Sunday, December 18, 2022

A young patient with diminishing pain with a subtle but diagnostic ECG.

Written by Emre Aslanger

(Emre is our newest editor.  He is an interventionalist in Turkey and one of 3 originators of the OMI/NOMI paradigm, along with Pendell and Smith.  Here are his publications.)


A 39-year-old male without prior medical history presents with chest pain that started 2 hours prior to presentation. He says that the pain intensity was 10/10 at home but now about 4/10. His medical exam is unremarkable. He has no cardiovascular risk factors except smoking for 10 pack-years. He denies any illicit drug use. His ECG is shown below.  

What do you think ?

Although not striking, this is clearly a diagnostic ECG for infero"posterior" myocardial infarction due to coronary occlusion (OMI), most likely due to left circumflex (LCx) artery occlusion. There is clear ST-segment depression in V2-5, which peaks around V4. The morphology in V2 is especially concerning for a reciprocal change to "posterior" ST-segment elevation (STE). There is also subtle STE in inferior leads, with hyperacute T-waves and accompanying Q waves in lead II and aVF. Lead III has a fractioned QRS complex. These all are highly unlikely to be seen in a 39-year-old man without previous cardiac history.   

Emergency physician doubts the diagnosis and wants to see another ECG with posterior leads. It is given below. The patient is highly stable and says his pain is now around 2/10. What would you do ?

Leads V4-6 here are actually V7-9. It is a good custom to write it on the paper as soon as the printout is acquired. Afterwards nobody can reliably guess what these leads actually are. Another suggestion is to keep V1-3 in place (here it seems that V1-3 are actually V4-6), as they show the greatest amount of ST depression and keeping them on the new ECG might ensure that STD in these leads did not disappear. If STD resolves at the time of the posterior ECG, it might be another reason for its false negativity. 

Here, there is STE in lead V8 and V9. It may be less than 1 mm but it is defined as at least 0.5 mm STE even in the fourth universal definition of myocardial infarction. However, we tend to assess it visually and STE is clearly there.  

Despite the clinical stability and decreasing pain, this patient needs an immediate angiogram. Chest pain may decrease due to multiple factors even if the artery is still occluded. I personally believe that among chest pain, ECG and troponin; the most reliable one is ECG. 

Another important pearl is that: Do not assume that a subtle ECG means a subtle MI. 

The patient was given 300 mg po acetylsalicylic acid, 180 mg ticagrelor and taken to the cath lab. 

Here is his angiogram:  
This shot shows that the left circumflex (LCx) is occluded at the ostium (origin).  This is seen just millimeters beyond the tip of the catheter.

Compare to the anatomy after stenting:
The lower of the 2 now easily seen branches is the circumflex, now with excellent flow.

The patient recovered well. His peak troponin was over 5000 ng/L. Next day echocardiogram showed inferolateral hypokinesia with an EF of %45-50. 

If you still have not read it, I strongly recommend that you read the following article on the diagnosis of "posterior" MI: Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion Myocardial Infarction (Versus Nonocclusive Ischemia), by Meyers HP et al.

Here is the link:
Note that the artery is still occluded, no visible collaterals are present (in other images), but the pain is diminished. Always remember that the pain is not so reliable if the ECG is clear.

A small note on "posterior MI":
You might have encountered the discussion about the naming of "posterior" MI. In the newer literature, it is usually called "lateral" MI, but "posterior" MI is also still in widespread use.

This appears to stem from using different coordinate frames interchangeably: one based on myocardial segments the other based on the lead locations on the chest wall.

