cor et vasa 56 (2014) e304–e310

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Review article – Special issue: Acute Coronary Syndromes

Biochemical markers in the diagnosis of myocardial

infarction

Tomáš Janota *
3rd Department of Internal Medicine, General University Hospital and 1st Medical School, Charles University, Prague,
Czech Republic

article info abstract

Article history: The diagnosis of myocardial necrosis due to acute myocardial infarction (AMI) and other
Received 9 May 2014 causes has long been based on the plasma levels of cardiac troponins. Other markers of
Received in revised form myocardial injury such as myoglobin, heart-type fatty acid binding protein, glycogen
18 June 2014 phosphorylase isoenzyme BB, or the early and sensitive total stress marker copeptin remain
Accepted 19 June 2014 to be just attractive options used primarily to early rule out AMI and in risk stratification.
Available online 19 July 2014 Recent years have seen the introduction of a routine practice of the high-sensitivity cardiac
troponin assays capable of detecting diagnostic elevations in plasma troponin levels as early
Keywords: as the first hours of myocardial injury. However, this assay tends to identify very often low
Biochemical markers of myocardial plasma troponin levels in primarily noncardiac conditions and also in healthy or apparently
necrosis healthy individuals. Hence, this novel technology warrants further study.
Acute myocardial infarction # 2014 The Czech Society of Cardiology. Published by Elsevier Urban & Partner Sp. z.o.o.
Troponins All rights reserved.
Copeptin

Contents

Cardiac troponins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 305

Causes of increased plasma troponin levels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 305
Troponin determination using high-sensitivity assays . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 306
Increase in cardiac troponins during heavy exertion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 307
Cardiac troponins in renal failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 307
Creatine kinase MB isoenzyme mass (CK-MB mass) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 307
Catalytic activity of total creatine kinase (CK). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 307
Myoglobin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 307
Heart-type fatty acid-binding protein (h-FABP) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 307
Isoenzyme BB glycogen phosphorylase (GPBB) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 307
Copeptin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 308
Other markers of myocardial necrosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 308

* Correspondence to: 3rd Department of Internal Medicine, General University Hospital and 1st Medical School, Charles University,
U Nemocnice 1, 128 08 Prague 2, Czech Republic. Tel.: +420 2 2496 2934/31; fax: +420 2 2496 2934.
E-mail addresses: tomasjanota@[Link], [Link]@[Link]
[Link]
0010-8650/# 2014 The Czech Society of Cardiology. Published by Elsevier Urban & Partner Sp. z .o.o. All rights reserved.
 cor et vasa 56 (2014) e304–e310 e305

The strategy in suspected AMI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 308

Periprocedural AMI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 308
Conflict of interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 308
Funding body . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 308
Ethical statement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 308
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 309

cTnI are comparable only when using the same assay of a

Introduction
specific manufacturer [6]. Using standard methods, cTn should
not be detected in healthy population. For a number of
Diagnosis of myocardial necrosis and, hence, diseases such as reasons, very low levels are also detected in healthy
acute myocardial infarction (AMI) has in the past decades individuals. The diagnostic cut-off point for AMI, the upper
become the domain of biochemical diagnostic tools. However, reference limit (URL), is an arbitrary value. In 2007, URL was
the potential of biochemical assays is substantially limited by defined as the 99th percentile of a normal reference popula-
the need for high sensitivity and specificity as well as the time tion. Optimal precision of determination, as described by the
needed and the simplicity of measurement of any of the coefficient of variation, should be ≤10%. The URLs for specific
markers. Table 1 provides an overview of the biochemical kits are indicated by the manufacturer. The high demands
markers, and both of those are currently being used in clinical placed on the biochemical accuracy of the assays have led to a
practice and those with the potential to find the widespread little bit reduced sensitivity. Despite this, when collecting
acceptance in the future. While some of the markers have blood at an appropriate interval since the onset of necrosis, the
become somewhat obsolete in the meantime, others are sensitivity is close to 100%. However, in the absence of other
unlikely to be employed in everyday practice. The increasingly attributes of AMI, an increase in cTn levels is only regarded as a
more sensitive assays entail increasingly more challenging manifestation of myocardial injury. While an increase in cTn
interpretation. Use of individual markers and interpretation of can be detected within 2–4 h, a diagnostically helpful increase
the values measured require a large body of knowledge and often does not occur until 4–6 h after the event. Release of cTn
experience, which continue to expand thus deserving ade- from necrotic myofibrils of cardiomyocytes is a gradual
quate attention. process. This explains why, in the presence of extensive
myocardial necrosis, the plasma levels of cTn could remain
elevated as long as 14 days. The total amount of released cTn
Cardiac troponins corresponds to the extent of necrosis. Accurate biochemical
assessment of the extent of necrosis would require an integral
Given their sensitivity and precision of determination, cardiac of values measured at short time intervals.
troponins (cTn) currently are and are likely to remain the gold
standard in the diagnosis of myocardial necrosis. There are Causes of increased plasma troponin levels
two types of cardiac troponins, I (cTnI) and T (cTnT). They are
released exclusively from the myocardium. In the diagnosis of The potential causes of increased plasma cTn levels are listed
AMI and cardiovascular risk stratification, both troponins in Table 2. The diagnosis of AMI is based on the detection of at
provide equal information [1–3]. Plasma cTn measurement least one cTn value higher than URL followed by a decrease,
provides the basis of the Universal definition of myocardial with the levels returning to a value below URL – depending on
infarction published in 2007 as well as its most recent version the magnitude of myocardial necrosis – within hours to days
during 2012 [4,5]. As cTnT examination is patented by a single [4,5]. Thus the diagnosis of AMI requires at least two
manufacturer, it is globally standardized; however, results of measurements. In case of protracted elevation of cTn levels

