If you were this patient, would you prefer to be managed with the Queen of Hearts?

Written by Pendell Meyers

A man in his early sixties with no significant medical history (including a "negative cardiac workup a few years ago" for unclear indication) called 911 for acute chest pain constantly for the past 5 hours. 

EMS arrived and recorded vital signs within normal limits and the following ECG during active pain:

EMS1 @ 0157:

What do you think?

Smith: There are hyperacute T-waves in inferior leads, with a reciprocally inverted hyperacute T-wave in aVL.  There is a negative T-wave in V2, suggesting posterior OMI, and minimal ST depression in V3 with a down-up T-wave, all but diagnostic (by itself) of posterior OMI.

If this patient was now pain free after chest pain, I might think the aVL is a reperfusion T-wave, with reciprocally large inferior T-waves.  And V3 is could conceivably be due to early posterior reperfusion.  And high lateral along with posterior is a syndrome of circumflex occlusion.  However, this patient has active chest pain, and thus this this is inferior-posterior OMI.

Here is the Queen's interpretation.  This is Version 1, which does not differentiate between active and reperfused OMI.  Version 2 will only say "OMI" if it is active.

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Pendell: The ECG shows diagnostic features of inferoposterior OMI, with massively hyperacute T waves in inferior leads and their reciprocally negative hyperacute T waves in I and aVL. There is inappropriate STD maximal in V2-V4 of posterior OMI. Really unusual to me that QOH V1 only has low confidence, but at least its correct.

Unfortunately you can see that the conventional Zoll algorithm sees nothing even to suggest AMI, let alone STEMI. 

During EMS transport, the pain suddenly resolved.

EMS2 @ 0210 with pain resolved:

13 minutes later, we see a very clear inferoposterior reperfusion pattern, with inverted inferior reperfusion T waves replacing the inferior HATWs, and large upright posterior reperfusion T waves replacing the STD maximal in V2-V4. Flow seems to be restored at this time.

Smith: Notice that Version 1 diagnoses "OMI" even though it is a reperfused OMI (and she knows it)

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ED1 @0249 with return of active pain:

What do you think?

Smith: There is Pseudonormalization of the inferior T-waves (they are not normal, but they have become upright again, due to re-occlusion)

This was not recognized, since it looks "normal" relative to earlier ECGs.

And the Queen's interpretation:

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The initial hs troponin T: 67 ng/L (URL for men is 20 ng/L)

ED2 @ 0336:

This needs no description

The patient was now recognized as acute coronary occlusion (because the providers use STEMI criteria to diagnose it, and did not recognize the diagnostic evidence on prior ECGs).

Angiogram showed no significant disease of the left main, LAD, or LCX, but acute culprit lesion of the proximal RCA with "99% stenosis" and TIMI 2 flow. 

After PCI, TIMI 3 flow was restored:

Subsequent troponins:

1,028 ng/L

6,363 ng/L

(none further measured)

This is the only post-procedure ECG recorded, about 6 hours after cath:

Echo next day showed EF 60%, Hypokinesis of the basal-mid inferior and basal-mid inferolateral myocardium.

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MY Comment, by KEN GRAUER, MD (10/10/2024):  

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I found today's case especially interesting because of: i) The excellent correlation between the timing of serial ECGs with the presence and severity of CP (Chest Pain); and, ii) The insightful interplay between acute posterior OMI with acute RV MI during the stages of acute occlusion — followed by spontaneous reperfusion — followed by reocclusion of the "culprit" artery.

• For clarity in Figure-1 — I've put together the first 3 ECGs in today's case, to which I've added the Mirror Test image for either lead V2 or V3 in the 3 tracings. (For review on how I apply the Mirror Test I devised — See My Comment in the September 21, 2022 post in Dr. Smith's ECG Blog).

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MY Thoughts on ECG #1:

In a patient with severe, new-onset CP — the initial EMS ECG is obviously abnormal and suggestive of acute OMI. That said — I found the pattern of ST-T wave abnormalities unusual, such that I was not immediately sure of what was going on.

