. The Joint European Society of Cardiology/American
College of Cardiology Committee. Myocardial
infarction redefined - a consensus document of
the Joint European Society of Cardiology/American
College of Cardiology Committee for the redefinition
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