An elderly woman with acute chest pain -- real or fake ST Elevation?

Written by Pendell Meyers

An elderly female called EMS with acute chest pain. 

Her vitals were within normal limits, and here is her EMS ECG:

What do you think?

Sinus rhythm, and QRS shows likely subtle RBBB, plus LAFB. While some STE could be expected by the large wide S wave in inferior leads, there is is STE and possibly HATW in II, III, and AVF, with reciprocal findings in aVL. While STD could be expected after a large R' of a RBBB in V2, that is not the case here: there is no R' in V2. So the STD in V2 is not explained, and is very large in proportion to its QRS complex, concerning for posterior OMI. The T waves in V4-6 are also a bit suspicious for hyperacute T waves. Overall, I would have high confidence for at least inferior and posterior OMI.

Queen of Hearts interpretation:

OMI with high confidence

Explainability image: 

I agree that the posterior OMI findings in V2 are the single most specific lead in this case.

It sounds like her pain improved before her first ECG obtained in the ED:

In context of the first ECG and resolution of symptoms, this shows reperfusion. however, if I interpreted this ECG alone and without context, I would have said it is nonspecific. This ECG is showing relative reperfusion compared to the first, and it briefly can pass through normal or near-normal before transitioning to reperfusion pattern.

QOH also sees no clear signs of active or reperfused OMI on this ECG (she cannot incorporate context or prior ECGs, yet).


Initial troponin (high sensitivity trop I): 212 ng/L.


She underwent angiogram within a few hours and was found to have mid-RCA culprit lesion, 99% stenosis, TIMI 3 flow. PCI was performed.

Here is her ECG several hours later:

Inferoposterior reperfusion findings.

Her peak troponin (high sensitivity trop I) was 23,893 ng/L.

Smith: 

This result shows you that troponin tells you what happened hours ago, not what is happening right now!  The artery was open, but the troponin rose from 212 to 23,000.  This patient was lucky to have spontaneous reperfusion.  Activating the cath lab so that the patient goes to angiogram "within a few hours" is too slow unless there is reperfusion.  I don't know if the delay was because they did not diagnose the OMI on the first ECG, or because they recognized reperfusion (by the ECG or pain resolution or both) on the second one.  If the latter, than the management was good.  If the former, then they could have risked an even larger MI than occurred.

What tells you the state of the artery right now?

1) The ECG with active ischemia or reperfusion or subendocardial ischemia or nonspecific (no ischemia)

2) presence or absence of symptoms.

(A specific finding on the ECG is much more reliable than symptoms)

What does not tell you what is going on right now? Rather, they tell you what has been going on in the last several hours:

1) Echocardiogram -- The myocardium remains stunned and hypokinetic after reperfusion.

2) Rising troponin -- troponin leaks from infarcted myocardium for a long time after ischemia is gone and will rise for a long time.

Queen of Hearts Update

We are working on upcoming models that are finally able to give more than a dichotomous yes/no for OMI. The most important distinct choices we will train first, are: 

Active OMI

Reperfused OMI

Subendocardial ischemia

Our very first such model correctly marks the first ECG in this series as "Active OMI, high confidence", and the last ECG as "Reperfused OMI, high confidence."

More to come!

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MY Comment, by KEN GRAUER, MD (12/10/2024):

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There are 2 aspects of today’s case that I found especially interesting: i) How despite the unusual appearance of the initial ECG — we knew there was acute OMI (TOP tracing in Figure-1); — and, ii) Some unexpected findings in ECG #2 (MIDDLE tracing in Figure-1).

Today’s Initial ECG:

As per Dr. Meyers — ECG #1 is diagnostic of acute OMI. The rhythm is sinus — and there is bifascicular block (RBBB/LAHB). That said — there are some atypical features:

In this older woman with new CP (Chest Pain) — my "eye" was immediately drawn to the 2 leads within the RED rectangles. 

• Regarding the inferior leads — there clearly is ST elevation in leads III and aVF, albeit with a saddleback shape that is often benign. In contrast — the T wave in lead II looks hyperacute (larger in size, with a disproportionately wide base — in comparison to modest dimension of the QRS in this lead).
• But any doubt that I may have had from the saddleback shape of ST elevation in leads III and aVF — was immediately dispelled by the shape of ST-T wave depression in lead aVL, which manifests a precise mirror-image opposite picture of the ST-T wave in lead III. In this older woman with new CP — there is no way lead aVL does not indicate acute OMI until proven otherwise.

As always — support in favor of acute inferior OMI can be forthcoming if there is also indication of acute posterior OMI.

• In ECG #1 — There is no way the distinct "shelf-like" flattened ST depression with terminal T wave positivity that we see in lead V2 is not indicative of associated posterior OMI until proven otherwise (within the 2nd RED rectangle).
• Instead of the gently upsloping, slight ST elevation that we normally see in lead V3 — the isoelectric flattened ST segment that we see in neighboring lead V3 confirms posterior OMI (BLUE arrow in this lead).

But what about the QRS widening in ECG #1?

• It is only if you look closely that we realize QRS width is ≥0.14 second (!) in ECG #1 (with true QRS width perhaps best appreciated by measuring QRS duration of the 1st complex within the RED rectangle in aVL).
• While RBBB/LAHB is clearly the best designation for QRS morphology in ECG #1 — the r' deflection is tiny and limited to lead V1 — and the rS complexes in leads V1-thru-V4 look surprisingly narrow. It could be easy to overlook the RBBB in this initial tracing.
• 
  
• P.S. — Could there be RV involvement? Whereas normally there is some ST-T wave depression in lead V1 with RBBB — there is none in ECG #1. In the setting of acute infero-postero OMI — this raises the question of whether there may be associated RV involvement? (which could be clinically relevant, depending on this patient's hemodynamic status).
• Obtaining right-sided leads would have been insightful ...

Figure-1: Comparison between the 3 tracings in today’s case.

What about ECG #2?

The "good news" in today's case — is that the patient's CP had decreased at the time ECG #2 was recorded, in association with near-return to the baseline for the inferior lead ST elevation — and, for the ST depression that had been seen in lead aVL. But what about the chest leads?

• I was puzzled by the appearance of new Q waves in leads V2,V3 (within the dotted BLUE ovals in these leads) — as well as by what appeared to be the suggestion of some new ST elevation in lead V1 that was not seen in ECG #1 (BLUE arrow in lead V1 of ECG #2).
• The increased size of the T waves in leads V2,V3 might be consistent with the limb lead changes suggesting some spontaneous reperfusion — But why the anterior Q waves and new ST elevation in lead V1?
• I suspected this patient might have multi-vessel disease and a changing pattern of collateral flow — but was content for the moment with the "good news" of clinical improvement and plan for prompt cath with PCI.

Putting It All Together

As per Dr. Meyers — the case ended well with cardiac cath showing an RCA "culprit" which was successfully stented. ECG #3 was obtained several hours after PCI.

• Both the anterior Q waves and the suggestion of ST elevation in lead V1 that we saw in ECG #2 are no longer seen in ECG #3.
• Wouldn't today's story "fit" better with events — if we didn't have to explain the above findings in ECG #2?

So — If we only had ECGs #1 and #3 for today's case:

• ECG #1 in this older woman with new CP — is immediately diagnostic of acute infero-postero OMI (in association with RBBB/LAHB).
• ECG #3 — is consistent with successful PCI when compared directly to ECG #1, in that it shows reperfusion ST-T wave changes (resolution of inferior lead ST elevation, now with T wave inversion in III and aVF — and taller, reperfusion T waves in leads V2,V3).
• P.S. — I'm curious if cardiac cath showed multi-vessel disease.