The current consensus proposed by the American Heart Association divides the LV into 17-segments (basal-, mid-, apical- anterior; basal-, mid-anteroseptum; basal-, mid-inferoseptum; apical septum; basal-, mid-, apical- inferior; basal-, mid-anterolateral; basal-, mid-inferolateral; apical lateral and apex). Many entities like “posterior MI” or “high-lateral MI” are still in use despite no LV segment bears these names. These names are a legacy of the second coordinate system, lead positions on the thoracic cavity. Indeed, the term “posterior MI” has such a historical connection. Since the LV diaphragmatic wall is opposed to the anterior wall, it has been first called as “posterior”. Later, a specific infarction entity that can be recognized using “posterior leads” or their anterior reflections (such as the presence of an R/S ratio >1 or an R-wave duration >40 milliseconds in lead V1) linked to the basal part of this wall. The term "true" posterior was coined for denoting that only the basal part of this wall curves upwards and truly constitutes a posterior structure. The remaining part named as inferior wall. Several later studies indicated that many patients do not have such a posteriorly curving wall. Cardiac magnetic resonance (CMR) studies indicated that these findings actually indicate MI of the inferolateral segments.

I believe that the nomenclature for the definition of MI should be based on the myocardium itself. However, I accept that many people may think the otherwise.

But if you choose to use this second approach, please be aware that "posterior" here means "the infarct diagnosed by ST depression in leads V1-V4 or by the "posterior" leads" not "the infarct of the myocardial wall just opposite to anterior wall". On echocardiogram you will not see a "posterior" hypokinesia (will see "inferolateral") and, as in this case, LCx may not give the blood supply of basal inferior segment (formerly called "posterior").

This may seem a bit detail but predicting the location of the culprit lesion from ECG may help interventionalists in the selection of guiding catheters, spotting the real culprit when multiple culprit-looking lesions are found on angiogram and decision making for revascularization strategies. Moreover, in addition to the extent of the infarcted myocardium being the single most important determinant of long-term prognosis, the involvement of specific left ventricular (LV) segments may also promote a vigilant search for associated complications. For example, mid-anterolateral and mid-inferior segments generally harbor papillary muscles and infarction of these segments may result in acute mitral regurgitation due to papillary muscle dysfunction or rupture. Post-myocardial infarction (MI) ventricular septal defects are frequently seen in mid-anteroseptal and apical septal segments, whereas apex and the basal inferior segment are prone to aneurysm formation.

These being said, the most important thing in this clinical situation is to diagnose OMI, whatever you call it.

Take home messages: 

- Never doubt your diagnosis when ECG is clear.
- A subtle ECG does not mean a subtle MI, especially in LCx territory.
- When taking a posterior ECG, keep leads V1-3 in place
- Posterior leads may be false negative, when V1-4 are diagnostic, do not use them to exclude "posterior" MI. 
- You may choose to say whatever you like, "posterior" or "inferolateral" MI, as long as you know how to diagnose and deal with it.


1. Meyers HP, Bracey A, Lee D, Lichtenheld A, Li WJ, Singer DD, Rollins Z, Kane JA, Dodd KW, Meyers KE, Shroff GR, Singer AJ, Smith SW. 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. doi: 10.1161/JAHA.121.022866. Epub 2021 Nov 15. PMID: 34775811; PMCID: PMC9075358.

2. Aslanger EK. Considerations on the naming of myocardial infarctions. J Electrocardiol. 2022 Mar-Apr;71:44-46. doi: 10.1016/j.jelectrocard.2022.01.006. Epub 2022 Jan 31. PMID: 35124348.

3. Cerqueira MD, Weissman NJ, Dilsizian V, Jacobs AK, Kaul S, Laskey WK, Pennell DJ, Rumberger JA, Ryan T, Verani MS; American Heart Association Writing Group on Myocardial Segmentation and Registration for Cardiac Imaging. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart. A statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association. Circulation 2002; 105(4): 539-42.

Comment by KEN GRAUER, MD (12/18/2022):
Important case with numerous diagnostic Pearls presented by Dr. Aslanger. I'd add the following thoughts to his excellent presentation.
  • We've presented numerous cases of acute posterior OMI that have been initially (and sometimes permanently) overlooked — because "there is no ST elevation". By definition — there won't be "ST elevation" in the standard 12 lead ECG with acute posterior OMI. As per Dr. Aslanger and his citation of the J Am Heart Assoc article by Meyers, Smith et al — posterior leads are not needed for the diagnosis of acute posterior OMI!

