In this ECG Cases blog we look at how the art of mirror images can help you identify acute coronary occlusion.
Written by Jesse McLaren; Peer Reviewed and edited by Anton Helman. December 2024
Six patients presented with potentially ischemic symptoms. Can you use mirror images to identify which patients had acute coronary occlusion?
Case 1: 55 year old with chest pain
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Case 2: 75yo history of aortic stenosis with fever and syncope
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Case 3: 55 year old with jaw and bilateral arm pain
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Case 4: 70 year old with chest pain
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Case 5: 30 year old with chest pain
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Case 6: 55 year old with chest pain
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The art of the mirror image in ECG interpretation
Let’s put the art in heart! ECGs are usually taught with math – using numbers for leads, and millimeters for interpretation. This can divert attention from the underlying cardiac pathology onto an abstract grid paper. STEMI criteria uses a ruler to measure ST segment elevation, and such a narrow focus leads to high rates of false positives and missed occlusions. But ECGs are more fascinating and can be better understood using concepts from art – like mirror image, scale and proportionality, and overall impression. There are many advances in ECG interpretation for Occlusion MI, and this science started with visual concepts. As OMI expert Dr. Smith explained, “the way I’ve come up with these formulas is I’ve been looking at EKGs for 30 years…what do I see in an EKG that other people aren’t seeing? Why do I see it? And all these formulas I’ve come up with, have to do with me trying to figure out what it is I see.”
This is the first in a series of blog posts on the Art of Occlusion MI, beginning with mirror image. The STEMI paradigm creates a false dichotomy between ST elevation and ST depression. But they can be mirror images of the same process, including secondary repolarization abnormalities or primary ischemia. As with the Renaissance painting above, mirrors produce flipped images that can confirm what you’re looking at and may provide more information depending on the view, but you need to know which is the mirror image and what you’re looking at. Similarly, reciprocal ST/T changes may be more obvious, but you need to determine what is the cause of the ST/T change and which is the mirror image. How can we use the art of mirror images to better identify occlusions?
- Determine what you’re looking at, and which is the mirror image
- Abnormal depolarization like LVH or LBBB produces secondary ST depression and T wave inversion, resulting in mirror image ST elevation and tall T waves; while acute coronary occlusion produces primary ischemic ST elevation and hyperacute T waves, with mirror image ST depression and T wave inversion
- In a patient with chest pain from acute coronary occlusion, hyperacute T waves result in mirror image T wave inversion; but in the same patient now painfree from reperfusion, T wave inversion results in mirror image tall T waves
- ST elevation in aVR is just a mirror image of diffuse ST depression towards the apex
- Remember where the mirrors are
The ‘PAILS’ mnemonic makes it seem like the ECG is a house of mirrors with a maze of reflections. This confuses frontal and horizontal planes, and breaks down especially for mid or distal LAD occlusions where there is no inferior ST depression. But we just have to remember how the leads relate to the heart to see which leads are mirrors to each other.
- Limb leads (frontal plane) mirrors:
- right inferior (III) and high lateral (aVL)
- aVR and apex (II)
- Chest leads (horizontal plane) mirrors:
- Anterior (V2-4) and posterior (V8-9)
- Right anterior/septal (V1) and left lateral (V6)
3. Learn the science of OMI based on mirror image
- Inferior OMI: primary ischemic STD in aVL is the mirror image for subtle inferior OMI [1]
- Posterior OMI: primary ischemic STD in V2-4 is the mirror image of posterior OMI [2]
- High lateral OMI: mirror in III can help identify subtle lateral STE and hyperacute T wave
- Anterior OMI: depends on the site of occlusion [3]
- mid LAD: no reciprocal change on 12 lead (because mirror to anterior is posterior)
- proximal LAD: reciprocal change inferior (mirror to diagonal branch) or V6 (mirror to septal)
- distal LAD: anterior plus inferior injury pattern (with mirror in high lateral)
- diffuse STD (with mirror STE in aVR) is a high risk but non-specific pattern that can be from tachy-arrhythmias, cardiac disease or non-cardiac shock states [4]
Back to the cases
Case 1: 55 year old with chest pain
- Heart rate/rhythm: normal sinus
- Electrical conduction: normal intervals
- Axis: right
- R-wave progression delayed
- Tall/small voltage: tall from LVH
- ST/T: secondary, discordant and proportional ST/T in III (with reciprocal in aVL) and V6 (with reciprocal in V1)
= LVH with secondary ST/T changes. Serial ECGs no change, serial troponins normal.