• ECG #1 shows sinus rhythm at ~65/minute — a normal PR interval — a borderline QTc — an incomplete RBBB pattern (rSrs' in lead V1 with terminal s waves in leads I,V6 — but without significant QRS widening) — and no chamber enlargement.
• The most striking finding is the deWinter-like T waves seen in each of the inferior leads. While I am much more used to seeing the gamut of deWinter-like ST-T wave changes in the chest leads (See My Comment in the April 17, 2023 post) — I don't know how else to describe the J-point depression rising to disproportionately huge T waves, other than as a deWinter-like equivalent of hyperacute changes in this patient with acute inferior OMI.
• Consistent with acute inferior OMI — are reciprocal ST-T wave changes seen in high-lateral leads I and aVL.
• Use of the Mirror Test facilitates appreciating associated posterior OMI (as per the inverted image of lead V3 in ECG #1). Consistent with posterior OMI is the straightened, downsloping ST depression in neighboring lead V4, with lack of ST depression in lateral leads V5,V6.
• The above said — the ST segment coving with symmetric T wave inversion seen in leads V1 and V2 of ECG #1 lacks the shelf-like ST depression typically seen in these leads with posterior OMI. Instead — this ST-T wave picture in leads V1,V2 is much more consistent with associated acute RV MI. The relatively modest amount of ST depression in leads V3,V4 is consistent with attenuation of the amount of anterior ST depression that is usually seen with posterior OMI — by opposing ST elevation from the acute RV MI.
• 
  
• KEY Point: The best way to confirm acute RV MI — is with use of right-sided leads (See My Comment in the July 19, 2020 and July 11, 2018 posts). That said — I thought the pattern of ECG changes seen in this initial EMS ECG was most consistent with a large, ongoing acute infero-postero OMI — with associated RV MI (and possibly with the T wave inversion in V1,V2 indicating some spontaneous RV reperfusion).
• PEARL #1: As we have often emphasized — recognition of acute RV MI is important because: i) It localizes the "culprit" artery to the proximal RCA; and, ii) Hemodynamic management of acute RV MI may be volume dependent (ie, avoidance of NTG — fluid infusion for hypotension).

Figure-1: Comparison between the first 3 ECGs in today's case. I've added the Mirror Test image for lead V2 in ECG #1 — and for lead V3 in ECGs #2 and #3 (See text).

MY Thoughts on ECG #2:

The change in ST-T wave appearance from ECG #1 to ECG #2 — is striking!

• In just 13 minutes (from 01:57 to 02:10) and simultaneously with the resolution of CP — the deWinter-like T waves in the inferior leads have evolved into the T wave inversion of spontaneous reperfusion.
• Reperfusion T waves are also now seen in the high-lateral leads I and aVL, in the form of prominent upright T waves.
• PEARL #2: This repeat ECG provides an insightful example of the tall, peaked T waves in leads V2,V3,V4 that signal posterior lead reperfusion!
• Note how the Mirror Test inverted image of lead V2 facilitates appreciation of how peaked, upright T waves in leads V2,V3 indicate posterior reperfusion!
• PEARL #3: Note that the T wave in lead V1 is also now positive — but that the amplitude of this upright T wave in lead V1 is so much smaller than the amplitude of the peaked T waves in leads V2,V3. This is another example of the attenuation of reperfusion T wave size by the interplay between posterior and RV OMIs.
• PEARL #4: Clinically — the above correlation between sudden resolution of CP and development of marked reperfusion T wave changes tells us that the "culprit" vessel has spontaneously reopened!

MY Thoughts on ECG #3:

Appreciation of ECG findings in the first 2 tracings — facilitates understanding the evolving pathophysiology occurring  39 minutes after ECG #2 — with the return of active CP:

• PEARL #5 (Beyond-the-Core): Be sure when comparing serial ECG findings — to look for any change in frontal plane axis and in QRS morphology. I thought that since ECG #1  was recorded — that there has been progressive axis shift to the left (more net negativity in the inferior leads) — such that limb lead morphology in ECG #3 is probably now consistent with LAHB (Left Anterior HemiBlock). Rather than LVH — the increased R wave amplitude in leads I and aVL may reflect discordance in the timing of ventricular depolarization due to the hemiblock.
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• PEARL #6: The above said — Limb lead ST-T wave changes in ECG #3 appear to be in process of returning to those that we first saw in ECG #1. Clinically — this return toward the ECG findings seen in the initial EMS ECG in association with the return of active CP — suggests reocclusion of the "culprit" artery. Awareness of this spontaneous reperfusion — followed soon after by reocclusion — emphasizes the need for prompt cath with PCI as soon as this is possible!

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P.S.: For those with an interest in another case illustrating the intriguing interplay between opposing electric forces, as may occur with acute RV and posterior MI evolving at different tempos — Check out My Comment in the October 7, 2019 post.