Author: Jason Kendall / Editor: Jason Kendall / Reviewer: Liz Florey, Jolene Rosario / Codes: CC1, CC2, CP1, SLO1, SLO3 / Published: 21/10/2021


Acute chest pain accounts for approximately 700,000 presentations to the emergency department (ED) per year in England and Wales and for 25% of emergency medical admissions [1].

Acute coronary syndromes (ACS) encompass a broad range of presentations including:

  • Unstable angina (UA)
  • Non-ST segment elevation myocardial infarction (NSTEMI)
  • ST segment elevation myocardial infarction (STEMI)

A clear understanding of the pathophysiology, classification and clinical presentation of these conditions is a pre-requisite for effective subsequent risk stratification and therapy.

Definition of Myocardial Infarction

Myocardial infarction (MI) is defined pathologically as myocardial cell death following prolonged ischaemia. Myocardial necrosis releases proteins (troponins, myoglobin, creatine kinase, etc.) into the circulation, which can be measured biochemically, and also gives rise to a clinical syndrome with characteristic symptoms and electrocardiographic changes. The criteria for acute, evolving or recent MI [2] are listed in the panel on the right.


In the context of cardiac marker rise, ST segment changes on the ECG define either STEMI or NSTEMI.

At the time of presentation, however, cardiac marker status is unknown, so the classification of patients presenting with ischaemic chest pain is based largely on the ECG.

Most patients with ST elevation at presentation have acute total coronary artery occlusion and progress to STEMI. However, many patients without ST elevation may not have a subsequent cardiac marker rise and are collectively termed non-ST elevation acute coronary syndromes (NSTE-ACS) until their markers define them as NSTEMI (marker rise) or UA (no marker rise) [3].

The image illustrates the classification of acute coronary syndromes. Click on the image to enlarge.


ACS occurs when myocardial oxygen demand exceeds circulatory supply.

This initially results in ischaemia; prolonged ischaemia results in infarction (myocardial cell necrosis).

A reduction in oxygen supply is precipitated by mechanical or inflammatory disruption (rupture or erosion) of an atherosclerotic coronary artery plaque associated with varying degrees of local vasoconstriction, thrombosis and micro-embolisation.

Atherosclerotic plaque disruption initiates thrombosis with platelet activation and platelet aggregation.

Thrombus formation

Thrombus formation in the context of STEMI is fibrin-rich; it causes coronary artery occlusion leading to myocardial ischaemia and subsequent infarction. This manifests electrocardiographically as ST segment elevation with a distribution of changes depending upon the coronary artery affected.

A thrombus occurring in the context of NSTE-ACS is platelet-rich; spontaneous thrombolysis and fragmentation into smaller particles release platelet emboli, which may cause small areas of more distal infarction (micro-infarction) without complete occlusion of the coronary artery. This is the process that is thought to be occurring in infarction without ST elevation, i.e. NSTEMI.

Dynamic Pathophysiology

The thrombotic response to plaque disruption is a dynamic process of thrombosis and thrombolysis, mediator induced vasoconstriction, and varying degrees of platelet aggregation and embolisation. Which particular process predominates determines the clinical syndrome, i.e. STEMI, NSTEMI or UA, and, in turn, the most appropriate subsequent therapy.

The incidence of NSTE-ACS is higher than STEMI and it appears that the number of NSTE-ACSs relative to STEMI is increasing with time [4].

Hospital mortality from STEMI is greater than that from NSTE-ACS but long term mortality is higher in NSTE-ACS [5]. In patients with NSTE-ACS, it is thought that greater age and higher incidence of co-morbidities, e.g. diabetes and renal impairment, contributes to the higher long term mortality.

Learning Bite

Short term mortality is higher with STEMI, but long term mortality is higher with NSTE-ACS.

Outcome from treated STEMI has improved significantly over the last few decades. In-hospital mortality prior to the 1960s was around 30% [4], dropped by the end of the 1980s to just below 20% [5], and currently is generally well under 10%, particularly in the research environment, where 30 day mortality figures as low as 5.4% have been reported [6].

Unfortunately, the overall natural history of AMI is more difficult to assess; the community and pre-hospital mortality of AMI appears to have changed little since the 1960s.

It is estimated that overall mortality from AMI is between 30% and 50% with the majority of deaths occurring within two hours of symptom onset, often prior to seeking or receiving definitive treatment. The above factors have underpinned health education programmes to encourage rapid decision-making on the part of the patient to call for help. However, there is little evidence that public education campaigns reduce patient delay [7].

Click here to go to the British Heart Foundation website.

