Myocardial infarction with non-obstructive coronary arteries

1. Myocardial infarction with non-obstructive
coronary arteries (MINOCA)
ANWER GHANI
FIBMS
IRAQ

2. .
 Acute coronary syndromes constitute a variety of
myocardial injury presentations that include a subset of
patients presenting with myocardial infarction with non-
obstructive coronary arteries (MINOCA).

3. .
 Myocardial infarction with non-obstructive coronary
arteries (MINOCA) is defined by clinical evidence of
myocardial infarction (MI) with normal or near-normal
coronary arteries on angiography.

4.  Gross-Sternberg Syndrome
Beltrame Syndrome
 Acute myocardial infarction (MI) without significant
coronary artery disease (CAD) was initially described
almost 80 years ago by Gross and Sternberg.
 Gross H, Sternberg WH. Myocardial infarction without significant lesions of coronary arteries. Arch Intern Med. 1939; 64:249–
267.CrossrefGoogle Scholar
 Whereas the term myocardial infarction with non-
obstructive coronary arteries (MINOCA) is recent.It has
been used by Beltrame to describe these patients
Beltrame JF. Assessing patients with myocardial infarction and non‐obstructed coronary arteries (MINOCA). J Intern Med. 2013;
273:182–185.CrossrefMedlineGoogle Scholar

5. .
 MINOCA differs from type 1 myocardial infarction (MI)
regarding patient characteristics, presentation,
physiopathology, management, treatment, and prognosis.

6. .
 MINOCA patient characteristics differ from those of other
Myocardial Infarction and Coronary Artery Disease (MI-
CAD) patients because:
 MINOCA subjects are younger, are more often female,
and tend to have fewer traditional cardiovascular risk
factors.

7. .
 In young patients (aged <55 years) presenting with AMI,
MINOCA is relatively frequent, occurring in >10% of the
population.

8.  Acute Coronary Syndrome
 The diagnosis of an acute coronary syndrome should be
established according to the fourth universal definition of
MI, which is :
 when there is evidence of acute myocardial injury
accompanied by clinical data suggesting acute myocardial
ischaemia such as relevant symptoms, new ischaemic electrocardiogram (ECG) changes, loss of viable
myocardium present in imaging, or identification of coronary thrombus.

9. .
 Non-obstructive coronary arteries on
angiography, is defined as no coronary
artery stenosis ≥ 50% in any potential
infarct-related artery.
 Clinical criteria and biomarker behaviour
of MINOCA remain similar to other acute
coronary event.

10.  MINOCA is not an uncommon presentation of acute coronary syndromes
 The prevalence of MINOCA is estimated to be 6-9%
among patients diagnosed with MI.
 With 11% in a recent prospective observational study.

11. .
 MINOCA is more common in women than men.
 MINOCA patients presenting with NSTEMI than in those
presenting with STEMI.
 Two-thirds of MINOCA subjects present ST-segment
elevation;
 MINOCA patients are younger, are more often female and
tend to have fewer cardiovascular risk factors.

12. .
 The risk of reinfarction was higher in the MICAD group,
the risk in the MINOCA group was lower.
 The mortality was higher among the MICAD pts.
 Although the characteristics of patients with MINOCA and their counterparts with AMI and CAD (AMI‐CAD) were different, the
mortality rates at 1 month (1.1% versus 0.6%, P=0.43) and 1 year (1.7% versus 2.3%, P=0.68) were not statistically different.
(2)

13.  MINOCA is a working diagnosis, and defining the
aetiologic mechanism is relevant because it affects patient
care and prognosis.
 Identification of underlying causes of MINOCA
-optimize treatment,
- improve prognosis,
- promote prevention of recurrent myocardial infarction.

14. .
 The prognosis is extremely variable, depending on the
cause of MINOCA.

15. Classification of myocardial injury
and infarction
 Cardiac troponin is the only recommended biomarker for
the detection of myocardial necrosis, and it is integral to
the diagnostic criteria for myocardial infarction.

