Myocardial Ischaemia

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Myocardial Ischaemia This page covers the ECG signs of myocardial ischaemia seen with non-ST-elevation acute coronary syndromes. ST-elevation / Q-wave myocardial infarction patterns are covered elsewhere (see links at bottom of page). Background Non-ST-elevation acute coronary syndrome (NSTEACS) encompasses two main entities: Non-ST-elevation myocardial infarction (NSTEMI). Unstable angina (UA). The differentiation between these two conditions is usually retrospective, based on the presence/absence of raised cardiac enzymes at 8-12 hours after the onset of chest pain. Both produce the same spectrum of ECG changes and symptoms and are managed identically in the Emergency Department. Patterns of Myocardial Ischaemia There are two main ECG abnormalities seen with NSTEACS: ST segment depression T wave flattening or inversion While there are numerous conditions that may simulate myocardial ischaemia (e.g. left ventricular hypertrophy , digoxin effect ), dynamic ST segment and T wave changes (i.e.

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Transcript of Myocardial Ischaemia

Page 1: Myocardial Ischaemia

Myocardial Ischaemia

This page covers the ECG signs of myocardial ischaemia seen with non-ST-elevation acute coronary

syndromes. ST-elevation / Q-wave myocardial infarction patterns are covered elsewhere (see links at bottom

of page). 

Background

Non-ST-elevation acute coronary syndrome (NSTEACS) encompasses two main entities:

Non-ST-elevation myocardial infarction (NSTEMI).

Unstable angina (UA).

The differentiation between these two conditions is usually retrospective, based on the presence/absence of

raised cardiac enzymes at 8-12 hours after the onset of chest pain. Both produce the same spectrum of ECG

changes and symptoms and are managed identically in the Emergency Department. 

Patterns of Myocardial Ischaemia

There are two main ECG abnormalities seen with NSTEACS:

ST segment depression

T wave flattening or inversion

While there are numerous conditions that may simulate myocardial ischaemia (e.g. left ventricular

hypertrophy, digoxin effect), dynamic ST segment and T wave changes (i.e. different from baseline ECG or

changing over time) are strongly suggestive of myocardial ischaemia.

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Click on the links above to read more about the different causes of ST segment and T wave abnormalities. 

Other ECG patterns of ischaemia

Hyperacute (peaked) T waves  or pseudonormalisation of previously inverted T waves (i.e. becoming

upright) suggest hyperacute STEMI.

Another, less well-known ECG feature of myocardial ischaemia is U-wave inversion.

Morphology Of ST Depression

ST depression can be either upsloping, downsloping, or horizontal (see diagram below).

Horizontal or downsloping ST depression ≥ 0.5 mm at the J-point in ≥ 2 contiguous

leads indicates myocardial ischaemia (according to the 2007 Task Force Criteria).

ST depression ≥ 1 mm is more specific and conveys a worse prognosis.

ST depression ≥ 2 mm in ≥ 3 leads is associated with a high probability of NSTEMI and predicts

significant mortality (35% mortality at 30 days).

Upsloping ST depression is non-specific for myocardial ischaemia.

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Distribution of ST segment depression

ST depression due to myocardial ischaemia may be present in a variable number of leads and with variable

morphology:

ST depression due to subendocardial ischaemia is usually widespread — typically present in leads I,

II, V4-6 and a variable number of additional leads.

A pattern of widespread ST depression plus ST elevation in aVR > 1 mm is suggestive of left main

coronary artery occlusion.

ST depression localised to a particular territory (esp. inferior or high lateral leads only) is more likely to

represent reciprocal change due to STEMI. The corresponding ST elevation may be subtle and

difficult to see, but should be sought. This concept is discussed further here.

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Widespread subendocardial ischaemia due to LMCA occlusion

T wave inversion

T wave inversion may be considered to be evidence of myocardial ischaemia if:

At least 1 mm deep

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Present in ≥ 2 continuous leads that have dominant R waves (R/S ratio > 1)

Dynamic — not present on old ECG or changing over time

NB. T wave inversion is only significant if seen in leads with upright QRS complexes (dominant R waves). T

wave inversion is a normal variant in leads III, aVR and V1.

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Widespread T wave inversion due to myocardial ischaemia (most prominent in the lateral leads)

Wellens’ Syndrome

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Wellens’ syndrome is a pattern of inverted or biphasic T waves in V2-4 (in patients presenting with

ischaemic chest pain) that is highly specific for critical stenosis of the left anterior descending

artery.

Patients may be pain free by the time the ECG is taken and have normally or minimally elevated cardiac

enzymes; however, they are at extremely high risk for extensive anterior wall MI within the next 2-3

weeks.

There are two patterns of T-wave abnormality in Wellens’ syndrome:

Type 1 Wellens’ T-waves are deeply and symmetrically inverted

Type 2 Wellens’ T-waves are biphasic, with the initial deflection positive and the terminal deflection

negative

Wellens’ Type 1

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Read more about Wellens’ syndrome here.

Non-specific ST segment and T wave changes

The following changes may occur with myocardial ischaemia but are relatively non-specific:

ST depression < 0.5 mm

T wave inversion < 1 mm

T wave flattening

Upsloping ST depression

More ECG Examples

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Example 1

Subendocardial ischaemia:

The most striking abnormality is the widespread ST depression, seen in leads I, II and V5-6. This is

consistent with widespread subendocardial ischaemia.

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There is also some subtle ST elevation in V1-2 and aVR with small Q waves in V1-2, suggesting that the

cause of the widespread ischaemia is a proximal LAD occlusion.

 

Example 2

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Reciprocal change:

The most obvious abnormality is the horizontal ST depression in III and aVF.

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This could be misinterpreted as “inferior ischaemia” — however, subendocardial ischaemia does not

localise.

Regional ST depression should prompt you to scrutinise the ECG for signs of reciprocal ST elevation…

In this case there is subtle ST elevation in aVL.

This is a high lateral STEMI!

Dr Stephen Smith covers two similar cases on his excellent ECG blog. 

 

Example 3

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Wellens’ Syndrome:

There are abnormal T waves in V1-4 — biphasic in V1-3 and inverted in V4.

This pattern is known as Type 2 Wellens’ Syndrome and is highly specific for a critical stenosis of the

proximal LAD artery.

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Example 4a

Dynamic ST depression in a patient with chest pain:

Widespread ST depression (leads I, II, V5-6) indicates subendocardial ischaemia.

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Q wave in lead III with slightly elevated ST segment suggests the possibility of early inferior STEMI.

 

Example 4b

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ECG of the same patient after treatment with oxygen, nitrates, heparin and antiplatelets:

The ST changes have now resolved.

Inferior ST segments and Q waves are stable — this patient had a history of prior inferior MI.

Troponin was raised, confirming that the initial ST depression was due to NSTEMI.

 

Example 5

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NSTEMI presenting with isolated U wave inversion:

There are inverted U waves, most prominent in leads V5-6.

This is an infrequently recognised but very specific sign of myocardial ischaemia — this patient had a

12-hour troponin of 4.0 ng/mL.

To find out the full story behind this ECG, click here.