Thursday, May 18, 2023

45 yo with jaw pain radiating to left shoulder for 6 hours

This case was provided by Steven Souchtchenko, a recent graduate of our Hennepin Healthcare EM/IM residency (i.e., a former trainee of mine).


A 45 yo man with no previous cardiac history presented to an ED not associated with a cath lab.  

He complained of jaw pain radiating to left shoulder for 6 hours.  He stated he had had a brief similar episode the evening prior.

Here is his ED ECG.

What do you think?

When this was shown to me I immediately said "Proximal LAD OMI".  Then I ran it through the Queen of Hearts AI app and she said "OMI with high confidence".

I showed it to Pendell, who said: "Clearly LAD OMI"

What features tell us that it is proximal LAD OMI?
1. There is a QS-wave in V2. That indicates old or subacute MI.  But the patient has no previous cardiac history, so we must assume it is new, and so subacute, and that is consistent with the 6-hour duration of pain.  
2. The T-wave is also large for old MI.  My rule is that if any lead has a T/QRS ratio >0.36, then it is acute OMI; if <0.36, then either old MI (LV aneurysm) or subacute OMI.
3. There is ST depression in V3 and V4.  Always abnormal.
4. There is coving of the ST segment in I and aVL, with large inverted T-waves and reciprocally upright large inferior T-waves (these actually suggest some reperfusion, but as the patient has persistent symptoms, one must assume there is continued ischemia).
5.  The proximal LAD will affect the territory of the LAD and of the 1st diagonal, which supplies the high lateral wall, resulting in the findings in I and aVL, and the reciprocal findings in III and aVF.

Dr. Souchtchenko immediately recognized OMI and activated the cath lab at the referral institution to which they transfer patients. 

The receiving cardiologist was not terribly receptive and did not think the ECG showed a problem with the LAD.

My colleague insisted and said "you will 100% find an LAD Occlusion."  The cardiologist then accepted the patient.

They then recorded another ECG just before transfer:

Now there is no question.

Angiogram showed a 100% proximal LAD OMI.

My Comment by KEN GRAUER, MD (5/18/2023):
GREAT case to illustrate a series of important points:
  • Point #1: You CAN teach clinicians to attain expertise in their ability to immediately recognize acute OMI. This was wonderfully demonstrated in today’s case — in which Dr. Smith’s former trainee instantly knew on hearing the history and seeing the initial ECG — that the patient had acute proximal LAD occlusion. Because of his training in recognizing OMI patterns — Dr. Smith's former trainee had no reservations about this diagnosis.

  • Point #2: The history is a KEY (and often ignored) component for optimal ECG interpretation. The history in today’s case was of new-onset cardiac-sounding symptoms that began the night before — then spontaneously resolved — and then recurred, ultimately leading to the patient's presentation in the ED. Appreciation of this history tells us that among the ECG findings that we might expect to see — there could be ST-T wave changes consistent with spontaneous reperfusion of the “culprit” artery (and there could be some "pseudo-normalization" if the initial ED ECG was obtained in between the stage of ST elevation — and the stage of reperfusion T wave inversion). This prepares us for the possibility that we may not see ST elevation on the initial ECG.

  • Point #3: The initial ECG in today's case (that I've reproduced in Figure-1) — is completely consistent with an acute proximal LAD occlusion that may have occurred the night before (when according to the history, the patient’s symptoms began) — and, which may have subsequently spontaneously reperfused.

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

What Do We See in ECG #1?
The initial ECG shows sinus rhythm at ~85/minute — normal intervals and axis — and no chamber enlargement.
  • The most concerning leads are leads V1 and V2 — which show QS complexes and abnormal ST elevation. Normally, there is slight, gently upsloping ST elevation in leads V2 and V3. Instead, there is distinct J-point ST elevation in lead V2, followed by straightening of the ST segment.
  • Lead V3 shows clearly abnormal slight J-point depression (instead of slight elevation) — with a hyperacute T wave ("fatter"-at-its-peak than it should be), followed by a biphasic T wave.
  • There is slight ST depression in lead V4 — with subtle terminal T wave negativity.
  • There is non-specific ST-T wave flattening in leads V5,V6. As a result of this flat T wave in lead V6 — there is T wave "imbalance", in that the T wave in lead V1 is taller than the T wave in lead V6 (See My Comment at the bottom of the page in the June 1, 2022 post in Dr. Smith's ECG Blog for more on T wave imbalance).

In the Limb Leads:
  • Lead aVL immediately caught my eye. There is a small Q wave (which may be significant given small size of the QRS in this lead) — clearly abnormal ST segment coving — and fairly deep and symmetric T wave inversion. In the absence of ST elevation — this ST-T wave appearance strongly suggests there has been recent spontaneous reperfusion.
  • The other high-lateral lead ( = lead I) — shows similar, albeit slightly less marked changes.
  • Lead III shows the mirror-image opposite ST-T wave picture of lead aVL. Note how disproportionate the T wave in lead III is compared to the tiny QRS complex in this lead.
  • Lead aVF shows a slightly smaller, but still obviously disproportionate T wave compared to the tiny QRS in this lead.

Putting It All Together:
Abnormal ST-T waves are seen in no less than 11/12 leads in ECG #1.
  • Although there is some resemblance between today's initial tracing and the South African Flag Pattern seen with acute occlusion of the 1st or 2nd Diagonal branch — the finding of ST elevation not only in lead V2, but also in lead V1 — suggests proximal LAD occlusion instead (See My Comment at the bottom of the page in the April 8, 2022 post of Dr. Smith's ECG Blog for more on the S. African Flag pattern).
  • That said — despite our suspicion of proximal LAD occlusion, no other leads show ST elevation. The slight-but-real J-point ST depression in lead V3 — with subtle biphasic T waves in leads V3,V4 could be consistent with evolving reperfusion T wave changes. There could be some "pseudo-normalization" producing the ST-T wave flattening in lateral chest leads.
  • As alluded to above — lack of ST elevation, in association with prominent T wave inversion in the high-lateral leads — with disproportionate (mirror-image opposite) ST-T wave changes in leads III and aVF — strongly suggest spontaneous reperfusion.

  • BOTTOM Line: The most logical "story" we can put together from correlation this patient's history and the initial ECG — is that acute proximal LAD occlusion probably occurred and lasted for some period of time the night before — followed by spontaneous reperfusion when symptoms temporarily resolved — only to have severe jaw and left shoulder pain return when the "culprit" vessel reoccluded. As per Dr. Smith — the 2nd ECG in today's case removed all doubt about the diagnosis!

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