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4/5/2017 DiagnosingType2MyocardialInfarctionAmericanCollegeofCardiology

DiagnosingType2MyocardialInfarction
May 18, 2016 |Paul Collinson, MD; Bertil Lindahl, M.D., Ph.D.

ExpertAnalysis

The ability to measure cardiac troponin, either cardiac troponin T (cTnT) or cardiac
troponin I (cTnI), marked a paradigm shift in the use of cardiac biomarkers for the
diagnosis of myocardial infarction (MI). For the rst time, a totally cardiac-specic
test was available that would detect myocardial injury even in the presence of
concomitant skeletal muscle injury. Comparison with the existing cardiac
biomarkers creatine kinase and creatine kinase-myocardial band (CK-MB) showed
diagnostic equivalence for detection of classical MI. More importantly, a large
proportion of patients with a diagnosis of unstable angina were found to have an
elevated cardiac troponin, and those patients were found to have a worse
prognosis compared with those who did not have elevated cardiac troponin.1
These ndings provided the impetus to shift to the use of cardiac troponin as the
cardiac biomarker of choice and the proposed redenition of MI.

There are some caveats that must be remembered. At this point in time, the
diagnostic "gold standard" biochemical test for diagnosis of MI was measurement
of CK-MB. Second, the usual threshold was a CK-MB twice the upper reference
limit, which reduced diagnostic sensitivity. It had previously been demonstrated
that minor rises in CK-MB about the upper reference limit but below the
diagnostic limit were associated with an adverse prognosis. It is therefore
unsurprising that cardiac troponin, a cardiac-specic test, was both more sensitive
and, because the diagnostic discriminant was optimised against CK-MB, more
specic.

The use of troponin as biochemical "gold standard" had an immediate result of


increasing the number of patients who had a nal diagnosis that excluded MI who
were noted to have an elevated troponin. Chronic elevation of both cTnT and cTnI
had been noted in renal failure early in the introduction of troponin testing.1 The
recommendation to use the 99th percentile as diagnostic discriminant and the
progressive improvements in assay sensitivity further increased the range of
clinical conditions with concomitant cardiac troponin elevation. This is illustrated
in the list included in the most recent iteration of the universal denition of MI.2
In addition, new clinical entities that mimic MI, such as spontaneous coronary
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artery dissection and Takotsubo (stress) cardiomyopathy, have been identied.3 As


it has been sardonically observed by Bob Jesse, "when troponin was a lousy assay
it was a great test, but now that it's becoming a great assay, it's getting to be a
lousy test."4 Therefore, in an attempt to address the problem of troponin
elevation outside of traditional MI, the concept of type 2 MI was introduced in the
universal denition of MI.5

Type 2 MI is dened as "myocardial infarction secondary to ischaemia due to


either increased oxygen demand or decreased supply, e.g. coronary artery spasm,
coronary embolism, anaemia, arrhythmias, hypertension or hypotension."

The denition of type 2 MI is unsatisfactory because it is not really dened by


what it is but rather what it is not.6 Nevertheless, the clinical problem remains: to
distinguish acute MI (associated with plaque rupture or erosion, traditional or type
1 MI)for which there is evidence-based treatmentfrom acute secondary
ischaemic cardiac injury, including type 2 MI, where such treatments are not
evidence based and may even be harmful.

The role of troponin measurement is in the dierential diagnosis of suspected


non-ST-segment elevation MI (NSTEMI). Patients presenting with ST-segment
elevation MI require immediate intervention based on current guidelines and thus
should not wait for troponin results.

The rst stage is to assess the probability that the patient has underlying acute
coronary artery disease (CAD) from the clinical history and that the symptoms are
caused by cardiac ischemia. The assessment of the probability that the patient has
underlying CAD may be an informal classication into high, medium, or low risk or
a more formal risk score. Cardiac ischemia is assessed by the electrocardiogram
(ECG) and interpretation of the symptoms. An initial troponin measurement
should be made as well as assessment of renal function and other appropriate
laboratory tests and investigations guided by the clinical presentation of the
patient.

A holistic assessment is required at this point. This must assess the totality of the
ndings in a circular rather than linear fashion. It is important that the results of
laboratory tests taken as a whole are consistent with the clinical features and the
ECG. If the troponin is not elevated, then repeat testing is required before acute
myocardial injury can be excluded with certainty. On the other hand, a single
elevated troponin is not, on its own, diagnostic of MI. However, an elevated
troponin along with other appropriate clinical and laboratory evidence raises the
probability that the diagnosis is NSTEMI. The higher the troponin value, the
greater the probability that the nal diagnosis will be MI. It must be stressed that
the data must be consistent. An elevated troponin plus a normal ECG or
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nonspecic changes should immediately raise suspicion of an alternate diagnosis.


