Title: Myocardial infarction with non-obstructive coronary arteries
1Myocardial 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 SyndromeBeltrame 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 64249267.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 273182185.Crossref
MedlineGoogle 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 lt55 years) presenting
with AMI, MINOCA is relatively frequent,
occurring in gt10 of the population.
8- 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, P0.43) and 1 year
(1.7 versus 2.3, P0.68) 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.
15Classification 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.
16Classification 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 ischemia, and last, - identification of a coronary thrombus by
angiography or autopsy. -
17Classification 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) - and coronary artery bypass grafting (type 5) are
also defined.
18Classification of myocardial injury
- Acute nonischemic myocardial injuryAcute
myocardial injury (rise and fall in biomarkers
cTn) in the absence of a primary ischemic cause
(ie, absence of MI) - Chronic myocardial injuryChronic myocardial
injury (cTn gt99th 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.
19(No Transcript)
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 of uncertain aetiology.
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 I from viable cardiomyocytes in
the absence of necrosis.
22Due 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.
- Furthermore, myocarditis or tako-tsubo
cardiomyopathy should be excluded by CMRI as
non-coronary causes.
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.
27Epicardial 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)
28Epicardial causes of MINOCA
- Coronary dissection
- DX IVUS/OCT
- RX Beta-blocker and simple antiplatelet therapy.
29Epicardial causes of MINOCA
- Coronary artery spasm
- DX Intracoronary nitrates, intracoronary Ach or
ergonovine test by experienced teams - RX Calcium antagonists, nitrates.
30Microvascular 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.
31Microvascular causes of MINOCA
- Takotsubo syndrome
- DX Ventriculography, echocardiography, troponin,
B-natriuretic peptide, CMR - RX Heart failure treatment, mechanical support
in cardiogenic shock.
32Microvascular 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.
33Microvascular 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, ß-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 ß-blockers, angiotensin-converting
enzyme inhibitors and angiotensin receptor II
blockers, and statins, but no significant
benefits were observed with P2Y12 inhibitors.
36- 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!
37References
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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) 305315. - 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.
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myocardial injury and infarction in clinical
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38THANKS