Acute coronary syndrome (ACS) is an umbrella term covering a number of acute presentations of ischaemic heart disease.

It covers a number of presentations, including
  • ST elevation myocardial infarction (STEMI)
  • non-ST elevation myocardial infarction (NSTEMI)
  • unstable angina


  • Incidence: 200.00 cases per 100,000 person-years
  • Peak incidence: 60-70 years
  • Sex ratio: more common in males 2:1
Condition Relative
Musculoskeletal chest pain5.00
Acute coronary syndrome1
Acute pericarditis0.50
Pulmonary embolism0.35
Aortic dissection0.02
<1 1-5 6+ 16+ 30+ 40+ 50+ 60+ 70+ 80+


Unmodifiable risk factorsModifiable risk factors
Increasing age
Male gender
Family history
Diabetes mellitus


Ischaemic heart disease is a complex process which develops over a number of years. A number of changes can be seen:
  • initial endothelial dysfunction is triggered by a number of factors such as smoking, hypertension and hyperglycaemia
  • this results in a number of changes to the endothelium including pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability
  • fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles
  • monocytes migrate from the blood and differentiate into macrophages. These macrophages then phagocytose oxidized LDL, slowly turning into large 'foam cells'. As these macrophages die the result can further propagate the inflammatory process.
  • smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque.

ACS generally develops in patients who have ischaemic heart disease, either known or previously undetected. Ischaemic heart disease is a term synonymous with coronary heart disease and coronary artery disease. It describes the gradually build up of fatty plaques within the walls of the coronary arteries. This leads to two main problems:
  • 1. Gradual narrowing, resulting in less blood and therefore oxygen reaching the myocardium at times of increased demand. This results in angina, i.e. chest pain due to insufficient oxygen reaching the myocardium during exertion
  • 2. The risk of sudden plaque rupture. The fatty plaques which have built up in the endothelium may rupture leading to sudden occlusion of the artery. This can result in no blood/oxygen reaching the area of myocardium.

Clinical features

Features of acute coronary syndrome (ACS) include:


A wide variety of ECG changes can be seen depending on what type of ischaemic event is happening, where it is happening and when it happened.

Acute myocardial infarction (MI)
  • hyperacute T waves are often the first sign of MI but often only persists for a few minutes
  • ST elevation may then develop
  • the T waves typically become inverted within the first 24 hours. The inversion of the T waves can last for days to months
  • pathological Q waves develop after several hours to days. This change usually persists indefinitely

STEMI criteria
  • clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:
    • 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
    • 1.5 mm ST elevation in V2-3 in women
    • 1 mm ST elevation in other leads
    • new LBBB (LBBB should be considered new unless there is evidence otherwise)

The table below shows the correlation between ECG changes and coronary territories:

ECG changesCoronary artery
AnteroseptalV1-V4Left anterior descending
InferiorII, III, aVFRight coronary
AnterolateralV4-6, I, aVLLeft anterior descending or left circumflex
LateralI, aVL +/- V5-6Left circumflex
PosteriorTall R waves V1-2Usually left circumflex, also right coronary


Acute coronary syndrome (ACS) is a very common and important presentation in medicine. The management of ACS has evolved over recent years, with the development of new drugs and procedures such as primary coronary intervention (PCI).

Emergency departments often have their own protocols based around local factors such as availability of PCI and hospital drug formularies. The following is based around the 2020 update to the NICE ACS guidelines.