Classical Presentation

The classic presenting symptom of ACS is chest pain, which is traditionally described as having a characteristic nature:

  • Heavy, aching or tight
  • Centre or left side of chest
  • Not related to respiration or movement
  • May radiate to one or both arms, neck or jaw

Likelihood ratios have been calculated that link features of the history with AMI [8-10].

Table of likelihood ratios

Table 1: Value of specific components of the chest pain history for the diagnosis of acute myocardial infarction
Historical factor Likelihood ratio
Ref 8 Ref 9 Ref 10
Increased likelihood of AMI:
Radiation to right arm/shoulder 4.7 2.9 2.6
Radiation to both arms/shoulders 4.1 7.1 4.1
Associated with exertion 2.4
Radiation to left arm 2.3 2.3 1.5
Associated with diaphoresis 2.0 2.0 2.1
Associated with nausea/vomiting 1.9 1.9 1.9
Worse than previous angina/similar to previous MI 1.8 1.3
Described as a pressure 1.3 1.4
Decreased likelihood of AMI:
Described as pleuritic 0.2 0.2 0.2
Described as positional 0.3 0.3 0.3
Described as sharp 0.3 0.3 0.3
Reproducible with palpation 0.3 0.2 – 0.4* 0.2
Inframammary location 0.8
Not associated with exertion 0.8

* In heterogenous studies, likelihood ratios are expressed as a range.

Learning Bite

No single factor in the history alone can confidently rule in or rule out AMI; characteristics of the pain with the highest likelihood for AMI are radiation of the pain to the right arm or shoulder, or to both arms or shoulders.

Risk Factors

Based on the analyses of the likelihood ratios for AMI, the history is a helpful, but not diagnostic, first step in the assessment of patients with chest pain.

Specifically, no single factor in the history carries with it a consistently powerful enough likelihood ratio to enable the emergency physician to robustly diagnose ACS or exclude it. The history does, however, form a start point in the diagnostic process, broadly establishing whether pain is likely to be cardiac ischaemic (or not) in origin; it provides information to add to baseline cardiac risk factors [3], which makes the diagnosis of ACS significantly more or less likely.

Atypical presentations of ACS are common, occurring in up to 33% of patients, mostly in the elderly, diabetics and women. Advanced age, co-morbid factors, delay in diagnosis, delayed or reduced use of reperfusion therapy, and reduced use of adjuvant therapies all contribute to the increased mortality in this population.

Physical findings associated with ACS are generally non-specific and include pallor, anxiety, sweating, tachycardia and tachypnoea. Generally, specific physical findings are associated with other causes for chest pain (i.e. not ischaemic cardiac) or are associated with the complications of AMI (see Table 2).

Table 2

Examination finding Likelihood ratio
Ref 9 Ref 10
Increased likelihood of AMI:
Third heart sound 3.2 3.2
Hypotension (systolic BP <80 mmHg) 3.1 3.1
Pulmonary crepitations 2.1 2.1
Decreased likelihood of AMI:
Chest pain reproducible by palpation 0.3 0.2-0.4*

* In heterogenous studies, likelihood ratios are expressed as a range.

Learning Bite

The finding of a third heart sound, hypotension or pulmonary crepitations makes AMI more likely.


Broadly speaking, the ECG will directly determine whether a patient’s further management follows:

  • An immediate fibrinoytic or mechanical reperfusion strategy, i.e. ST segment elevation and left bundle branch block
  • An anti-thrombotic and anti-platelet strategy (ST segment depression or T-wave inversion)
  • A ‘rule out’ strategy (normal ECG)

The image shows partial and complete coronary occlusion.

What ECG changes are indicative of myocardial ischaemia that may progress to AMI [2]?

ST segment changes, new conduction defects, Q waves and T wave changes may indicate AMI [2].

Example of a Non-STE ACS ECG:

Example of a STEMI ECG showing myocardial infarction:

Table 3 below shows the likelihood ratios for the association of various ECG changes with AMI [9,10]:

Table 3: Value of specific components of the ECG for the diagnosis of acute myocardial infarction [9,10]
ECG finding Likelihood ratio
Ref 9 Ref 10
Increased likelihood of AMI:
New ST segment elevation 5.7 – 53.9* 13.1
New Q wave formation 5.3 – 24.8* 5.0
New conduction deficit 6.3
New ST segment depression 3.0 – 5.2* 3.13
T wave peaking and/or inversion 3.1 1.9
Decreased likelihood of AMI:
Normal ECG 0.1 – 0.3 0.1

* In heterogenous studies, likelihood ratios are expressed as a range.

