Acute coronary

syndrome

Acute coronary syndrome (ACS) is a

syndrome (a set of signs and symptoms)
due to decreased blood flow in the
coronary arteries such that part of the
heart muscle is unable to function
properly or dies.[1] The most common
symptom is centrally located pressure-
like chest pain, often radiating to the left
shoulder[2] or angle of the jaw, and
associated with nausea and sweating.
Many people with acute coronary
syndromes present with symptoms other
than chest pain, particularly women,
older people, and people with diabetes
mellitus.[3]

Acute coronary syndrome

Blockage of a coronary artery

Specialty Cardiology

Acute coronary syndrome is subdivided

in three scenarios depending primarily on
the presence of electrocardiogram (ECG)
changes and blood test results (a change
in cardiac biomarkers such as troponin
levels):[4] ST elevation myocardial
infarction (STEMI), non-ST elevation
myocardial infarction (NSTEMI), or
unstable angina.[5] STEMI is
characterised by complete blockage of a
coronary artery resulting in necrosis of
part of the heart muscle indicated by ST
elevation on ECG, NSTEMI is
characterised by a partially blocked
coronary artery resulting in necrosis of
part of the heart muscle that may be
indicated by ECG changes, and unstable
angina is characterised by ischemia of
the heart muscle that does not result in
cell injury or necrosis.[6][7]

ACS should be distinguished from stable

angina, which develops during physical
activity or stress and resolves at rest. In
contrast with stable angina, unstable
angina occurs suddenly, often at rest or
with minimal exertion, or at lesser
degrees of exertion than the individual's
previous angina ("crescendo angina").
New-onset angina is also considered
unstable angina, since it suggests a new
problem in a coronary artery.[8]
Signs and symptoms
Symptoms of the acute coronary
syndromes are similar.[8] The cardinal
symptom of critically decreased blood
flow to the heart is chest pain,
experienced as tightness, pressure, or
burning.[9] Localisation is most
commonly around or over the chest and
may radiate or be located to the arm,
shoulder, neck, back, upper abdomen, or
jaw.[9] This may be associated with
sweating, nausea, or shortness of
breath.[8][9] Previously, the word "atypical"
was used to describe chest pain not
typically heart-related, however this word
is not recommended and has been
replaced by "noncardiac" to describe
chest pain that indicate a low likelihood
of heart-related pain.[9]

In unstable angina, symptoms may

appear on rest or on minimal exertion.[6]
The symptoms can last longer than
those in stable angina, can be resistant
to rest or medicine, and can get worse
over time.[8][10]

Though ACS is usually associated with

coronary thrombosis, it can also be
associated with cocaine use.[11] Chest
pain with features characteristic of
cardiac origin (angina) can also be
precipitated by profound anemia, brady-
or tachycardia (excessively slow or rapid
heart rate), low or high blood pressure,
severe aortic valve stenosis (narrowing
of the valve at the beginning of the
aorta), pulmonary artery hypertension
and a number of other conditions.[12]

Pathophysiology
In those who have ACS, atheroma rupture
is most commonly found 60% when
compared to atheroma erosion (30%),
thus causes the formation of thrombus
which block the coronary arteries. Plaque
rupture is responsible for 60% in ST
elevated myocardial infarction (STEMI)
while plaque erosion is responsible for
30% of the STEMI and vice versa for Non
ST elevated myocardial infarction
(NSTEMI). In plaque rupture, the content
of the plaque is lipid rich, collagen poor,
with abundant inflammation which is
macrophage predominant, and covered
with a thin fibrous cap. Meanwhile, in
plaque erosion, the plaque is rich with
extracellular matrix, proteoglycan,
glycoaminoglycan, but without fibrous
caps, no inflammatory cells, and no large
lipid core. After the coronary arteries are
unblocked, there is a risk of reperfusion
injury due spreading inflammatory
mediators throughout the body.
Investigations is still underway on the
role of cyclophilin D in reducing the
reperfusion injury.[13]
Other, less common, causes of acute
coronary syndrome include spontaneous
coronary artery dissection,[14] ischemia in
the absence of obstructive coronary
artery disease (INOCA), and myocardial
infarction in the absence of obstructive
coronary artery disease (MINOCA).[15]

Diagnosis

Classification of acute coronary syndromes.[16]

Electrocardiogram

In the setting of acute chest pain, the

electrocardiogram (ECG or EKG) is the
investigation that most reliably
distinguishes between various causes.[17]
The ECG should be done as early as
practicable, including in the ambulance if
possible.[18] ECG changes indicating
acute heart damage include: ST
elevation, new left bundle branch block
and ST depression amongst others. The
absence of ECG changes does not
immediately distinguish between
unstable angina and NSTEMI.[6]
Blood tests

Change in levels of cardiac biomarkers,

such as troponin I and troponin T, are
indicative of myocardial infarction
including both STEMI and NSTEMI,
however their levels are not affected in
unstable angina.[6]