Acute coronary syndrome can be classified as follows:
  • ST-elevation myocardial infarction (STEMI): ST-segment elevation + elevated biomarkers of myocardial damage
  • non ST-elevation myocardial infarction (NSTEMI): ECG changes but no ST-segment elevation + elevated biomarkers of myocardial damage
  • unstable angina

The management of ACS depends on the particular subtype. NICE management guidance groups the patients into two groups:
  • 1. STEMI
  • 2. NSTEM/unstable angina

Common management of all patients with ACS
  • aspirin 300mg
  • oxygen should only be given if the patient has oxygen saturations < 94% in keeping with British Thoracic Society oxygen therapy guidelines
  • morphine should only be given for patients with severe pain
    • previously IV morphine was given routinely
    • evidence, however, suggests that this may be associated with adverse outcomes
  • nitrates
    • can be given either sublingually or intravenously
    • useful if the patient has ongoing chest or hypertension
    • should be used in caution if patient hypotensive

The next step in managing a patient with suspected ACS is to determine whether they meet the ECG criteria for STEMI. It is, of course, important to recognise that these should be interpreted in the context of the clinical history.

Management of STEMI

Once a STEMI has been confirmed the first step is to immediately assess eligibility for coronary reperfusion therapy. There are two types of coronary reperfusion therapy:
  • primary coronary intervention
    • should be offered if the presentation is within 12 hours of onset of symptoms AND PCI can be delivered within 120 minutes of the time when thrombolysis could have been given (i.e. consider thrombolysis if there is a significant delay in being able to provide PCI)
    • if patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered
    • drug-eluting stents are now used. Previously 'bare-metal' stents were sometimes used but have higher rates of restenosis
    • radial access is preferred to femoral access
  • thrombolysis
    • should be offered within 12 hours of onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when thrombolysis could have been given
    • a practical example may be a patient who presents with a STEMI to a small district general hospital (DGH) which does not have facilities for PCI. If they cannot be transferred to a larger hospital for PCI within 120 minutes then thrombolysis should be given. If the patient's ECG taken 90 minutes after thrombolysis failed to show resolution of the ST elevation then they would then require transfer for PCI

If patients are eligible this should be offered as soon as possible.

Primary coronary intervention for patients with STEMI

Further antiplatelet prior to PCI
  • this is termed 'dual antiplatelet therapy', i.e. aspirin + another drug
  • if the patient is not taking an oral anticoagulant: prasugrel
  • if taking an oral anticoagulant: clopidogrel

Drug therapy during PCI
  • patients undergoing PCI with radial access:
    • unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) - this is the action of using a GPI during the procedure when it was not intended from the outset, e.g. because of worsening or persistent thrombus
  • patients undergoing PCI with femoral access:
    • bivalirudin with bailout GPI

Other procedures during PCI
  • thrombus aspiration, but not mechanical thrombus extraction, should be considered
  • complete revascularisation should be considered for patients with multivessel coronary artery disease without cardiogenic shock

Thrombolysis for patients with STEMI

Thrombolysis used to be the only form of coronary reperfusion therapy available. However, it is used much less commonly now given the widespread availability of PCI.

The contraindications to thrombolysis and other factors are described in other notes.

Patients undergoing thrombolysis should also be given an antithrombin drug.

If patients have persistent myocardial ischaemia following thrombolysis then PCI should be considered.

Management of NSTEMI/unstable

The management of NSTEMI/unstable is complicated and depends on individual patient factors and a risk assessment. The summary below provides an overview but the full NICE guidelines should be reviewed for further details.

Further drug therapy
  • antithrombin treatment
    • fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography immediately
    • if immediate angiography is planned or a patients creatinine is > 265 µmol/L then unfractionated heparin should be given

Risk assessment

The Global Registry of Acute Coronary Events (GRACE) is the most widely used tool for risk assessment. It can be calculated using online tools and takes into account the following factors:
  • age
  • heart rate, blood pressure
  • cardiac (Killip class) and renal function (serum creatinine)
  • cardiac arrest on presentation
  • ECG findings
  • troponin levels

This results in the patient being risk stratified as follows:

Predicted 6‑month mortalityRisk of future adverse cardiovascular events
1.5% or belowLowest
> 1.5% to 3.0%Low
> 3.0% to 6.0%Intermediate
> 6.0% to 9.0%High
over 9.0%Highest

Based on this risk assessment key decisions are made regarding whether a patient has coronary angiography (with follow-on PCI if necessary) or has conservative management. The detailed pros/cons of this descision are covered in other notes.