Table 1 – Biochemical markers of myocardial necrosis and dynamics of their changes during acute myocardial infarction.
Marker of necrosis Onset of the Max. increase – without Duration of the
plasma levels reperfusion (h) increase
increase (h)
cTnI 2–6 12–30 1–10 days
cTnT 2–6 12–75 1–15 days
hs-cTn I/T 1 – –
CK-MB mass 3–8 9–24 1–3 days
CK 3–8 8–58 1–4 days
Myoglobin 1–3 5–8 <12 h
GPBB 0.5 1 <4 h
h-FABP 0.5 1–3 –
cTnI, cardiac troponin I; cTnT, cardiac troponin T; hs-cTnI/T, high sensitive assay for troponin I or T; CK-MB mass, creatine kinase MB
isoenzyme mass; CK, total creatine kinase; GPBB, glycogen phosphorylase isoenzyme BB; h-FABP, heart type fatty acid binding protein.
e306 cor et vasa 56 (2014) e304–e310

would often persist for several days without a decrease or even

Table 2 – The causes of increased plasma concentrations
of cardiac troponin. continue to increase. The elevations in cTn levels seen in the
presence of cardiac contusion, after cardioversion, endomyo-
Prolonged myocardial ischemia
cardial biopsy or ablation for arrhythmia are very small.
Myocarditis, pericarditis, endocarditis
Heart contusion Elective cardiac pacing results in modest elevation in cTn
Cardioversion, cardiostimulation, endomyocardial biopsy, above the URL in more than one in three patients; however, the
arrhythmia ablation increase disappears within 24 h [14]. An increased risk of
Severe heart failure cardiovascular complications is heralded by mildly elevated
Hypertensive emergencies cTn also in sepsis and other serious conditions. However, cTn
Tachyarrhythmias, bradyarrhythmias
elevations associated with these conditions are not a so
Aortic stenosis
reliable prognostic marker.
Hypertrophic cardiomyopathy
Takotsubo syndrome
Stroke, subarachnoid hemorrhage Troponin determination using high-sensitivity assays
High doses of catecholamines
Pulmonary embolization, pulmonary hypertension Besides conventional or standard methods of cTn assessment,
Aortic dissection high-sensitive cTn assays have recently become available,
Infiltrative diseases – sarkoidosis, amyloidosis, sclerodermia,
referred as hs-TnT and high-sensitive or ultra-sensitive TnI
hemochromatosis
Severe burns
(hs-TnI) [15]. The cTn is identical. High sensitive is only the
Rhabdomyolisis method. The term high-sensitivity assays refers to those
Cardiotoxic medicine (adriamycin, 5-fluorouracil, etc.) allowing cTn detection in 50–90% of the healthy adults. URL is
Snake poisons the 99th percentile of values determined in a reference group
Severe hypothyreosis of healthy individuals with a coefficient of variation <10% as
Sepsis, severe respiratory diseases with standard assays. However, URL is equal to the upper limit
Severe renal failure
of normal. High-sensitivity assays have gained widespread
acceptance, particularly the patented hs-cTnT assay. The
without an obvious decrease, the cause is more likely values determined using hs-cTn in males are slightly higher
myocarditis or another long-term cause. Mild elevations of compared with that of females [16]. The URL for males and
cTn are very often associated with tachyarrhythmias, severe females is described as 14.5 and 10 ng/l, respectively, being
heart failure, pulmonary embolism, hypotension or uncon- 13.5 ng/l in a mixed population. The differences when using
trolled hypertension. These elevations are due to a combina- hs-cTnI are likely to be even greater. The recommendation is to
tion of various mechanisms. Severe heart failure is associated use units providing results in whole numbers, that is, ng/l in
