Sunday, September 13, 2020

A man in his 50s with 2 hours of chest pressure

 Case submitted by Anonymous, written by Pendell Meyers

A man in his 50s with history only smoking presented to the ED with chest pressure for the past 2 hours. His vitals were within normal limits except BP 163/109. 

No prior ECG was available. Here is his triage ECG:

What do you think?
This is probably obvious to regular readers of this blog, but it is NOT obvious to most emergency providers and cardiologists.

Findings include:

 - Sinus rhythm

 - Normal QRS complex

 - Hyperacute T waves in leads II, III, and aVF

 - reciprocal STD and T wave inversion in aVL

 - STD in V2-V4 (max in V3)

 - Likely hyperacute T waves in V5 and V6 as well

Interpretation: diagnostic for inferoposterolateral STEMI(-) OMI. There is always a small possibility of takotsubo or myocarditis, but this ECG is OMI until proven otherwise.

In our most important upcoming study, we are about to show that ECG experts are superior to simple STEMI criteria. We found that at least one of 7 key ECG findings were documented in the vast majority of cases where the expert outperformed the STEMI criteria. This case has at least three of these findings: hyperacute T waves, STE/hyperacute T waves in inferior leads with any STD/TWI in aVL, and STD max in V2-V4. 

The triage ECG was brought back to the ED physician immediately for review. The ED physician recognized this pattern and called a "heart alert" (this allows immediate cath consult via phone consultation and review of the ECG between EM and Cardiology). 

Aspirin and heparin were given. Cardiology came immediately to evaluate the patient. 

The cardiology team was not convinced of ACS and required that the patient be negative for Covid before further consideration of emergent cath would be entertained (reasoning unclear). So the swab was sent as rapidly as possible.

The first contemporary troponin T resulted undetectable, less than 0.01 ng/mL.

The second troponin T resulted elevated at 0.13 ng/mL (around 6pm, roughly 3 hours after arrival).

The rapid Covid swab returned negative, but by this time the patient was already admitted to cardiology who had no plans for emergent cath despite rising troponin (reasoning unclear).

This ECG was done just before the patient went upstairs to the cardiology floor. It shows continued active OMI of the inferior, posterior, and lateral walls.

Troponin at 9pm resulted at 4.74 ng/mL. This is a very high troponin T, roughly equivalent to a troponin I of 40-50 ng/mL.

The plan was for cath in the morning.

The troponin had already started falling by 6am, resulting at 3.20 ng/mL.

The delayed angiogram showed total thrombotic occlusion (100%, TIMI 0 flow) of the First Obtuse Marginal (OM1). So it was OMI of the OM1. There was also scattered other chronic lesions including 70% circumflex and 75% RCA. Ejection fraction was estimated at 40%, and echo showed hypokinesis of the inferobasal and lateral walls.

 Before intervention, showing OM1 occlusion.

Annotated showing where the occlusion is.

After intervention, showing now patent OM1.

Here is his ECG the next day:

There are new Q-waves in inferior leads. It is not clear whether the T waves in the precordial leads are large enough to be considered posterior reperfusion T waves, and if this is a completed MI as suspected then reperfusion T-waves would not really be expected (they may invert but with very low voltage).

Learning Points:

This case is an obvious example of how expert ECG interpreters can recognize OMI far earlier than the current management of the STEMI paradigm.

ST depression maximal in V1-V4 in the setting of a normal QRS should be concerning for posterior OMI until proven otherwise.


MY Comment by KEN GRAUER, MD (9/13/2020):


Today’s case provides an example of an acute OMI that should not have been overlooked by the Cardiology team.

  • Among the goals of our ECG Blog — is to provide constructive feedback in the hope of improving the care of acute coronary syndromes. One of the KEYS for doing this — is to enhance awareness of which ECG findings emergency providers should look for when a patient with new-onset cardiac symptoms does not manifest readily identifiable millimeter-criteria that satisfy the definition of an acute STEMI.
  • Drs. Smith and Meyers continue their laudatory work on dispelling the fallacy of dependence on millimeter-based STEMI criteria — which results in overlooking an estimated 25-30% of acute coronary occlusions (SEE our September 3, 2020 post for Dr. Meyers’ concise 17-minute presentation of the OMI Manifesto).
  • In the hope of facilitating recall of Which ECG Findings To Look For — when STEMI-criteria ST elevation are not evident — I’ve adapted from the research and teachings of Drs. Smith and Meyers the features I list in Figure-1.