Which patients with NSTEMI/unstable angina should have a coronary angiography (with follow-on PCI if necessary)?
  • immediate: patient who are clinically unstable (e.g. hypotensive)
  • within 72 hours: patients with a GRACE score > 3% i.e. those at immediate, high or highest risk
  • coronary angiography should also be considered for patients is ischaemia is subsequently experienced after admission

Primary coronary intervention for patients with NSTEMI/unstable angina

Further drug therapy
  • unfractionated heparin should be given regardless of whether the patient has had fondaparinux or not
  • further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug) prior to PCI
    • if the patient is not taking an oral anticoagulant: prasugrel or ticagrelor
    • if taking an oral anticoagulant: clopidogrel

Conservative management for patients with NSTEMI/unstable angina

Further drug therapy
  • further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug)
    • if the patient is not at a high-risk of bleeding: ticagrelor
    • if the patient is at a high-risk of bleeding: clopidogrel


Patients are at risk of a number of immediate, early and late complications following a myocardial infarction (MI).

Cardiac arrest

This most commonly occurs due to patients developing ventricular fibrillation and is the most common cause of death following a MI. Patients are managed as per the ALS protocol with defibrillation.

Cardiogenic shock

If a large part of the ventricular myocardium is damaged in the infarction the ejection fraction of the heart may decrease to the point that the patient develops cardiogenic shock. This is difficult to treat. Other causes of cardiogenic shock include the 'mechanical' complications such as left ventricular free wall rupture as listed below. Patients may require inotropic support and/or an intra-aortic balloon pump.

Chronic heart failure

As described above, if the patient survives the acute phase their ventricular myocardium may be dysfunctional resulting in chronic heart failure. Loop diuretics such as furosemide will decrease fluid overload. Both ACE-inhibitors and beta-blockers have been shown to improve the long-term prognosis of patients with chronic heart failure.


Ventricular fibrillation, as mentioned above, is the most common cause of death following a MI. Other common arrhythmias including ventricular tachycardia.


Atrioventricular block is more common following inferior myocardial infarctions.


Pericarditis in the first 48 hours following a transmural MI is common (c. 10% of patients). The pain is typical for pericarditis (worse on lying flat etc), a pericardial rub may be heard and a pericardial effusion may be demonstrated with an echocardiogram.

Dressler's syndrome tends to occur around 2-6 weeks following a MI. The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.

Left ventricular aneurysm

The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. This is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.

Left ventricular free wall rupture

This is seen in around 3% of MIs and occurs around 1-2 weeks afterwards. Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy are required.

Ventricular septal defect

Rupture of the interventricular septum usually occurs in the first week and is seen in around 1-2% of patients. Features: acute heart failure associated with a pan-systolic murmur. An echocardiogram is diagnostic and will exclude acute mitral regurgitation which presents in a similar fashion. Urgent surgical correction is needed.

Acute mitral regurgitation

More common with infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle. Acute hypotension and pulmonary oedema may occur. An early-to-mid systolic murmur is typically heard. Patients are treated with vasodilator therapy but often require emergency surgical repair.


The 2006 Global Registry of Acute Coronary Events (GRACE) study has been used to derive regression models to predict death in hospital and death after discharge in patients with acute coronary syndrome

Poor prognostic factors
  • age
  • development (or history) of heart failure
  • peripheral vascular disease
  • reduced systolic blood pressure
  • Killip class*
  • initial serum creatinine concentration
  • elevated initial cardiac markers
  • cardiac arrest on admission
  • ST segment deviation

*Killip class - system used to stratify risk post myocardial infarction

Killip classFeatures30 day mortality
INo clinical signs heart failure6%
IILung crackles, S317%
IIIFrank pulmonary oedema38%
IVCardiogenic shock81%