with an increase in cTn in up to 40% of the cases. More often, the SI system, although the pg/ml predominantly used in the
cTn elevations due to heart failure are seen in patients with English-language literature are numerically identical.
coronary heart disease, hypertension, diabetes mellitus and A mild elevation of hs-cTn is detected in an even larger
renal failure. In these conditions, the elevations are associated spectrum of the patients without AMI as compared with
with higher mortality rates and early rehospitalization [7]. In standard methods, e.g., in the patients with chronic, seem-
the presence of supraventricular arrhythmias, mild elevations ingly stable heart failure or in stable coronary heart disease, in
in cTn frequently occur just within the first hours of the onset those taking a variety of drugs or with more serious
of arrhythmia. In pulmonary embolism and pulmonary inflammatory diseases [17,18]. An increase in hs-cTn values
hypertension, the increase in cTn levels correlates with the is associated with increased risk of cardiovascular complica-
severity of the condition, magnitude of EKG alterations, tions. A question to be answered yet is the benefit of
echocardiographic signs of right ventricular overload and, therapeutic measures in response to these minimal detected
most importantly, with prognosis. The absence of an increase values. However, use of the triple diagnostic cut-off in an effort
in cTn implies virtually zero mortality and a minor risk of to enhance the assay specificity resulted in subsequent
complications. The negative predictive value is in the range of increased mortality [19]. It is not yet clear whether unstable
97–99%. However, cTn elevations may occasionally be detected angina can occur without being reflected in elevated hs-cTn
also in patients with mild pulmonary embolism. The positive levels. An undisputed advantage of the high-sensitivity
predictive value is relatively low (34–42%) [8–12]. In addition to methods is the earlier detection of increased plasma cTn
natriuretic peptides, increased cTn may help guide the levels [20,21]. A diagnostically useful hs-cTn elevation occurs
selection of patients benefiting from thrombolytic therapy. as early as 1 h since the onset of necrosis. The diagnosis of AMI
However, its indication cannot be based solely on this can be excluded based on the magnitude of changes in cTn
parameter [13]. A more marked increase in cTn is associated levels within the first hours of the event. The 2011 European
with takotsubo cardiomyopathy. The reason for this is unclear Society of Cardiology guidelines recommend to repeat cTn
and, perhaps, also ambiguous. The suggested action of examination at an interval of 3 h [22]. A change in cTn levels
elevated levels of circulating catecholamines may also be at (delta) can be expressed as relative (>20%) or absolute. Studies
play in stroke and subarachnoidal hemorrhage as mild cTn have suggested that the assessment based on the absolute
elevations are a frequent occurrence. Without clinical man- change is more reliable. In the case of hs-cTnT, the diagnostic
ifestations of myocardial ischemia, there is no need to value of a change is reported to be 9.2 ng/l. Using this cut-off
measure cTn repeatedly to rule out AMI. Perimyocarditis in value, the negative predictive value (NPV) was 97% and the
most cases results in a mild elevation of cTn. The elevation positive predictive value (PPV) 49%. In a subpopulation of
 cor et vasa 56 (2014) e304–e310 e307

