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Angina pectoris affects approximately 112 million people globally.
Up to 70% of patients undergoing invasive angiography do not have obstructive coronary artery disease, more
common in women than in men, and a large proportion have INOCA as a cause of their symptoms.
INOCA patients present with a wide spectrum of symptoms and signs that are often misdiagnosed as non-cardiac
leading to under-diagnosis/investigation and under-treatment.
INOCA can result from heterogeneous mechanism including coronary vasospasm and microvascular dysfunction and is
not a benign condition.
Compared to asymptomatic individuals, INOCA is associated with increased incidence of cardiovascular events,
repeated hospital admissions, as well as impaired quality of life and associated increased health care costs.
• Pathophysiology and endotypes :
• Microvascular angina and epicardial coronary artery spasm
• In the absence of flow-limiting coronary artery disease, myocardial
ischaemia can result from specific pathways of microcirculatory
dysfunction.
• Two microcirculatory dysfunction endotypes MVA:
• 1. Structural microcirculatory remodelling
• 2. Functional arteriolar dysregulation.
• The diagnosis of MINOCA is made after coronary angiography in a patient
presenting with an acute myocardial infarct based on the following criteria
• 1. AMI criteria
• (a) Positive cardiac biomarker (preferably cardiac troponin) defined as a rise
and/or fall in serial levels, with at least one value above the 99th percentile
upper reference limit
• (b) Corroborative clinical evidence of infarction including at least one of the
following:
• (i) Symptoms of ischemia
• (ii) New or presumed new significant ST-T changes or new LBBB
• (iii) Development of pathological Q waves
• (iv) Imaging evidence of new loss of viable myocardium or new RWMA
• (v) Intracoronary thrombus evident on angiography or at autopsy
• 2. Nonobstructive coronary arteries on angiography
• (a) Defined as the absence of obstructive CAD on angiography (no coronary
artery stenosis ≥ 50%) in the infarct-related artery
• (b) This includes patients with the following:
• (i) Normal coronary arteries (no stenosis > 30%)
• (ii) Mild coronary atherosclerosis (stenosis > 30% but < 50%)
• 3. No clinically overt specific cause for the acute presentation
• (a) At the time of angiography, the specific diagnosis is not apparent
• (b) It is necessary tofurther evaluate the patient for the underlying cause
of MINOCA
Proposal for a diagnostic algorithm in patients with
myocardial ischaemia with non-obstructive coronary arteries.
aUnless renal function <35ml/min per 1.73 m2. bHaemoglobin,
C-reactive protein, leucocytes, oxygen saturation, D-dimers,
(NT-pro) brain natriuretic peptide. cWithin 48h. AMI acute myocardial
infarction, MINOCA myocardial ischaemia with nonobstructive
coronary arteries, ICA invasive coronary angiography,
CMP cardiomyopathy, IVUS intravascular ultrasound,
OCT optical coherence tomography, RWMA regional wall motion
abnormalities, PFO patent foramen ovale, ASD atrial septal
defect, CT computed tomography, CMR cardiac magnetic
resonance imaging, LGE late gadolinium enhancement.
ACS acute coronary syndrome
Inoca and minoca
Inoca and minoca
Inoca and minoca
Inoca and minoca
Inoca and minoca
Inoca and minoca
Inoca and minoca
Inoca and minoca
Inoca and minoca
Inoca and minoca
Inoca and minoca
Inoca and minoca

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Inoca and minoca

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  • 2. Angina pectoris affects approximately 112 million people globally. Up to 70% of patients undergoing invasive angiography do not have obstructive coronary artery disease, more common in women than in men, and a large proportion have INOCA as a cause of their symptoms. INOCA patients present with a wide spectrum of symptoms and signs that are often misdiagnosed as non-cardiac leading to under-diagnosis/investigation and under-treatment. INOCA can result from heterogeneous mechanism including coronary vasospasm and microvascular dysfunction and is not a benign condition. Compared to asymptomatic individuals, INOCA is associated with increased incidence of cardiovascular events, repeated hospital admissions, as well as impaired quality of life and associated increased health care costs.
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  • 6. • Pathophysiology and endotypes : • Microvascular angina and epicardial coronary artery spasm • In the absence of flow-limiting coronary artery disease, myocardial ischaemia can result from specific pathways of microcirculatory dysfunction. • Two microcirculatory dysfunction endotypes MVA: • 1. Structural microcirculatory remodelling • 2. Functional arteriolar dysregulation.
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  • 31. • The diagnosis of MINOCA is made after coronary angiography in a patient presenting with an acute myocardial infarct based on the following criteria • 1. AMI criteria • (a) Positive cardiac biomarker (preferably cardiac troponin) defined as a rise and/or fall in serial levels, with at least one value above the 99th percentile upper reference limit • (b) Corroborative clinical evidence of infarction including at least one of the following: • (i) Symptoms of ischemia • (ii) New or presumed new significant ST-T changes or new LBBB • (iii) Development of pathological Q waves • (iv) Imaging evidence of new loss of viable myocardium or new RWMA • (v) Intracoronary thrombus evident on angiography or at autopsy
  • 32. • 2. Nonobstructive coronary arteries on angiography • (a) Defined as the absence of obstructive CAD on angiography (no coronary artery stenosis ≥ 50%) in the infarct-related artery • (b) This includes patients with the following: • (i) Normal coronary arteries (no stenosis > 30%) • (ii) Mild coronary atherosclerosis (stenosis > 30% but < 50%) • 3. No clinically overt specific cause for the acute presentation • (a) At the time of angiography, the specific diagnosis is not apparent • (b) It is necessary tofurther evaluate the patient for the underlying cause of MINOCA
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  • 37. Proposal for a diagnostic algorithm in patients with myocardial ischaemia with non-obstructive coronary arteries. aUnless renal function <35ml/min per 1.73 m2. bHaemoglobin, C-reactive protein, leucocytes, oxygen saturation, D-dimers, (NT-pro) brain natriuretic peptide. cWithin 48h. AMI acute myocardial infarction, MINOCA myocardial ischaemia with nonobstructive coronary arteries, ICA invasive coronary angiography, CMP cardiomyopathy, IVUS intravascular ultrasound, OCT optical coherence tomography, RWMA regional wall motion abnormalities, PFO patent foramen ovale, ASD atrial septal defect, CT computed tomography, CMR cardiac magnetic resonance imaging, LGE late gadolinium enhancement. ACS acute coronary syndrome