Figure-1: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG. For more on this subject — SEE our September 3, 2020 post with Dr. Meyers OMI Manifesto Talk. For my clarifying Figure illustrating T-QRS-D (2nd bullet) — See My Comment in our November 14, 2019 post.

Let’s take another look at 2 of the 3 tracings from today’s case (Figure-2). For clarity — I’ve put the initial ECG ( = ECG #1) together with the ECG done the following day after PCI ( = ECG #3).

Figure-2: Comparison between the initial ECG and the ECG done the next day after PCI. I’ve added a magnified mirror-image view of leads V2 and V3 to the right of each tracing (See text).

Dr. Meyers has highlighted the abnormal ECG findings in ECG #1 (above). I’d like to add the following thoughts to his excellent discussion:

  • The term, hyperacute T waves” — is interpreted differently by different observers. As I indicate in the 1st bullet of my Figure-1 — I favor defining hyperacute T waves as being disproportionately tall and/or fatter-at-their-peak or wider-at-their-base than should be expected given R wave and S wave amplitude in whatever lead you are looking at.

PEARL #1: To facilitate recognition of hyperacute T waves — I favor the concept I’ve named, Patterns-of-Leads”. By this I mean that IF there is an ongoing acute coronary syndrome, and you identify an ST-T wave abnormality in one lead — the chances are excellent that one or more neighboring leads will also manifest a similar ST-T wave abnormality.

  • For example — Isn’t the peak of the T wave in lead aVF fatter-than-you-would-normally-expect it to be? Compared to the 9 mm tall R wave in this lead — Isn’t the 5 mm tall T wave disproportionately taller-than-it-should-be? I’d add that the base of the T wave in lead aVF is also wider than I’d expect. Given the history ( = chest “pressure” of 2 hours duration that brought today’s patient to the ED!) — the T wave in lead aVF has to be considered a “hyperacute” T wave until you prove otherwise.
  • Using the principle of Patterns-of-Leads — I agree with Dr. Meyers that the other 2 inferior leads ( leads IIand III) show similar hyperacute T waves.
  • Elsewhere on this tracing (as per Dr. Meyers) — lateral chest leads V5 and V6 also show similar hyperacute changes. By way of comparison — a much more normal T wave appearance is seen in leads V5 and V6 of ECG #3 done the next day.

Dr. Meyers also highlights the reciprocal ST-T depression seen in lead aVL. We have commented often in Dr. Smith’s Blog how helpful the finding of a reciprocal relationship for ST-T wave appearance between leads III and aVL is for recognizing acute OMI.

  • Beyond-the-Core (and admittedly subtle): The reciprocal relationship between leads III and aVL is subtle in the initial ECG from today’s case. This is because of 2 factors: i) The amplitude of the QRS complex and T wave in lead aVL of ECG #1 is tiny; andii) The T wave in lead aVL may normally be negative in cases in which the QRS is predominantly negative (as it is in ECG #1). That said — even though the amplitude of the QRS and ST-T wave in lead aVL of ECG #1 is tiny — the relative width of this negative T wave is wider-than-I-would-have-expected, and this wider shape of the inverted T wave in aVL is a miniaturized mirror-image match of the disproportionate T wave dimensions in lead III.

PEARL #2: The purpose of the 5th bullet in my Figure-1 — is that the finding of maximal ST segment depression in leads V2-to-V4 is highly suggestive of acute posterior involvement (since anterior leads V2,V3,V4 provide a mirror-image view of the LV posterior wall). As a visual aid to facilitate recognition of the distinct ST-T wave depression shape that is characteristic of acute posterior MI — I favor what I call, the Mirror Test” (See My Comment in the February 16, 2019 post of Dr. Smith’s ECG Blog).