patients with ST-segment elevations without AMI, the ideal international studies still require CK-MB mass determination.
diagnostic value was 6.9 ng/l with NPV of 93% and PPV of 83% While, similar to cTn, an increase in CK-MB mass is in most
[23]. Similar values are also recommended for follow-up cases diagnostic within 4–6 h of the onset of problems. The
measurement after 1–2 h [24,25]. As a result, AMI can be ruled levels normalize, despite extensive necrosis, as early as 48–
out as early as 2–3 h after the onset of the index event [22]. In 72 h. Creatine kinase MB mass may thus serve as an adjunct
patients experiencing earlier recurrence of AMI in the presence marker for the diagnosis of reinfarction at a time when
of a persisting increase in cTn, another AMI should be heralded circulating cTn levels are still high.
by another increase in hs-cTn by at least 20% [5]. In risk
stratification of cardiovascular complications, hs-cTn has
Catalytic activity of total creatine kinase (CK)
been shown to be more sensitive than cTn determined by a
standard method [26,27]. However, routine examinations for
the purpose of risk stratification without suspected myocardi- Due to its nonspecificity, determination of CK as a marker of
al injury are not recommended. myocardial necrosis can currently only be used as an inexpen-
sive adjunct method to assess the dynamics and extent of
Increase in cardiac troponins during heavy exertion myocardial injury, e.g., in the patients after catheter-based
recanalization of an occluded artery in a diagnostically clear AMI.
Quite often, elevated cTn and, especially, hs-cTn are detected
following an endurance activity such as the marathon race. In
Myoglobin
fact, a mildly elevated cTn does not necessarily be a
manifestation of irreversible injury but only of what is referred
to as a metabolic turnover. Myocyte regeneration occurs Given its relatively low molecular weight, in the presence of
throughout our life, and acceleration of this regenerative myocyte injury, myoglobin escapes quickly into the circulation
process after a bout of exercise resulting in myocyte death may to remain there, due to its short half-life, for only 10–30 min.
not imply irreversible myocardial injury [28–31]. What we do An increase in its plasma levels becomes apparent within 1 h
know is that the increase in cTn in trained athletes is smaller of the onset of the index event. An increase helpful in the early
compared to that seen in individuals pursuing recreational diagnosis of AMI is apparent between hours 2 and 12 of the
activities. A major increase in hs-cTn is likely to signal an event. However, myoglobin is not myocardium-specific and its
already inadequate workload for the body. plasma levels tend to rise in renal failure. The cut-off values for
males and females differ and vary according to the manufac-
Cardiac troponins in renal failure turer. Given the quick and relatively short rise, myoglobin is a
suitable adjunct marker in early diagnosis of AMI and
In moderate renal failure, cTnT levels are often mildly elevated, diagnosis of reinfarction.
with the increase being smaller with cTnI levels [32]. The reason
for the increase is not understood. Although the cause remains
Heart-type fatty acid-binding protein (h-FABP)
unclear, elevated cTn levels correlate significantly with the risk
of total mortality. Consequently, some authors recommend
measuring the cTn levels at least once a year so, when an AMI is As this specific cardiac protein, which binds fatty acids, begins to
suspected, the current cTn levels could be compared against the be released from an injured myocardium within 30 min of onset
‘‘baseline’’. Other authors do not advocate use of any ‘‘baseline’’ of the index event, it should be used to quickly rule out AMI [34].
levels claiming they have very low diagnostic value [33]. The Using semiquantitative h-FABP examination with a point-of-
most difficult findings to assess are those of dialysis patients as care test within 3 h of the first manifestations of AMI, its
TnI levels after a dialysis session drop by almost 90%. While sensitivity in study conditions has been shown to be close to
troponin should not cross the dialysis membrane, it may be up 70%, yet its performance in early diagnosis in everyday practice
taken on its surface. By contrast, postdialysis troponin T levels is still lower [34,35]. Assays for h-FABP assessment by ELISA are
tend to rise, likely as a result of hemoconcentration. The now available for the standard clinical use. There have been
diagnosis of AMI in dialysis patients thus cannot be established reports showing that the predictive value of h-FABP in
until after a more appreciable rise in cTn with a subsequent recurrence of acute coronary syndrome and death may be
relatively rapid decrease typical of AMI. It may be helpful to superior to standard cTn [36]. Couple of studies have suggested
assess the increase in levels after an interval of 1–3 h. The body that combining h-FABP with hs-cTn provides for an almost
of experience with hs-cTn is still fairly limited. negligible improvement in sensitivity of early AMI diagnosis [37].

Creatine kinase MB isoenzyme mass (CK-MB mass) Isoenzyme BB glycogen phosphorylase (GPBB)

Creatine kinase MB isoenzyme is not myocardium-specific Yet another potential early biochemical marker of myocardial
occurring for instance in a small amount in skeletal muscle. Its necrosis is an increase in the plasma levels of GPBB. Within the
use in the diagnosis AMI is considered acceptable only in cases first hour of the index event, GPBB determined by ELISA proved
where cTn assays are unavailable [4]. Although the 2011 to be the most sensitive indicator of myocardial injury with a
European guidelines for the diagnosis of non-ST-elevation sensitivity of 96%, clearly superior to that of myoglobin (71%),
acute coronary syndromes do no longer mention CK-MB, some CK-MB mass (63%), and cTnT (54%) [38]. While its predictive
e308 cor et vasa 56 (2014) e304–e310

