11/14/24, 10\:33 AM Acute Coronary Syndrome (ACS)

Acute Coronary Syndrome (ACS)

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Succinct notes to superpower your revision
Acute coronary syndrome (ACS)\: encompasses STEMI, NSTEMI, and unstable angina. STEMI and NSTEMI are types of
myocardial infarction.
Myocardial infarction (MI)\: rise/fall in cardiac biomarkers (troponin) with at least one of the following\: symptoms of
ischaemia, ECG changes, imaging evidence of new myocardial damage, or intracoronary thrombus.
Classi
Type 1\: spontaneous MI (atherosclerosis, plaque rupture).
Type 2\: MI secondary to ischaemia (imbalance between blood supply and demand).
Type 3\: MI diagnosed post-mortem.
Type 4a\: MI related to PCI.
Type 4b\: MI due to stent thrombosis.
Type 5\: MI related to CABG.
Clinical features\: chest pain (radiating to arms, back, jaw), nausea, vomiting, sweating, breathlessness, haemodynamic
instability, new/worsening angina.
Initial management\: resting 12-lead ECG, morphine, oxygen (if low SpO ), nitrates, aspirin (300 mg), second antiplatelet
2
(ticagrelor, prasugrel).
STEMI\: acute chest pain, persistent ST-segment elevation, complete coronary occlusion, risk of ventricular arrhythmias;
managed with primary PCI (gold standard) or thrombolysis if PCI not available within 90 minutes.
NSTEMI\: partial coronary occlusion, worse long-term outcomes than STEMI; managed with beta-blockers, ACE inhibitors,
atorvastatin, and assessment for invasive angiography using the GRACE score.
Unstable angina\: prolonged (>20 min) rest angina, new severe angina, increasing frequency/duration/threshold of angina;
managed similarly to NSTEMI.
Troponin\: elevated in MI, but can also be raised due to tachy/bradyarrhythmias, aortic dissection, severe valve disease,
hypertrophic cardiomyopathy, severe respiratory failure, severe anaemia, coronary spasm, heart failure, Takotsubo
cardiomyopathy, sepsis, renal failure, stroke, subarachnoid haemorrhage.
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A comprehensive topic overview

Introduction

Chest pain is a common presentation, and the diagnosis of acute coronary syndrome is frequently suspected. Acute
coronary syndrome (ACS) encompasses a variety of diagnoses and can be subcategorised into\:
ST-elevation ACS\: ST-elevation myocardial infarction (STEMI)
Non-ST elevation ACS\: Non-ST elevation myocardial infarction (NSTEMI) and unstable angina

Aetiology

Two of the three diagnoses that exist under the umbrella of ACS are types of myocardial infarction (STEMI and NSTEMI).
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De

The European Society of Cardiology's de
Detection of a rise and/or fall in cardiac biomarker values (preferably troponin) with at least one value above the 99
th
percentile (upper reference limit) with at least one of the following\:
Symptoms of ischaemia (the patient's history and clinical presentation and the history are vital to guide your
interpretation of the tests you are about to perform)
New or presumed new signi
Pathological Q wave changes on the ECG
Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
Identi
A 'new left bundle branch block' does not mean 'a left bundle branch block that has just been found because the patient
has never had an ECG before'
. Nor does it mean 'a left bundle branch block that is present now but was not present on an
ECG in 2006'
.
A new LBBB due to ischaemia is the result of an occluded proximal left anterior descending (LAD) or left main stem
artery. A large amount of myocardium and conductive tissue needs to be a
patients are usually acutely unwell.
Development of Q waves on the ECG
The Q wave re
ventricular wall depolarisation. If the ventricular wall is dead, a 'window' is created that allows the septal depolarisation to
show up on the surface ECG.
Imaging evidence of new regional wall abnormality
The sequence of changes and signs of ischaemia (the ischaemic cascade) on various tests is shown in Figure 1.
Figure 1. Ischaemic cascade
Troponin
A troponin level is only a number. It is only relevant when applied in the context of other clinical
There are many causes of a raised troponin, including\:
1
Myocardial infarction
Tachy/bradyarrhythmias
Aortic dissection
Severe aortic valve disease
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Hypertrophic cardiomyopathy
Severe respiratory failure
Severe anaemia
Coronary spasm
Heart failure
Takotsubo cardiomyopathy
Sepsis
Renal failure
Stroke
Subarachnoid haemorrhage

