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Brain & Heart A review on MINOCA

1. Introduction means that no coronary stenosis ≥50% that could represent
a potential infarction-related lesion should be present
Myocardial infarction with non-obstructive coronary on the angiography. Third, there should be no other
artery (MINOCA) was first reported by gross and Steinberg clinical condition present that could mimic AMI, such as
in 1939, but the term was first used in a study published pulmonary embolism or myocarditis. Cases meeting these
1
in 2013. Studies show that myocardial infarction (MI) can three criteria may be classified as MINOCA.
2
occur in the absence of coronary artery obstruction, but
physicians’ awareness and interest in this phenomenon 4. Pathophysiology
have only recently increased due to the widespread use of
coronary angiography in MI treatment. Even though our Numerous factors can contribute to the heterogeneous
understanding of MINOCA is burgeoning, there are still pathophysiology of MINOCA, such as coronary plaque
significant gaps. MINOCA refers to acute MI due to non- disruption and rupture, spontaneous coronary artery
obstructive coronary arteries or stenosis ≤50% on coronary dissection (SCAD), coronary vasospasm, coronary
thrombus or embolism, and myocardial bridging.
angiography. Around 15% of MI cases are caused by
MINOCA, which increases the risk of morbidity and death 4.1. Coronary plaque disruption and rupture
following diagnosis. Effective management of MINOCA
is challenging due to its complex nature and difficult AMI (type 1) can be caused by plaque rupture, erosion,
diagnostics. Even though there have been significant recent or calcified nodules. Damage to the vascular endothelium
leads to thrombosis, which can then result in platelet
advancements in our understanding of this disorder, the micro-emboli to the microvasculature or partial or
true pathophysiology of this condition remains poorly complete obstruction of the coronary arteries. Coronary
known and is currently undergoing additional research. plaques that are at high risk of rupture include those with
Several studies suggest that MINOCA is a collection of a lipid-rich core, a thin fibrous cap with macrophage/
diverse illnesses with various pathogenic processes and the lymphocyte infiltration, decreased smooth muscle cell
condition is not always benign, even though people with it content, and expansive remodeling. Large- and medium-
typically have a somewhat better prognosis than those with sized arteries with atherosclerotic plaque rupture cause
MI due to coronary artery disease (MI-CAD). platelet activation, which results in the formation of a
2. Epidemiology thrombus and a reduction in coronary blood flow. There
are three phases of platelet-activated thrombus: the initial
According to several studies, about 1 – 15% of patients phase of platelet adhesion, the extension phase (which
with MI are diagnosed with MINOCA. Patients with involves activation), and the perpetuation phase. During
3-7
MINOCA typically have lower levels of hyperlipidemia the initiation phase, the platelets roll, adhere, and spread
and are younger in age. Studies suggest an increased over the collagen matrix. The glycoprotein (GP) Ib/V/IX
8
incidence of severe cardiovascular events, such as acute receptor complex on the platelet surface interacts with von
MI (AMI) and death as a result of MINOCA in recent Willebrand factor and the GP VI and GP Ia proteins with
8
years. Evidence suggests that depression and anxiety are collagen at the site of plaque rupture to mediate adhesion.
more common in MINOCA patients and are strongly Platelets can get activated as a result of these interactions.
associated with poor prognosis as compared to patients Following platelet activation, local platelet-activating
with MI-CAD. 9-11 MINOCA and MI-CAD exhibit distinct factors recruit additional circulating platelets to expand
seasonal variations, with MINOCA showing a modest and stabilize the hemostatic plug. These platelet-activating
rise in occurrence during the summer and fall. However, agents include thromboxane A2 (TXA2), serotonin,
both conditions are more prevalent in the mornings, and thrombin, collagen, and adenosine diphosphate (ADP).
research has indicated that MINOCA’s time of onset is not The most powerful of them is thrombin. Importantly, the
correlated with its prognosis. 12,13 prothrombinase complex on the active platelet surface
mostly produces thrombin, which breaks fibrinogen into
3. Diagnostic criteria fibrin. Adherent platelets release ADP and TXA2, which
The European Society of Cardiology published the Fourth help draw in circulating platelets and cause different platelet
Universal Definition of MI in 2018, which included activation forms, such as alterations in platelet morphology
MINOCA as a new category of MI. According to and elevated proinflammatory molecule expression. In the
13
this publication, three requirements must be met for a end, this process allows for platelet aggregation, resulting
MINOCA diagnosis. First, a definite diagnosis of AMI in thrombosis.
must be made. Second, non-obstructive coronary disease The second most frequent cause of atherothrombosis is
must be demonstrated by coronary angiography. This plaque erosion. A plaque that has lost or malfunctioned

Volume 3 Issue 3 (2025) 2 doi: 10.36922/bh.5811