Prediction scores

A combination of cardiac biomarkers and

risk scores, such as HEART score and
TIMI score, can help assess the
possibility of myocardial infarction in the
emergency setting.[19][13]
Prevention
Acute coronary syndrome often reflects a
degree of damage to the coronaries by
atherosclerosis. Primary prevention of
atherosclerosis is controlling the risk
factors: healthy eating, exercise,
treatment for hypertension and diabetes,
avoiding smoking and controlling
cholesterol levels; in patients with
significant risk factors, aspirin has been
shown to reduce the risk of
cardiovascular events. Secondary
prevention is discussed in myocardial
infarction.[20]
After a ban on smoking in all enclosed
public places was introduced in Scotland
in March 2006, there was a 17%
reduction in hospital admissions for
acute coronary syndrome. 67% of the
decrease occurred in non-smokers.[21]

Treatment
People with presumed ACS are typically
treated with aspirin, clopidogrel or
ticagrelor, nitroglycerin, and if the chest
discomfort persists morphine.[22] Other
analgesics such as nitrous oxide are of
unknown benefit.[22] Angiography is
recommended in those who have either
new ST elevation or a new left or right
bundle branch block on their ECG.[1]
Unless the person has low oxygen levels
additional oxygen does not appear to be
useful.[23]

STEMI

If the ECG confirms changes suggestive

of myocardial infarction (ST elevation in
specific leads, a new left bundle branch
block or a true posterior MI pattern),
thrombolytics may be administered or
percutaneous coronary intervention may
be performed. In the former, medication
is injected that stimulates fibrinolysis,
destroying blood clots obstructing the
coronary arteries . In the latter, a flexible
catheter is passed via the femoral or
radial artery and advanced to the heart to
identify blockages in the coronary
arteries. When occlusions are found, they
can be intervened upon mechanically
with angioplasty and usually stent
deployment if a lesion, termed the culprit
lesion, is thought to be causing
myocardial damage. Data suggest that
rapid triage, transfer and treatment is
essential.[24] The time frame for door-to-
needle thrombolytic administration
according to American College of
Cardiology (ACC) guidelines should be
within 30 minutes, whereas the door-to-
balloon percutaneous coronary
intervention (PCI) time should be less
than 90 minutes. It was found that
thrombolysis is more likely to be
delivered within the established ACC
guidelines among patients with STEMI as
compared to PCI according to a 2009
case control study.[25]

NSTEMI and NSTE-ACS

If the ECG does not show typical changes

consistent with STEMI, the term "non-ST
segment elevation ACS" (NSTE-ACS) may
be used and encompasses "non-ST
elevation MI" (NSTEMI) and unstable
angina.

The accepted management of unstable

angina and acute coronary syndrome is
therefore empirical treatment with
aspirin, a second platelet inhibitor such
as clopidogrel, prasugrel or ticagrelor,
and heparin (usually a low-molecular
weight heparin), with intravenous
nitroglycerin and opioids if the pain
persists. The heparin-like drug known as
fondaparinux appears to be better than
enoxaparin.[26]

If there is no evidence of ST segment

elevation on the electrocardiogram,
delaying urgent angioplasty until the next
morning is not inferior to doing so
immediately.[27] Using statins in the first
14 days after ACS reduces the risk of
further ACS.[28]
Cocaine-associated ACS should be
managed in a manner similar to other
patients with acute coronary syndrome
except beta blockers should not be used
and benzodiazepines should be
administered early.[29]

Prognosis

Prediction scores

The TIMI risk score can identify high risk

patients in non-ST segment elevation MI
ACS[30] and has been independently
validated.[31][32]

Based on a global registry of 102,341

patients, the GRACE risk score estimates
in-hospital, 6 months, 1 year, and 3-year
mortality risk after a heart attack.[33] It
takes into account clinical (blood
pressure, heart rate, EKG findings) and
medical history.[33]

Biomarkers

The aim of prognostic markers is to

reflect different components of
pathophysiology of ACS. For example:

Natriuretic peptide – both B-type

natriuretic peptide (BNP) and N-
terminal proBNP can be applied to
predict the risk of death and heart
failure following ACS.
 Monocyte chemo attractive protein
(MCP)-1 – has been shown in a
number of studies to identify patients
with a higher risk of adverse outcomes
after ACS.

Coronary CT angiography combined with

troponin levels is also helpful to triage
those who are susceptible to ACS. F-
fluoride positron emission tomography is
also helpful in identifying those with high
risk, lipid-rich coronary plaques.[13]

Day of admission

Studies have shown that for ACS

patients, weekend admission is
associated with higher mortality and
lower utilization of invasive cardiac
procedures, and those who did undergo
these interventions had higher rates of
mortality and complications than their
weekday counterparts. This data leads to
the possible conclusion that access to
diagnostic/interventional procedures
may be contingent upon the day of
admission, which may impact
mortality.[34][35] This phenomenon is
described as weekend effect.

See also
Allergic acute coronary syndrome
(Kounis syndrome)

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