  • More than this — posterior leads that fail to show ST elevation may provide false reassurance (Please see My Comment at the bottom of the page in the September 21, 2022 post in Dr. Smith's ECG Blog)Failure of posterior leads to consistently demonstrate ST elevation in association with subtle posterior OMI — should not be surprising. This is because posterior placement of leads V7, V8 and V9 situates these leads in a position from which electrical activity must pass through the thick musculature of the back before being recorded on the ECG. As a result — even under optimal circumstances, QRST amplitudes (and therefore the amount of ST-T wave elevation) in posterior leads is often modest.

  • As per Dr. Aslanger — it is essential when using additional monitoring leads to specify in writing on the actual ECG which leads are being used. In today's 2nd tracing — I guessed that leads V4,V5,V6 were replaced by posterior leads V7,V8,V9 — but I had no idea that leads V1,V2,V3 were replaced by leads V4,V5,V6. When one considers that 1 or more right-sided leads might also be ordered in addition to (instead of) posterior leads — the number of possible lead switches that might be made is numerous.

  • PEARL #1: I would strongly suggest that when posterior leads V7,V8,V9 are recorded (and substituted for leads V4,V5,V6) — that a 2nd ECG with the standard 12 leads is also recorded! This is an especially important suggestion for those clinicians who obtain posterior leads for the sole purpose of "convincing the cardiologist that there is ST elevation!" As noted above, even in the best of circumstances — the relative amount of ST elevation in posterior leads is modest compared to the amount of ST depression in anterior leads. I have seen cases when 10-15 minutes after the initial ECG, a 2nd ECG is obtained in which leads V7,V8,V9 are substituted for V4,V5,V6 — and because of spontaneous reperfusion that was evident only in leads V4,V5 (which were omitted on the repeat tracing, being replaced by posterior leads) — this spontaneous reperfusion was not recognized! (and as a result — posterior leads no longer showed any ST elevation).

PEARL #2: Several lead electrodes in ECG #1 are malpositioned ...
As we've shown many times on Dr. Smith's ECG Blog — too-high placement of the V1,V2 electrode leads is disturbingly common (Please see My Comment at the bottom of the page in the April 17, 2022 post and in the November 4, 2018 post in Dr. Smith's ECG Blog)

KEY Point: Suspect that leads V1 and/or V2 have been placed 1 or 2 interspaces too high on the chest — IF one or more of the following clues are present:
  • CLUE #1 — If there is an r’ in leads V1 and/or V2, especially if the other finding for incomplete RBBB (ie, terminal s waves in lateral leads I and V6) is absent.
  • CLUE #2 — If there is a significant negative component to the P wave in lead V1 and/or V2.
  • CLUE #3 — If the appearance of the QRS complex and the ST-T wave in leads V1 and V2 looks very much like the QRS and ST-T wave in lead aVR.

Note that in the initial ECG from today's case (which I have reproduced in Figure-1) — all of the above 3 Clues are present, which strongly suggests that leads V1 and V2 are malpositioned.
  • In addition — Morphology of the QRS complex and ST-T wave of lead V3 does not make physiologic sense in ECG #1, considering the relative size and shape of the QRST complex in neighboring leads V2 and V4.

  • KEY Point: Given that the treating clinician in today's case was uncertain enough about the diagnosis of acute OMI, that he/she felt the need to repeat the ECG with posterior leads — the fact that the V1, V2 and V3 electrode leads are almost certainly malpositioned should have prompted immediate repeat of the standard 12-lead ECG after verifying lead placement.

Our THANKS to Dr. Aslanger for presenting today's case!

Figure-1: I've reproduced the initial ECG in today's case.

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