  • Note in the magnified mirror-image view of leads V2 and V3 (to the right of ECG #1) — that the taller-than-expected anterior R waves in leads V2 and V3 of ECG #1 in the mirror-image view “become” Q waves. Note also that the straightened, downsloping depressed ST segment in lead V2  and, the straightened, upsloping depressed ST segment in lead V3 — in the mirror-image view “become” readily apparent as acute infarction-like ST elevation with terminal T inversion. KEY: With a little bit of practice — use of the Mirror Test should facilitate near-instant recognition of even subtle changes of acute posterior MI.

PEARL #3: In the 3rd bullet in Figure-1 — I’ve underlined that, “the more leads with suspicious findings — the greater the concern for an acute ongoing event”. As soon as I’ve identified which of the 12 leads manifest clearly abnormal ST-T wave findings — I reapply the “Patterns-of-Leads” principle, by GOING BACK and taking another look at the remaining leads, to see if they might also show subtle abnormalities that I may not have initially identified.

  • Leads in ECG #1 that I have already identified (above) as clearly manifesting abnormal ST-T waves in this patient with new-onset symptoms include — leads II,III,aVF  lead aVL  leads V2,V3 — and leads V5,V6.
  • Among the remaining leads in ECG #1 — I believe subtle-but-real ST-T wave abnormalities are also present in leads I, V1 and V4. Lead I — shows slight J-point ST depression and ST segment straightening. Regarding lead V1 — in the context of clear indication of acute posterior MI (given the appearance of leads V2 and V3) — the T wave in V1 looks broader and more deeply inverted than I’d normally expect (subtle). And, Lead V4 is definitely abnormal — as it shows ST depression and an overly fat-and-peaked T wave, similar to the ST-T wave appearance in lead V3.
  • BOTTOM Line Regarding ECG #1: No less than 11 of 12 leads manifest what I consider abnormal (and potentially acute) ST-T wave changes in this patient with new-onset symptoms.

Putting It All Together: As per Dr. Meyers — the abnormal findings in ECG #1 are “probably obvious to regular readers of this blog”. They should be obvious to all providers charged with rendering emergency care.

  • The BEST ways to facilitate recognizing these acute changes in ECG #1 are: i) To look at all 12 leads for the ECG findings listed in Figure-1 in all of your patients with new symptoms who do not manifest obvious STEMI criteria; andii) To actively seek out follow-up (whenever at all possible) on the patients you see — andto learn from that follow-up!

To anyone questioning the detail of my above commentary — I suggest making a lead-by-lead comparison in Figure-2 of QRS and ST-T wave appearance for each of the 12 leads between ECG #1 and ECG #3.

  • It should be noted that there has been some change in QRS morphology for both limb leads (due to slight frontal plane axis shift) and chest leads (perhaps due to slight change in precordial lead placement). Despite this — I believe that for the most part, the changes in ST-T wave morphology that we see between ECG #1 and ECG #3 are real.
  • Note that each of the leads with hyperacute T wave changes that we identified for ECG #1 — no longer look “hyperacute” in ECG #3.
  • As per Dr. Meyers — the Q in lead III of ECG #3 is now much deeper (almost equal in amplitude to the small R wave in this lead).
  • Perhaps the shallow T inversion in lead III of ECG #3 — and the now upright T wave in lead aVL — both reflect some reperfusion. Similarly, the ST depression in leads V2-V4 that was seen in ECG #1 — is no longer present in ECG #3. As suggested by the magnified mirror-image view of leads V2 and V3 (to the right of ECG #3) — the now upright T waves in leads V1-thru-V4 may also represent reperfusion.

Our THANKS to Dr. Meyers for presenting this case. LOTS of lessons to be learned!