16. Classification of myocardial injury
and infarction
Myocardial injury is defined by only one criterion: the
elevation of cardiac troponin.
A myocardial infarction is a myocardial injury attributed
specifically to ischemia, i.e., with clinical evidence of a
rise in troponin and at least one of the following:
ischemic symptoms or electrocardiographic changes,
development of pathologic Q waves,
imaging evidence of new loss of viable myocardial or
regional wall motion abnormalities consistent with

17. Classification of myocardial injury
and infarction
 The classification distinguishes between type 1 myocardial
infarction due to thrombosis of an atherosclerotic plaque
and
 type 2 myocardial infarction due to myocardial oxygen
supply-demand imbalance in the context of another acute
illness.
 Myocardial infarctions presenting as sudden death (type
3),
 or after percutaneous coronary intervention (type 4)

18. Classification of myocardial injury
 Acute nonischemic myocardial injury:Acute myocardial injury (rise and fall in
biomarkers [cTn]) in the absence of a primary ischemic cause (ie, absence of MI)
 Chronic myocardial injury:Chronic myocardial injury (cTn >99th percentile URL
without an acute change).
 Acute myocardial injury is classified where troponin concentrations are elevated with
evidence of dynamic change in the absence of overt myocardial ischaemia, whereas
in chronic myocardial injury troponin concentrations remain unchanged on serial
testing.

20.  The most common causes of
MINOCA
 coronary plaque disease,
 coronary dissection,
 coronary artery spasm,
 coronary microvascular spasm,
 Takotsubo cardiomyopathy,
 Myocarditis,
 coronary thromboembolism,
 other forms of type 2 myocardial infarction and MINOCA

21.  Mechanisms of myocardial injury
It is now recognised that cardiac troponin may be released
out with the context of myocardial ischaemia and necrosis,
with several purported mechanisms.
 Cardiomyocytes undergo mechanical stretch in response
to pressure or volume overload, and this may trigger
activation of intracellular proteases associated with
intracellular degradation of troponin.
 Furthermore, there is evidence that tachycardia may
stimulate stress-responsive integrins within the
cardiomyocyte, triggering release of intact cardiac troponin

22. Due to multiple potential causes, MINOCA should be considered rather as a
working diagnosis after coronary angiography and further efforts should be
taken to define the cause of MI in each individual patient.
 The MINOCA is a working diagnosis that requires a further
diagnostic work-up by
 invasive techniques, such as intravascular ultrasound
(IVUS) and optical coherence tomography (OCT) or
 non-invasive imaging with cardiac magnetic resonance
imaging (CMRI).

23. .
 When it is ascertained that obstructive coronary artery
disease has not been inadvertently overlooked, other
coronary disorders, such as
 plaque rupture or erosion,
 Thrombosis,
 Dissection,
 spasms
 or microvascular dysfunction should be evaluated.

24.  In the absence of relevant coronary artery disease,
myocardial ischaemia might be triggered by an acute
event in epicardial coronary arteries, coronary
microcirculation, or both.
 Epicardial causes of MINOCA include coronary plaque
disruption, coronary dissection, and coronary spasm.
 Microvascular MINOCA mechanisms involve
microvascular coronary spasm, takotsubo syndrome
(TTS), myocarditis, and coronary thromboembolism.
 Patients with elevated cardiac markers due to presumed myocarditis or Takotsubo were not included in the VIRGO registry.

25. .
 Coronary angiography with non-significant coronary
stenosis and left ventriculography are first-line tests in the
differential study of MINOCA patients.

26.  MINOCA is not a benign diagnosis, and its polymorphic
forms differ in prognosis.
 . MINOCA care varies across centres, and future multi-
centre clinical trials with standardized criteria may have a
positive impact on defining optimal cardiovascular care for
MINOCA patients.