Similarly, there should be no other occult but acknowledged causes of minor
troponin elevation, such as renal failure or signicant age. Other potential acute
causes of troponin elevation associated with CAD such as tachycardia or other
conditions causing increased oxygen demand or reduced oxygen supply indicate a
type 2 MI. However, even if the clinical probability of underlying CAD is high, a
nal diagnosis of MI requires demonstration of a changing troponin value.
Contemporary sensitive assays are able to detect a signicant troponin change on
retesting if the initial value is elevated with a repeat test performed 2-3 hours
later and with high sensitivity assays within 1 hour.

Repeat testing allows the immediate distinction between an acute myocardial


injury and underlying chronic myocardial damage causing troponin elevation. This
resolves the dilemma of the patient with renal disease (or high age). An elevated
troponin in the rst sample is to be expected in the patient with renal failure. A
changing troponin indicates acute injury and may be due to an acute MI. In
contrast, an elevated troponin that does not change signicantly is due to chronic
myocardial injury and may require further investigation but possibly not as an in-
patient and not necessarily by a cardiologist.

The next phase of the evaluation is to distinguish between an acute troponin rise
that is consistent with acute MI and one that is due to another cause. The
diagnosis of acute MI should never be made on the basis of a troponin elevation
alone. Again, a complete evaluation of the patient requires that the troponin rise
is consistent with the clinical ndings and the ECG. An elevated troponin with
minimal ECG ndings can occur with myocarditis or pulmonary embolism. The
most important factor is to be aware that other clinical conditions can cause a
troponin elevation. Troponin elevation is specic for myocardial injury, but not
every troponin elevation is an MI. The presence of other clinical conditions such as
pneumonia or pulmonary embolus should shift the clinical focus to an
appreciation that the troponin elevation is an additional prognostic rather than
diagnostic nding. If there is diagnostic uncertainty, cardiac imaging, either
invasive or noninvasive, as well as other types of cross sectional imaging is
necessary to provide additional information.

Therefore, the key features to diagnose a type 2 MI (more properly secondary


ischaemic cardiac injury), can be summarised as follows:

An elevated but changing troponin value


Clinical features inconsistent with type 1 acute MI
Clinical conditions known to increase the oxygen demand or decrease the
oxygen supply like tachycardia

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Potentially confounding clinical conditions or comorbidities that are potentially


associated or known to be associated with myocardial injury
Absence of symptoms and/or signs indicating other nonischemic causes of
troponin elevations like myocarditis.

Treatment of type 2 MI is to treat the underlying condition and hence remove the
cardiac insult. To adequately assess the prognosis and determine appropriate
further treatment in patients with type 2 MI, information about whether the
patient has (or is likely to have) signicant underlying CAD is essential.7 In
addition, it is important to remember that elevated troponin in the patient with
non-acute MI is not redundant information but also indicates an adverse
prognosis (Figure 1).8

Figure 1

References

1. Collinson PO, Garrison L, Christenson RH. Cardiac biomarkers - A short


biography. Clin Biochem 2015;48:197-200.

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2. Thygesen K, Alpert JS, Jae AS, et al. Third universal denition of myocardial
infarction. Eur Heart J 2012 ;33:2551-67.
3. Lettieri C, Zavalloni D, Rossini R, et al. Management and Long-Term Prognosis
of Spontaneous Coronary Artery Dissection. Am J Cardiol 2015;116:66-73.
4. Jesse RL. On the relative value of an assay versus that of a test: a history of
troponin for the diagnosis of myocardial infarction. J Am Coll Cardiol
2010;55:2125-8.
5. Thygesen K, Alpert JS, White HD, et al. Universal denition of myocardial
infarction. Circulation 2007;116:2634-53.
6. Collinson P, Lindahl B. Type 2 myocardial infarction: the chimaera of
cardiology? Heart 2015;101:1697-703.

Clinical Topics: Acute Coronary Syndromes, Arrhythmias and Clinical EP, Heart
Failure and Cardiomyopathies, Prevention, Vascular Medicine, ACS and Cardiac
Biomarkers, Implantable Devices, SCD/Ventricular Arrhythmias, Atrial
Fibrillation/Supraventricular Arrhythmias, Heart Failure and Cardiac
Biomarkers, Hypertension

Keywords: Anemia, Angina, Unstable, Arrhythmias, Cardiac, Biological Markers,


Comorbidity, Coronary Artery Disease, Creatine Kinase, Creatine Kinase, MB Form, Diagnosis,
Dierential, Electrocardiography, Fibrinogen, Hypertension, Hypotension, Muscle, Skeletal,
Myocardial Infarction, Myocardial Ischemia, Myocarditis, Phthiraptera, Pneumonia,
Pulmonary Embolism, Renal Insuciency, Spasm, Tachycardia, Troponin I, Troponin T, Acute
Coronary Syndrome

2017 American College of Cardiology Foundation. All rights reserved.

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