Is this OMI reperfused or active?

These ECGs were texted to me by one of our previous ultrasound fellows, Will Smoot

An elderly male arrived via EMS for acute substernal chest pain with radiation to left shoulder and arm that awakened him from sleep at 0030.  

He took two full strength aspirin prior to EMS arrival.  The pain was relieved by one prehospital NTG spray.  

He arrived at the ED just shy of two hours after onset, pain free.  

No prior similar symptoms or known CAD.  

PMHX significant for hypertension and BPH.  Family history significant for father with MI at age 56, lived to age 83.  No acute infectious prodrome, known pulmonary disease, or recent trauma.  

Here is the initial ED ECG:

Here that first ECG is cleaned up by PM Cardio app:

What do you think?

Smith: this ECG is diagnostic of inferior-posterior OMI.  There is subtle STE in III and aVF, with a domed T-wave and some terminal T-wave inversion.  There is precordial STD maximal in V2 and V3, diagnostic of posterior OMI.

The question is: is this Active OMI or is it Reperfused OMI?

I think the ECG is equivocal on this point.  The fact that the patient's pain is resolved is good evidence (but not fool-proof) that the artery is reperfused.

Before concluding that there is reperfusion, one should record another ECG to ascertain if there is evolution of reperfusion.

The Queen of Hearts Diagnosed "STEMI/STEMI equivalent" on that first ECG (she now uses "STEMI Equivalent" rather than OMI). This is the new version of the Queen.  The old version would diagnose "OMI" even if it was a reperfused OMI.  The fact that she states "STEMI-Equivalent" here means that she does not think it is reperfused, but she does not  know that the patient is pain free now.

And here is explainability:

Will Smoot: "Initial ECG upon arrival, high concern for OMI."   (Will ran the ECG through Queen of Hearts and received the "OMI" result.)

Bedside cardiac ultrasound (Will is an ultrasound fellowship trained EP) did not demonstrate severe LV systolic dysfunction, acute valvular abnormality, severe RV dilation, or pericardial effusion. 

Initial high sensitivity Troponin I:  36.5 (ng/L) -- slightly elevated.


Here is the repeat 12 Lead ECG approximately 20 minutes later (still pain free)

Now it shows definite reperfusion

More inferior T-wave inversion

Less STD in V2, V3.

Cleaned up:

 2 hr repeat troponin:  2820.4 ng/L (No further troponin obtained during hospitalization)

Will: "I discussed high suspicion for OMI with cardiology, and he recommended standard NSTEMI management and will plan to cath later that day.  Admitted to hospitalist service on heparin."  

Angiogram:

99% Circumflex occlusion (reperfused).  

TIMI flow is not specified, but presumably was adequate.

No peak troponin was measured.

TTE results:
Normal LV size.  LVEF 55-60%.  Mild hypokinesis of basal-mid inferolateral and inferior walls. 
Normal RV size and function. 

Learning Points:

1) Learn to recognize Subtle OMI

2) Before assuming an OMI is reperfused, verify it by obtaining more ECGs to see evolution of reperfusion.

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MY Comment, by KEN GRAUER, MD (11/19/2024):

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Today's initial ECG provides yet another example of a tracing with a "Quick" Answer — as well as a slower, more complete Answer.

• The "Quick" Answer — addresses how to approach this case assuming you are working in a busy ED (Emergency Department) in which 3 patients present at the same time with new CP (Chest Pain) — and YOU have just seconds to decide if the initial ECG does (or does not) represent acute OMI until proven otherwise?
• The slower more complete Answer — addresses one of the primary goals of Dr. Smith's ECG Blog, namely time-efficient assessment of KEY findings for the tracing in front of us, including more subtle changes that may be relevant to the case.

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First — the "Quick" Answer:

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For clarity in Figure-1 — I've reproduced those findings in the initial ECG that "jumped out to me", allowing me literally to know within 5 seconds that regardless of what follow-up ECGs and serial Troponins might show — this patient needs prompt cath!

• The History in today's case is very concerning! = a 72yo man awakened from sleep by severe CP radiating to his left arm and shoulder. This history immediately places this patient in a higher-risk category for having an acute cardiac event (ie, meaning we need to rule out an acute event, rather than the other way around). Therefore, even subtle ECG abnormalities need to be assumed acute until proven otherwise.
• PEARL #1: Given this history — my "eye" jumped to the ST-T waves in leads V2 and V3 (within the RED rectangle in Figure-1). As we often emphasize in Dr. Smith's ECG Blog — in a patient with new CP, the finding of ST depression maximal in leads V2, V3 and/or V4 = acute posterior OMI until proven otherwise.
• Knowing that additional support may be needed to convince a skeptical interventionist — my "eye" next jumped to the 2 leads within the light BLUE rectangles (ie, to inferior leads III and aVF). Each of these leads shows subtle-but-real ST segment coving with slight elevation.
• PEARL #2: The BEST way to confirm that potentially acute ST-T wave findings in lead III are "real" — is to engage the "magical" reciprocal ST-T wave relationship between lead III and lead aVL (which works because lead aVL lies almost directly opposite to lead III in the frontal axis plane). So my "eye" next jumped to lead aVL (within the PURPLE rectangle in Figure-1) — where I immediately saw reciprocal ST depression with terminal T wave positivity — thereby confirming probable acuity for the subtle inferior lead ST elevation.

