ST depression does not localise

I have had a few people ask me about the following statement from ECG Case 121:

“The reciprocal ST depression seen in leads III and aVF (in high lateral infarction) is often mistaken for inferior ischaemia. One must recall that ST depression does not localise, and such ST depression should be assumed to be a reflection of ST elevation in mirror image leads.”

Buttner, Aslanger: ECG Case 121

“ST depression does not localise” – what does this mean?

The term “localise” has two relevant interpretations here.

Firstly, contrary to common belief and computer interpretation, ST depression alone does not accurately represent the location of myocardial ischaemia. Terms such as “inferior ischaemia” based on ST depression in inferior leads are misnomers.

Secondly, subendocardial ischaemia produces a fairly typical pattern of ST depression, most commonly involving leads II and V4-6, with reciprocal ST elevation in aVR. This is regardless of which part of the myocardium is under stress. As such, ST depression localised to other regions such as inferior and/or anterior leads is unusual for “ischaemia” and should raise concern for reciprocal infarction. ST depression due to subendocardial ischaemia typically does not localise to specific myocardial territories on the ECG

So, let’s look more closely at these two aspects.

In patients undergoing exercise stress testing with known single vessel disease, ST depression seen does not accurately reflect the regions of ischaemia and is often non-specific. For example, patients with right coronary artery (RCA) stenosis do not necessarily manifest inferior lead ST depression.

Unfortunately, the electrophysiology behind this is not fully understood — we know that ST elevation, Q waves, and T wave inversion (TWI) all do accurately reflect the location of ischaemia or infarction. ST depression is thought to represent the boundary between ischaemic and non-ischaemic myocardium, and thus while it may overlap the underlying non-transmural ischaemia, it likely spans a much wider, non-specific area.

Here are four examples:

Where is the disease?

We are all familiar with this pattern of ST elevation in aVR and widespread ST depression. This ECG pattern simply tells us there is an oxygen supply/demand mismatch causing subendocardial ischaemia. In a clinical context, this can be due to:

• Hypotension
• Hypoxia
• Fixed stenosis limiting flow

However, the ECG here cannot localise such ischaemia and it is not necessarily global. It is likely that patients with this pattern in hypotension and/or hypoxia are essentially giving themselves a stress test, and may have single vessel, two vessel or triple vessel disease manifesting ischaemic changes.

The same pattern can be seen in patients with single vessel disease undergoing exercise stress testing, even in those with isolated inferior ischaemia on myocardial perfusion scan (MPS) due to RCA stenosis. Of course, in the absence of physiological stress, collateral supply means these patients would be unlikely to manifest ECG changes clinically. Such a pattern in suspected acute coronary syndrome (ACS) is therefore often due to LMCA critical stenosis or triple vessel disease.

Emergency Physician Dr Sam Ghali provides a great video example of this ECG pattern occurring in a patient with an unstable GI bleed and the importance of recognising this as oxygen supply/demand mismatch.

Note: ST elevation in aVR seen in subendocardial ischaemia is simply a reciprocal change to ST depression usually present in V4-6, I and II. Remember, aVR is a not real lead, it is calculated from leads I and II. Therefore, if there is ST depression in lead I and II, ST elevation in aVR is a corollary, not a magic sign.

As we have seen above, oxygen supply/demand mismatch produces a consistent ECG pattern with an ST vector pointing towards aVR, as a result of ST depression in leads V4-6 and II. As such, localised ST depression not involving these leads should be a major red flag for reciprocal occlusion myocardial infarction (OMI).

Example 1: “Anterior ischaemia”

55 year-old man presents with central chest pain

This ECG was signed off as “ST depression in V2-4, anterior ischaemia, repeat in 15 minutes”. The machine interpretation agreed, stating >> ST depression anteriorly, consider ischaemia <<. Posterior leads V7-9 were normal with no ST elevation seen.

We know from above that this interpretation is incorrect for for two reasons. Firstly, we cannot localise myocardial ischaemia based on ST depression alone. Secondly, the absence of ST depression in leads II and V5-6 (and associated ST elevation in aVR) here should raise flags for reciprocal infarction.

Indeed, if we look closely, we note:

• Pathological Q waves and trace ST elevation in inferior leads II, III, aVF
• Trace ST depression in aVL

This ECG is diagnostic for acute inferoposterior occlusion myocardial infarction (OMI). The patient went on to have delayed angiography revealing a complete left circumflex artery occlusion.

Example 2: “Inferior ischaemia”

74 year-old man presents with central chest pain

ST depression in leads III and aVF here is often misinterpreted as “inferior ischaemia”. Once again, this does not fit with the ECG pattern produced by subendocardial ischaemia, and such localised ST depression should be assumed to be a reflection of ST elevation in mirror image leads. ST elevation in I, aVL and V2 here is diagnostic for high lateral OMI.