27. Epicardial causes of MINOCA
 Coronary artery disease (plaque rupture)
 DX: IVUS/OCT, FFR/iFR
 RX: Antiplatelet therapy, statins, ACEi/ARB, beta-blockers
Studies of intracoronary imaging have shown that ≈40% of patients with MINOCA have some evidence of plaque disruption. Since
coronary angiography cannot evaluate the vascular lumen, intracoronary imaging modalities such as intravascular ultrasound
(IVUS) might play a determinant role in evaluating the lesion.
 IVUS: Intravascular ultrasound; OCT: Optical coherence tomography; FFR: Fractional flow reserve; iFR: Instantaneous wave-
free ratio..
 Although intravascular ultrasound is helpful in demonstrating plaque rupture, optical coherence tomography is a better tool for
identifying patients with plaque erosion and may be superior for the assessment of patients with spontaneous coronary artery
dissection.(2)

28. Epicardial causes of MINOCA
 Coronary dissection
 DX: IVUS/OCT
 RX: Beta-blocker and simple antiplatelet therapy.

29. Epicardial causes of MINOCA
 Coronary artery spasm
 DX: Intracoronary nitrates, intracoronary Ach or
ergonovine test by experienced teams
 RX: Calcium antagonists, nitrates.

30. Microvascular causes of MINOCA
 Microvascular coronary spasm
 DX: Objective evidence of ischaemia (ECG, LV wall
motion abnormalities, PET). Impaired microvascular
function (CFR, intracoronary Ach test, abnormal CMR,
slow coronary flow)
 RX: Beta-blockers and nitrates, calcium antagonist,
possibly ranolazine
 CMR: Cardiac magnetic resonance; PET: Positron emission tomography.

31. Microvascular causes of MINOCA
 Takotsubo syndrome
 DX: Ventriculography, echocardiography, troponin, B-
natriuretic peptide, CMR
 RX: Heart failure treatment, mechanical support in
cardiogenic shock.

32. Microvascular causes of MINOCA
 Myocarditis
 Dx: CMR, EMB, viral serologies, high c-reactive protein
 Rx: Heart failure treatment if complication, autoimmune
therapy in autoimmune forms.
 EMB: Endomyocardial biopsies.

33. Microvascular causes of MINOCA
 Coronary embolism
 Dx: History of potential thromboembolic sources,
thrombophilia screen, TTE, TOE, bubble contrast
echography
 Rx: Antiplatelet therapy, anticoagulation, transcatheter
closure or surgical repair.

34. .
 Among patients with AMI, there is a higher prevalence of
nonobstructive coronary arteries among women,
particularly young women. Nevertheless, the prognosis for
young women with AMI is worse than that for young men.It
is possible that this result is due to suboptimal (less
aggressive and/or less targeted) therapeutic strategies in
patients with “nonatherosclerotic” AMI. (2)

35. .
 Discharge therapies (eg, aspirin, β‐blockers,
angiotensin‐converting enzyme inhibitors and angiotensin
receptor II blockers, and statins) were less frequently
prescribed for MINOCA patients.
 Favorable outcomes when MINOCA patients were treated
with β‐blockers, angiotensin‐converting enzyme inhibitors
and angiotensin receptor II blockers, and statins, but no
significant benefits were observed with P2Y12 inhibitors.

36.  Summary
 MINOCA has comparable outcomes to MI‐CAD up to 1
year of follow‐up. Nevertheless, there is a paucity of
evidence‐based data to guide our approach to the
evaluation and management of MINOCA patients.
 This results in variable and suboptimal practice patterns
and disparities in care. The time has come to make a
change!

37. References
 1- Myocardial infarction with non-obstructive coronary arteries: A comprehensive review and future research directions. Rafael
Vidal-Perez, Charigan Abou Jokh Casas, Rosa Maria Agra-Bermejo, Belén Alvarez-Alvarez, Julia Grapsa, Ricardo Fontes-
Carvalho, Pedro Rigueiro Veloso, Jose Maria Garcia Acuña, and Jose Ramon Gonzalez-Juanatey. World J Cardiol. 2019 Dec
26; 11(12): 305–315.
 2- Myocardial Infarction With Nonobstructive Coronary Arteries (MINOCA): It's Time to Face Reality! Jacqueline E.
Tamis‐Holland, and Hani Jneid. Originally published28 Jun 2018https://doi.org/10.1161/JAHA.118.009635Journal of the
American Heart Association. 2018;7:e009635.
 3- Assessment and classification of patients with myocardial injury and infarction in clinical practice. Andrew R Chapman, Philip
D Adamson, http://orcid.org/0000-0003-1926-5925Nicholas L Mills.Heart 2017;103:10-18.

38. THANKS