ST Segment Elevation

The presence of ST segment elevation, new Q wave formation or a new conduction deficit (e.g. left bundle branch block), in the context of acute ischaemic chest pain, is associated with such significantly positive likelihood ratios for AMI (see Table 1) that the diagnosis can usually be made with confidence and appropriate therapy commenced.

Table 4

Table 4: Value of specific components of the ECG for the diagnosis of acute myocardial infarction [9,10]
ECG finding Likelihood ratio
Ref 9 Ref 10
Increased likelihood of AMI:
New ST segment elevation 5.7 – 53.9* 13.1
New Q wave formation 5.3 – 24.8* 5.0
New conduction deficit 6.3
New ST segment depression 3.0 – 5.2* 3.13
T wave peaking and/or inversion 3.1 1.9
Decreased likelihood of AMI:
Normal ECG 0.1 – 0.3 0.1

* In heterogenous studies, likelihood ratios are expressed as a range.

However, the ECG by itself cannot define AMI, which also requires the demonstration of a cardiac marker rise. There are situations where this ‘injury’ pattern (i.e. ST segment elevation) does not necessarily indicate that myocardial necrosis has or will occur, such as:

  • ‘Aborted’ myocardial infarction where early reperfusion has occurred [11]
  • Coronary artery vasospasm with spontaneous resolution

Pitfall: There are occasional situations where ST elevation in the setting of ischaemic chest pain does not indicate that necrosis has or will occur.

ST segment elevation will typically be found in a ‘territorial’ distribution on the ECG that reflects, and is determined by, coronary artery anatomy

Click on the links below to view the ECGs.

Fig 1

Fig 2

ST Segment Depression and T Wave Changes

The presence of ST segment depression and/or T wave changes (see Fig 1), in the context of acute ischaemic chest pain, normally indicates myocardial ischaemia (i.e. unstable angina) but is also associated with a positive likelihood ratio for AMI (i.e. NSTEMI – see Table 1). Fig 1 Table 5

Table 5: Value of specific components of the ECG for the diagnosis of acute myocardial infarction [9,10]
ECG finding Likelihood ratio
Ref 9 Ref 10
Increased likelihood of AMI:
New ST segment elevation 5.7 – 53.9* 13.1
New Q wave formation 5.3 – 24.8* 5.0
New conduction deficit 6.3
New ST segment depression 3.0 – 5.2* 3.13
T wave peaking and/or inversion 3.1 1.9
Decreased likelihood of AMI:
Normal ECG 0.1 – 0.3 0.1

* In heterogenous studies, likelihood ratios are expressed as a range. Approximately 50% of patients with ST depression and 33% of patients with T wave inversion will subsequently be shown to have myocardial infarction [2,12]. This group of patients are presenting with an ACS (i.e. UA or NSTEMI).

Following a standard (12 lead) ECG, if posterior (V7, V8, V9) or right sided (V4R) infarction is suspected, additional chest leads are required in:

  • Patients with inferior ST segment elevation because the majority of right-sided infarcts and posterior infarcts occur as extensions of inferior infarcts. This may affect management – patients with right sided MI and hypotension may respond to fluid resuscitation.
  • Patients with anteroseptal ST segment depression (indicating ischaemia) because this may be masking true posterior infarction; this will, if demonstrated, affect immediate treatment.

Standard and posterior ECG lead placement

Figure 1: Standard and posterior ECG lead placement

Click on the links below to see standard-lead and posterior-lead ECG traces.

Standard chest lead

Additional posterior leads

Learning Bite

Be alert to the need for right sided or posterior leads when diagnosing STEMI – they should be performed as routine in all patients with inferior ST elevation or anteroseptal ST depression.

What About Left Bundle Branch Block?

Patients with ischaemic cardiac chest pain and left bundle branch block (LBBB) should be assumed to be having an AMI. These patients should be considered for immediate reperfusion therapy, because they have been shown to have amongst the highest mortality of patients with AMI, and they also gain the greatest benefit from thrombolysis [13].

Learning Bite

The default position for patients presenting with ischaemic chest pain and LBBB should be to assume that the presentation is due to AMI.

A normal ECG significantly reduces the probability of AMI [9,10]. It does not, however, reduce this probability enough to allow confident safe discharge based upon the history and ECG alone [15]. Therefore, patients who present with chest pain, in whom cardiac ischaemia is suspected and who have a normal ECG, should undergo further diagnostic testing (i.e. delayed cardiac markers, exercise testing, etc.) before they can be confidently ascribed to a low risk group.


A normal ECG in a patient with chest pain does not allow safe discharge without further investigation.


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