This patient had a 100% occlusion of the first diagonal branch of the LAD, as well as severe triple vessel disease. This ECG was featured in ECG Case 121.

Example 3: aVL, the neglected lead

52 year-old man presents with chest pain

aVR has traditionally been considered the “neglected lead” in the diagnosis of LMCA or triple vessel disease, which we now know simply reflects oxygen supply/demand mismatch.

aVL is likely the neglected lead in the diagnosis of occlusion. ST depression in aVL in the setting of subendocardial ischaemia is rare (2-5% of cases), and when present is usually associated with changes in V4-6 and II. Isolated ST depression in aVL should raise concern for reciprocal changes and inferior OMI. The above patient had a 95% sub-total occlusion of his RCA.

What about when we have occlusion in the setting of subendocardial ischaemia?

There will be two ST vectors present:

• ST elevation relating to subendocardial ischaemia, directed towards aVR
• ST elevation due to occlusion, directed towards the infarcted territory

The above ECG, known as Aslanger pattern, is representative of acute inferior OMI in the setting of concomitant multi-vessel disease:

• The ST vector of subendocardial ischaemia directs towards aVR, reflecting ST depression in V4-6 and II
• The ST vector of inferior infarction directs towards II, III and aVF
• The resultant average ST vector directs rightwards, producing ST elevation in lead III and aVR only

Summary

Localised ST depression may be the first indicator of subtle occlusion

ST depression localised to a specific myocardial territory on the ECG is a frequent yet overlooked sign of occlusion myocardial infarction. Often misinterpreted as “localised ischaemia”, these changes should raise suspicion for subtle reciprocal ST elevation and associated infarction. Localised ST depression in anterior precordial leads is recognised as a sign of posterior infarction, but the same awareness is not as prevalent for these changes elsewhere.

ST elevation in aVR? Clinical context is everything

As Dr Stephen Smith outlines in this great case example, the pattern of diffuse ST depression (involving V4-6 and II) and ST elevation in aVR simply represents oxygen supply/demand mismatch, and does not necessarily indicate severe coronary artery disease. The same pattern can be seen in hypotension secondary to other causes, including post-resuscitation following cardiac arrest. We must be cautious to not allow this to distract from attending to other underlying pathology.

A 2019 single-centre retrospective analysis found that in patients undergoing code STEMI activations with this ECG pattern, only 59% had severe coronary artery disease, and none had LMCA or LAD occlusions. 36% of these patients had presented in cardiac arrest. In suspected ACS, ST elevation in aVR and diffuse ST depression warrants early discussion with cardiology and prompt (within 24-48 hours) angiography, but in the absence of ST elevation in V1-2 or elsewhere, is usually not indicative of occlusion.

Related topics

• Occlusion Myocardial Infarction (OMI)
• ST elevation in aVR
• Aslanger Pattern
• ECG Case 121

Expert review

• Smith SW. Subendocardial ischaemia does not localize. Dr Smith’s ECG Blog. 2010 August
• Smith SW. Diffuse subendocardial ischaemia on the ECG. Dr Smith’s ECG Blog. 2016 November

References

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• Kurata et al. Localization of Exercise-Induced Myocardial Ischaemia with ST Depression. Internal Medicine 1992; 31(5): 583-588
• Birnbaum et al. ST segment depression in a VL: a sensitive marker for acute inferior myocardial infarction. Eur Heart J. 1993 Jan;14(1):4-7
• Kang X, Berman DS, Lewin HC, Miranda R, Agafitei R, Cohen I, Friedman JD, Germano G. Comparative localization of myocardial ischemia by exercise electrocardiography and myocardial perfusion SPECT. J Nucl Cardiol. 2000 Mar-Apr;7(2):140-5.
• Landesberg et al. Perioperative Myocardial Ischemia and Infarction: Identification by Continuous 12-lead Electrocardiogram with Online ST-segment Monitoring. Anesthesiology February 2002, Vol 96, 264-270
• Bischof et al. ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis. Am J Emerg Med. 2016 Feb;34(2):149-54
• Aras et al. Spatial Organization of Acute Myocardial Ischaemia. J Electrocardiol. 2016 May-Jun; 49(3): 323-326
• Harhash et al. aVR ST Segment Elevation: Acute STEMI or Not? Incidence of an Acute Coronary Occlusion. Am J Med. 2019 May;132(5):622-630
• Kharel et al. Implications of Localized ST Depression in a Vascular Territory and Altered Precordial T-Wave Balance in Ischemic Heart Disease. Cureus. 2020 Jun; 12(6): e8580

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