value for mortality and rehospitalization was also high, GPBB URL in patients with nonelevated baseline values [5]. A rise of
specificity was very low (43.7%) [38]. In a study comparing point- cTn values >20% at 3 h is necessary for the diagnosis of the
of-care assays, GPBB was a less sensitive marker than h-FABP. periprocedural reinfarction if the baseline values are elevated
and are stable or falling. Smaller cTn values or smaller values
elevations would only suggest myocardial injury which is found
Copeptin
after an apparently uncomplicated elective PCI in up to a quarter
of patients. Some studies have suggested that a periprocedural
Copeptin is the C-terminal prohormone arginine-vasopressin increase in cTn significantly increases the risk of cardiovascular
(CT-proAVP). Unlike the arginine-vasopressin (antidiuretic complications including in-hospital death as well as cardiovas-
hormone), it is stable and consistently reflects any changes cular complications during follow-up [42–44]. A very mild
in arginine-vasopressin circulating levels in response to a elevation heralds the risk of cardiovascular complications in
variety of stimuli including AMI. Its plasma levels are only the early postprocedural period [45]. Determination of
dependent on gender, renal function, and a host of other CK-MB mass with a shorter half-life of the increase is also
factors. Copeptin levels correlate with left ventricular systolic helpful for the diagnosis of periprocedural AMI [46].
dysfunction. A meta-analysis of studies of baseline examina- For the diagnosis of AMI associated with cardiac surgery the
tions of the patients with suspected AMI showed the elevation of cardiac biomarker values should be >10 99th
sensitivity of copeptin alone of 63%, cTn alone 87%, yet a percentile URL in case of baseline nonelevated values. A
combination of copeptin and cTn improved sensitivity for the smaller elevation again suggests only a periprocedural
AMI diagnosis to 95–98%. Combining cTn with copeptin myocardial necrosis [4,5,47]. Even a tenfold increase above
decreased the specificity from 87% (when using cTn alone) the URL is not infrequent.
to 56%. On the other hand, a positive result of combined It has been recently recommended to determine cTn even
copeptin and cTn determination did correlate with morbidity after noncardiac surgery in at-risk patients over 45 years of age
and mortality. An increase in copeptin levels without a parallel and all those above 65 years. An increase in cTn on
increase in cTn could help earlier focusing on other conditions postoperative days 1 and 2 is reported in 8% of the patients
associated with some risk. As repeat examination of hs-cTn who are usually without complaints and EKG alterations.
after 3 h has a sensitivity of up to 100% and a high specificity, Unless there is another obvious cause, this cTn elevation is
routine introduction of copeptin examination for quick rule- considered a manifestation of ‘‘myocardial injury after
out of AIM currently seems to be quite unlikely [37,39–41]. noncardiac surgery’’ (MINS). MINS is associated with markedly
increased risk of cardiovascular and 30-day mortality and
MINS patients require closer care [48].
Other markers of myocardial necrosis

Conclusion
At present, assays of several other sensitive biomarkers – e.g.,
cysteine and glycine-rich protein 3 (Csrp3) – are available that
can be used even in very early diagnosis of myocardial injury. Given their high sensitivity, specificity, and reasonable avail-
However, none of the novel markers have been to date used in ability, cTn examinations are currently the gold standard of
clinical practice for a variety of reasons, most importantly biochemical diagnosis of myocyte necrosis whatever the
because of technical complexity and high costs involved. etiology [49,50]. Repeating an hs-cTn examination at 3 h will
provide a helpful clue in early diagnosis, diagnosis of recurrent
AMI and quick rule-out of AMI. Interpretation of mild elevations
The strategy in suspected AMI
of plasma cTn levels in healthy or apparently healthy
individuals poses a diagnostic challenge. All in all, the use
The first cTn determination is performed immediately even in and utility of other biochemical markers, especially for the
patients with a short duration of complaints. Elevated cTn purpose of early rule-out of AMI, are yet to be assessed in future.
levels may signal the onset of AMI earlier that one would guess
from the patient's medical history data or consider as just
Conflict of interest
another cause of the increase. In severe renal failure, early
blood analysis may also provide a baseline value for future
monitoring of the patient. Additional examinations to confirm The author has no conflict of interest.
the increase and subsequent decrease in cardiac markers at
standard cTn are recommended at an interval of 6–9 h, or
Funding body
within 3 h of the first hs-cTn assay. As the onset of complaints
may not coincide with that of myocardial necrosis, the
examination may need to be repeated. The preparation of this article did not use any financial support.

Periprocedural AMI Ethical statement

For the diagnosis of AMI associated with percutaneous coronary The article was prepared in accordance with the ethical
angioplasty (PCI), cTn levels should be >5 the 99th percentile principles.
 cor et vasa 56 (2014) e304–e310 e309

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