My Impression (on seeing ECG #1 and learning the history): 

• Acute infero-postero OMI — until proven otherwise.
• Total time that I needed to appreciate the above KEY findings that appear within the colored rectangles in Figure-1 — literally less than 5 seconds.
• For any provider who might still be uncertain about their "quick" Answer interpretation of Figure-1 — Use of the QOH application would confirm your impression of acute OMI in need of prompt cath (as shown by the QOH interpretation, discussed above by Dr. Smith).
• BUT — simple appreciation of the importance of the clinical history and the 2 concepts reviewed in Pearl #1 and Pearl #2 (stated above) — allows you to confidently diagnose acute OMI with need for prompt cath either with (or without) assistance from QOH application.

Figure-1: The initial ECG in today's case. I've labeled KEY findings that give us the "Quick" Answer. (To improve visualization — I've digitized the original ECG using PMcardio).

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Now — the Slower, More Complete Answer:

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I've labeled today's initial ECG more completely in Figure-2 — to include additional more subtle but relevant ECG findings.

• ST depression in lead V2 and lead V3 is not only deeper than in other chest leads — but the ST segments in these 2 leads are downsloping with terminal T wave positivity. This supports acute posterior OMI until proven otherwise.
• That said — the ST segment is straightened in the remaining chest leads ( = leads V4,V5,V6).
• ST segment straightening is also seen in lead I — and in lead II. 
• PEARL #3: While concern in today's case is greatest for ST-T wave changes suggestive of acute infero-postero OMI — ST segment straightening and/or depression is seen in no less than 8/12 leads (ie, in leads I,II,aVL; V2-thru-V6). The fact that this diffuse distribution of ST flattening/depression occurs in association with ST elevation in leads III,aVF and in lead aVR — suggests that this patient probably has underlying multi-vessel disease in addition to whatever acute abnormality may be ongoing (with features and clinical implications similar to Diffuse Subendocardial Ischemia and/or Aslanger Pattern).

The above leaves us with assessment of the ECG appearance of the QRST complex in lead V1. Potential clinically relevant implications of the lead V1 QRST appearance include the following:

• The rSr' morphology in lead V1 — is consistent with IRBBB (Incomplete Right Bundle Branch Block), given narrow terminal S waves in left-sided leads I and V6 — and QRS width that falls shy of 0.11 second.
• While possible that this rSr' morphology in lead V1 that we do not see in lead V2, is the result of too-high lead placement of the V1 chest electrode (which does show a negative P wave not seen in lead V2) — I interpreted this rSr' complex in lead V1 as most consistent with IRBBB given the lateral lead terminal S waves.
• Finally — Isn't the ST segment in lead V1 coved and slightly elevated? While difficult to appreciate because of small QRS amplitude in V1 — the BLUE arrow in this lead highlights a different ST-T wave appearance than the expected ST segment depression that should generally be seen in lead V1 with IRBBB.
• Confirmation that the ST segment in lead V1 is truly elevated and abnormal is forthcoming from: i) Comparison with the ST segment in neighboring lead V2 that is unmistakably depressed; — and, ii) The luxury we have of not just 2 beats — but 11 beats (ie, "looks") at the ST-T wave in the long lead V1 rhythm strip — all-11-of-which show similar ST segment coving with slight-but-real ST elevation (BLUE arrows in the long lead V1).

PEARL #4: What is the clinical relevance of this ST appearance in lead V1? In answer to this question — 2 considerations came to mind:

• In the setting of acute infero-postero OMI that we have in today's case — the ST elevation in lead V1 but not in neighboring leads V2,V3 — could reflect acute RV involvement. If this were true — this would localize the "culprit" artery to the proximal RCA, because the LCx does not supply the right ventricle.
• Alternatively — the ST coving and elevation that we see in lead V1 — in association with ST depression in 8/12 leads + ST elevation in leads III,aVR,aVF and V1 (with the most ST elevation being in lead aVR) — could simply be a reflection of DSI (Diffuse Subendocardial Ischemia) from altered collateral patterns and significant underlying multi-vessel coronary disease in addition to acute infero-postero OMI.

BOTTOM Line: It is disappointing that the consulting cardiologist in today's case delayed prompt cath because he/she misinterpreted the initial ECG as indicative of a "NSTEMI".

• Cardiac cath ultimately confirmed inf.-post OMI with significant multi-vessel coronary disease. 

Figure-2: The initial ECG showing the more complete Answer.