  1. I don't understand why with continued pain (I assume?) And actively rising enzymes why not immediate cath. Also I would think a point of care echocardiogram or formal stat echo would go a long way here

    1. A great case!
      1. As a matter of fact, the ECG changes in ER are more than subtle. When there is a disagreement between ER docs and Cardiology team, how do we reconcile it?: next level of testing: Echo right away and of course, cath would have been real helpful (in hindsight). There should have been an insistence by ER docs to pursue the diagnosis further sooner. You know why for the #2 reason, at least.
      2. Suppose that patient coded on the floor/ICU with VT/VF and died, the case went to the court and ER docs were also implicated, what would they say, "Not my problem!" Likely wont work.
      Great explanation as always. Thank you for sharing.

    2. @ jpmishra — TOUGH issues you raise. These are discussed all the time by us on Dr. Smith’s ECG Blog — as when emergency providers recognize acute OMI but cardiology consultants are not convinced. As illustrated in many of our cases — additional testing (ie, serial troponins, frequent repeat ECGs looking for dynamic changes, comparison with prior tracings, and ideally a stat Echo at the bedside during chest pain looking for localized wall motion abnormalities) + frequent discussion with cardiology are effective measures in many cases to get agreement on the need for prompt cath. Hopefully, with time — your consulting cardiology team will get to know emergency providers better (and will hopefully value and respect their opinion on ECG interpretation). That said, as some of our cases show — sometimes nothing works to convince the Cardiology team … Sometimes cardiology refusal to cath the patient is done from afar, or by a junior member of the team (resident or fellow). All I can suggest under such circumstances is to insist that the Cardiology Attending come in to DIRECTLY see and examine the patient — and that they then take over care (with the ED physician documenting it all on the chart).

  2. Not posterior leads was obtained?

    1. @ PB — Posterior leads are NOT needed to make the diagnosis of acute posterior involvement. I explain and illustrate this with my Mirror Test in My Comment above. Please realize that the size of changes with posterior leads tends to be much less obvious that what can plainly be seen by mirror-image of the anterior leads — so it is RARE indeed (if it ever happens ... ) that posterior leads will tell you something that can't be seen by the standard 12 leads (using the mirror-image technique). Send us a case if you have one of a posterior MI not apparent on standard 12-lead ECG but diagnosed only by posterior leads — :)

  3. Replies
    1. Yes. Cath confirmed OMI with total (100%) occlusion of the 1st obtuse marginal branch of the LCx (including other narrowings) and localized hypokinesis.

  4. I'm curious when there is close to a net isoelectric complex whether we should V2 and V3 to be contiguous concordant STE. In the end the clinical picture and enzymes along with many atypical leads trumps any nitpicking about millimeters or concordant vs discordant but I might even have called it STEMI positive based on V2-4.

    1. I’m afraid I do not understand all of your question — but YES, if the ONLY thing we saw that was abnormal on ECG #1 was that shape and that amount of ST depression in leads V2,V3 and V4 — this alone is enough to call it an “OMI” ( = Occlusion-based acute MI). We get into semantics as to whether this is a “STEMI” — since technically there isn’t ST “elevation” — but practically speaking NONE of that matters. What counts is whether or not there is acute occlusion of a major coronary artery — and maximal ST depression of the shape we see in V2-V4 in ECG #1 in a patient with new chest pain IS diagnostic of acute OMI (This is the 5th bullet in my Figure-1). I hope that addresses your concerns — :)

  5. Ken and Pendell...

    A very, very sad case. Fortunately, the outcome wasn't as bad as it might have been.

    Personally, I thought the initial ECG was obvious. The T waves were too large, too wide and too symmetrical to be normal T waves. They were literally screaming "HYPERACUTE!"

    I always teach my students that it is just as important to recognize normal as abnormal - especially when "abnormal" is a bit subtle. A practice tip I give is to take two leads - Lead II and V3, for instance - and for the next twenty or thirty ECGs that you see, study the T waves in those two leads (after assessing all the others, of course). Learn what normal looks like - check the height and width, check for asymmetry, compare inferior T waves to lateral T waves. Learn to recognize all the shades of normal. Once done, the T waves in this ECG will immediately grab your attention.

    Jerry W. Jones, MD FACEP FAAEM


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