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Case 2: 75yo history of aortic stenosis with fever and syncope
- H: sinus tach
- E: normal
- A: right
- R: mild delay
- T: normal
- S: primary ischemic STD inferolateral, with mirror image in aVR/V1
= non-specific global ischemia
Cath lab activated for “ST elevation in aVR”, with no acute coronary occlusion. Diffuse ST depression from was severe aortic stenosis with sepsis, and changes resolved with treatment:
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Case 3: 55 year old with jaw and bilateral arm pain
- H: normal
- E: normal
- A: normal
- R: normal
- T: normal
- S: primary ischemic STE anterior (with STD V6 mirror to V1), and high lateral (with STD III mirror to aVL)
= proximal LAD occlusion
Cath lab activated: 100% proximal LAD occlusion, peak trop 22,000 ng/L. Follow up reperfusion T wave inversion anterior and lateral T (with mirror relatively tall T in III):
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Case 4: 70 year old with chest pain
- H: sinus brady
- E: normal
- A: normal
- R: Q wave V2-3
- T: normal
- S: primary ischemic ST elevation and hyperacute T wave V2-4, no mirror inferior STD because no ST elevation or hyperacute T wave in aVL
= Mid LAD occlusion.
No reciprocal change seen so cath lab not activated. Stat cardiology consult and 15 lead done, showing mirror image in V8-9 (unnecessary for diagnosis, but shows that anterior lead mirror is posterior):
Cath lab activated: 99% mid LAD occlusion, first trop 125 and peak 37,000 ng/L. Follow up showed anterior reperfusion T wave inversion:
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Case 5: 30 year old with chest pain
- Heart rate/rhythm: normal sinus
- E: normal
- A: right
- R: normal
- T: tall voltate with early repolarization
- S: mild proportional ST elevation and concordant T waves, aVL mirrors lead III
= normal, no sign of pericarditis or occlusion MI. Normal investigations.
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Case 6: 55 year old with chest pain
- H: normal
- E: incomplete RBBB
- A: normal
- R: normal
- T: normal
- S: inferior primary ischemic ST elevation and hyperacute T waves with mirror in aVL, and primary ischemic anterior ST depression which is mirror to posterior wall
=infero-posterior STEMI(-) occlusion MI
Did not meet STEMi criteria so 15 lead done: now meeting STEMI criteria inferiorly but posterior leads tiny voltages and less obvious ischemic STE than mirror anterior STD:
Cath lab activated: 99% RCA occlusion, peak troponin 45,000 ng/L
Discharge ECG showed reperfusion T wave inversion inferior (with mirror tall T in aVL) and posterior (with mirror tall T in V2-3):
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Take home points for The Art of Occlusion MI Part 1: Mirror Image
- Remember which leads are reciprocal to each other, and identify which is the main ST/T change (and whether secondary or primary) and which is the mirror
- Reciprocal change can be more obvious than the primary injury pattern, and help highlight subtle inferior (mirror in aVL), lateral (mirror in III) or posterior (mirror V2-4) OMI
- STE-aVR is a mirror to widespread ST depression, which is a high risk but non-specific pattern that can be from tachy-arrhythmias, cardiac disease or non-cardiac shock states
- LAD occlusion may or may not produce reciprocal change on the 12-lead depending on the location of occlusion
For more cases see ECG Cases 24: reciprocal change and Occlusion MI
For online, live and interactive ECG courses, visit www.heartsECGcourse.com.
References
- Bischof JE, Worral C, Thompson P, et al. ST depression in lead aVL differentiates inferior ST-eelvatino mycoardial infarction from pericarditis. Am J Emerg Med 2016 Feb;23(2):149-154
- Meyers HP, Bracey A, Lee D, et al. Ischemic ST-segment depression maximal in V1-V4 (versus V5-V6) of any amplitude is specific for occlusion myocardial infarction (versus nonocclusive ischemia). J Am Heart Assoc 2021 Dec 7;10(23):e022866
- Fiol M, Cygankiewicz I, Guindo J, et al. Evolving myocardial infarction with ST elevation: ups and downs of ST in different leads identifies the culprit artery and location of the occlusion. Ann Noninvasive Electrocardiol 2004 Apr;9(2):180-6
- Harhash AA, Huang JJ, Reddy S, et al. aVR ST segment elevation: acute STEMI or not? Incidence of an acute coronary occlusion. Am J Med 2019, 132(5):622-630
Beautifully simplified! OMI ECGs make a lot more sense after learning this concept, sir. I’m out of words to thank you, sir.
Excellent article! I’m glad to see someone else disabusing people who read ECGs as part of their profession of the idea that ST depression in V1-V3 is always reciprocal to ST elevation in Leads II, II and aVF. While ST depression in Leads V1 – V3 does indeed represent (usually) reciprocal changes, those changes are reciprocal to deviations in Leads V7 – V9, not II, III or aVF.
One thing I have learned over the years is that although two leads may be situated to react reciprocally to each other, other factors can intervene that change the dynamic and create confusion. ST depression in Leads V5 and V6 in the presence of STE in the inferior leads, without STE in V1 or V2, is usually suggestive of a superdominant RCA that was the main supplier of circulation to the apicolateral wall of the LV (V5 and V6). Occlusion of the RCA results in a subendocardial ischemia in that area with reduced contributions from the LAD, LCx and perhaps an RI preventing the ischemia from becoming transmural.
Again, excellent article and very well presented!