Classi

Type 1\: spontaneous myocardial infarction
This is your 'typical' myocardial infarction. Atherosclerosis originates from damage to the endothelium and a build-up of
cholesterol.
The in
(eventually) calcium to build up with a
When this cap cracks, the exposed debris triggers thrombus formation in the con
(which are only typically between 2 and 5mm in diameter), causing partial or total occlusion of the artery.
Type 2\: myocardial infarction secondary to ischaemia
A type 2 myocardial infarction is a common event in hospitals where patients with stable coronary artery disease +/-
previous coronary intervention (PCI or CABG) are unwell and put additional stress on their heart that would not normally be
present.
If there is a su
demand for blood (e.g. sepsis/hypovolaemic shock, tachyarrhythmia) then the myocardium can become ischaemic
without a plaque rupture event.
Type 3 MI\: post-mortem
A type 3 myocardial infarction is diagnosed post-mortem.
Type 4a MI\: percutaneous coronary intervention
This is related to percutaneous coronary intervention (i.e. caused by an angioplasty procedure blocking a side branch or
damaging the main coronary artery causing ischaemia)
Type 4b MI\: stent thrombosis
This is related to stent thrombosis. If patients stop anti-platelets early post-angioplasty or continue to smoke, stents can
occlude (this usually results in a STEMI if complete sudden thrombosis or NSTEMI if gradual re-stenosis over time).
Type 5 MI\: bypass
Type 5 myocardial infarction is related to a bypass graft (CABG) operation.

Clinical features

The clinical features of ACS are similar, regardless of the underlying diagnosis (e.g. NSTEMI, STEMI or unstable angina).
Typical clinical presentations of ACS include\:
2
pain in the chest and/or other areas (for example, the arms, back or jaw) lasting longer than 15 minutes
chest pain associated with nausea and vomiting, marked sweating and breathlessness
chest pain associated with haemodynamic instability
new-onset chest pain, or abrupt deterioration in previously stable angina, with recurrent chest pain occurring frequently
and with little or no exertion, and with episodes often lasting longer than 15 minutes.
For more information, see the Geeky Medics guide to a chest pain history.
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Management

When ACS is suspected, initial management should be commenced as soon as possible\:
2
Resting 12-lead ECG
Morphine
Oxygen\: only if low SpO
2
Nitrates (e.g. glyceryl trinitrate)
Aspirin (300 mg) and a second rapid-acting antiplatelet such as Ticagrelor or Prasugrel
For more information, see the Geeky Medics guide to the emergency management of ACS.

ST-elevation ACS

ST-elevation myocardial infarction (STEMI)

Patients with STEMI typically present with acute chest pain and persistent (>20 minutes) ST-segment elevation.
ST elevation is a sign of complete occlusion of an epicardial coronary artery by thrombus causing immediate myocardial
death relating to the territory a
Anterior\: V1-V4
Inferior\: II, III, aVF
High lateral\: I, aVL
Low lateral\: V5, V6
Posterior\: a dominant R wave in V1-3 with ST depression in V1-3 (the mirror image of an anterior MI)
These patients are at elevated risk of ventricular arrhythmias and myocardial damage can be minimised by rapidly
opening the artery.
ST elevation
Management of STEMI
3
The current gold standard treatment option is primary percutaneous intervention (PCI) to allow the vessel to be opened
as quickly as possible (as 'time is muscle').
Studies have shown that it is bene
rather than resorting to thrombolysis.
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There is a bene
trial suggests that there is limited bene
4
The recommended treatment used to be thrombolysis to try and break down the clot in the artery. However, this has
signi
angioplasty' with higher bleeding risks associated due to the pre-medication.

