year) and very late (>1 year) stent/scaffold
thrombosis1. Type 4c MI describes an in-stent
restenosis or restenosis after balloon angioplasty
in the infarct-related artery. 1
Finally, type 5 MI denotes peri-procedural
infarctions in the setting of CABG. 1 In contrast to
type 4a MI (PCI-related MI), type 5 MI is defined as
increase of cTn >10-times the 99th percentile URL
in case of normal baseline cTn, or increase of
post-procedural cTn >20% in case of chronically
elevated pre-procedural cTn-concentration. 1 In
addition to cTn dynamics, elements of ischaemia
including new pathological Q waves, new graft
occlusion or native coronary artery occlusion as
detected by angiography or loss of viable
myocardium or new regional wall motion
abnormality by cardiac imaging are necessary
for the diagnosis of type 5 MI. 1
One of the most
important
elements of
the updated
Universal MI
Definition is the
emphasis on the
differentiation
between
myocardial
injury and MI
Key clinical messages
One of the most important elements of the
updated Universal MI Definition is the emphasis
on the differentiation between myocardial injury
and MI. Only the laboratory finding of elevated
cTn or increase of cTn in serial measurements
without any clinical evidence of ischaemia should
not be labelled as MI but as myocardial injury. 1
Moreover, the new consensus paper highlights
that myocardial injury should not only be clearly
differentiated from MI but also represents an
entity in itself, which comprises a variety of
diseases requiring further diagnostic workup.
A large number of cardiac (for example, heart
failure, myocarditis, Takotsubo syndrome,
revascularisation procedure, catheter ablation,
defibrillator shocks, cardiac contusion) and
non-cardiac (for example, sepsis, chronic kidney
disease, stroke or subarachnoid haemorrhage,
pulmonary embolism, chemotherapy) pathologies
and conditions can lead to myocardial injury
unrelated to ischaemia. 1 Depending on the
presence or absence of a dynamic cTn pattern, the
condition of myocardial injury should be declared
as acute or chronic. 1 The clinical differentiation
between the various causes of myocardial injury
can be challenging and often requires
comprehensive diagnostics. In this regard, the
2018 Universal Definition of MI has particularly
emphasised the use of cardiac magnetic
resonance (CMR) imaging to define the aetiology
of myocardial injury. 1 Indeed, CMR enables a
unique in vivo view on myocardial tissues and the
use of late gadolinium-enhanced sequences allows
for a reliable distinction between ischaemic and
non-ischaemic patterns of myocardial scarring. 1,7,8
Contingent upon the primary disease, a clear
differentiation between myocardial injury and MI
might be difficult. As highlighted by a new
References
1 Thygesen K et al. Fourth
Universal definition of
myocardial infarction 2018.
Circulation 2018;138:e618–e651.
2 Roth GA et al. Global, regional,
and national burden of
cardiovascular diseases for 10
causes, 1990 to 2015. J Am Coll
Cardiol 2017;70:1–25.
3 Thygesen K et al. Universal
definition of myocardial
infarction. Circulation
2007;116:2634–53.
4 Nomenclature and criteria
for diagnosis of ischemic heart
disease. Report of the Joint
International Society and
Federation of Cardiology/World
Health Organization task force
on standardization of clinical
nomenclature. Circulation 1979;
59: 607–9.
5 Mair J. High-sensitivity
cardiac troponins in everyday
clinical practice. World J Cardiol
2014;6:175–82.
6 Twerenbold R et al. Clinical
use of high-sensitivity cardiac
troponin in patients with
suspected myocardial infarction.
J Am Coll Cardiol 2017;70:
section in the 2018 consensus document,
chronic kidney disease (CKD) especially represents
a condition that often results in clinical
misinterpretation because a high proportion
of patients with CKD displays elevated cTn
concentrations. 1 Importantly, renal clearance
of cTn has only minor effects on serum cTn
concentrations 9 , whereas increased ventricular
pressure, microvascular dysfunction, anaemia,
hypotension and direct toxic effects of uraemia
are considered as main mechanisms explaining
the myocardial injury in CKD patients. 1,10 Acute
volume overload in CKD, for example, may lead
to both acute myocardial injury and type 2 MI;
a clear differentiation, however, may be
challenging and often remains insufficient
in clinical routine. 1 Not only in CKD patients,
but also in a large number of other patients,
including patients with multiple morbidities
or those who are critically ill, the differentiation
between myocardial injury and type 2 MI has
remained the key clinical challenge following
publication of the 2018 Universal Definition
of MI. 1
Routine primary PCI in the acute setting of
MI has revealed that a considerable proportion
of MI patients (approximately 10%) does not show
significant coronary artery disease. 11,12 This
clinical scenario has gained more and more
attention over the past few years and is referred
to as MI with non-obstructive coronary arteries
(MINOCA). 13 After publication of a position paper
of the ESC working group in 2017, 13 MINOCA has
now for the first time been included in the
Universal Definition of MI. 1 As the name implies,
MINOCA is defined as MI according to the criteria
as described in detail above as well as non-
obstructive coronary arteries (no coronary artery
stenosis of ≥50%) as displayed by acute
angiography. 13 MINOCA is a heterogeneous entity
with several potential underlying causes that
should be elucidated by a comprehensive
diagnostic algorithm incorporating additional
imaging modalities including CMR. 1,13
Conclusions
The Fourth Universal Definition of MI published in
2018 provides updated criteria for the definition
of the five types of MI established by the
preceding consensus documents, with particular
focus on the differentiation between myocardial
injury and MI. The entity of myocardial injury
describes a clinical scenario of elevated or
increasing cTn concentration without any signs
of ischaemia. Particularly due to therapeutic
consequences, it is crucial to distinguish
myocardial injury from MI, which displays both
cTn dynamics and clinical evidence of ischaemia.
996–1012.
7 Reinstadler SJ, Thiele H, Eitel
I. Risk stratification by cardiac
magnetic resonance imaging
after ST-elevation myocardial
infarction. Curr Opin Cardiol
2015;30:681–9.
8 Motwani M et al. Advances
in cardiovascular magnetic
resonance in ischaemic heart
disease and non-ischaemic
cardiomyopathies. Heart
2014;100:1722–33.
9 Friden V et al. Clearance of
cardiac troponin T with and
without kidney function. Clin
5
HHE 2019 | hospitalhealthcare.com
Biochem 2017;50:468–74.
10 Januzzi JL Jr et al. Troponin
elevation in patients with
heart failure: on behalf of the
third Universal Definition of
Myocardial Infarction Global Task
Force: Heart Failure Section. Eur
Heart J 2012;33:2265–71.
11 DeWood MA et al. Coronary
arteriographic findings soon
after non-Q-wave myocardial
infarction. N Engl J Med
1986;315:417–23.
12 Gehrie ER et al.
Characterization and outcomes
of women and men with
non-ST-segment elevation
myocardial infarction and
nonobstructive coronary
artery disease: results from the
Can Rapid Risk Stratification
of Unstable Angina Patients
Suppress Adverse Outcomes
with Early Implementation of the
ACC/AHA Guidelines (CRUSADE)
quality improvement initiative.
Am Heart J 2009;158:688–94.
13 Agewall S et al. ESC working
group position paper on
myocardial infarction with non-
obstructive coronary arteries.
Eur Heart J 2017;38:143–53.