Non-ST-elevation ACS

Non-ST-elevation myocardial infarction (NSTEMI)

Non-ST elevation myocardial infarctions (NSTEMIs) are often seen as a more 'routine' heart attack. However, they have
worse long-term outcomes than STEMIs (although a lower risk of death in the short term).
They tend to be associated with partial coronary occlusion.
Diagnosis of an NSTEMI involves a combination of, clinical assessment, serial troponin measurement and ECG analysis (see
deNSTEMIs.
Management of NSTEMI
5
Initiate further medical treatment once a diagnosis of NSTEMI is con
Beta blockade (or alternative rate-limiting agent if contraindicated - aim HR of 50-60 bpm)
ACE inhibitor (unless contraindicated - aim for a systolic blood pressure of 120 mmHg or less)
Atorvastatin 80mg OD
Once someone is diagnosed with a type I NSTEMI and commenced on appropriate medical therapy, there are various risk
scores that can be calculated to assess the value of invasive angiography.
NICE recommends the use of the GRACE score which is used to predict in-hospital and post-discharge to 6-month
mortality.
Other factors that should be considered before proceeding to angiography include\:
Renal function (there is a risk of contrast nephropathy and this can leave predialysis patients permanently dependent on
dialysis)
Bleeding risk (as above)
Can the patient lie
it is not fun for the operator, cath lab team or the patient. In a non-urgent setting, angiography should be delayed until
the patient is able to tolerate lying
Other signi
(age/dementia/malignancy) may not gain any prognostic bene
medically.
When to perform angiography
O
cardiovascular events (predicted 6-month mortality 3.0% or less).
O
cardiovascular events (predicted 6-month mortality 3.0% or less) if ischaemia is subsequently experienced or is
demonstrated by ischaemia testing.
O
who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality above 3.0%)
if they have no contraindications to angiography (such as active bleeding or comorbidity). Perform angiography as
soon as possible for patients who are clinically unstable or at high ischaemic risk.
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Unstable angina

Stable (or 'exertional') angina is de
Typical cardiac pain
Brought on by exertion and relieved by rest
Lasting less than 20 minutes
Unstable angina is an acute coronary syndrome that is de
biochemical evidence of myocardial damage. It is characterised by speci
6
of\:
prolonged (>20 minutes) angina at rest
new onset of severe angina
angina that is increasing in frequency, longer in duration, or lower in threshold
angina that occurs after a recent episode of myocardial infarction
Diagnosis of unstable angina is based on clinical assessment. Troponin measurements will be normal as there has not
been any ischaemic damage (yet) and the ECG may be normal for similar reasons.
Management of unstable angina
5
Management of unstable angina is the same as for NSTEMI discussed above.

References

Third Universal De
Acute coronary syndromes (including myocardial infarction); NICE Quality Standard, Sept 2014. Available from\: [LINK]
NICE Guideline. Myocardial infarction with ST-segment elevation\: acute management. Clinical guideline [CG167]. Published
date\: 10 July 2013. Available from\: [LINK]
Yousef ZR, Redwood SR, Bucknall CA, Sulke AN, Marber MS. Late intervention after anterior myocardial infarction\: e
left ventricular size, function, quality of life, and exercise tolerance\: results of the Open Artery Trial (TOAT Study). J Am Coll
Cardiol 2002;40\:869-876
NICE Guideline. Unstable angina and NSTEMI; NICE Clinical Guideline (March 2010 - last updated November 2013).
Available from\: [LINK]
Ro
presenting without persistent ST-segment elevation\: Task Force for the Management of Acute Coronary Syndromes in
Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). Eur Heart J. 2016
Jan 14;37(3)\:267-315.

Acute Heart Failure
Atrial Fibrillation (AF)
Atrioventricular Block
Brugada Syndrome
Bundle Branch Block

Test yourself

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