An ECG with only «marginal» change

This is by Magnus Nossen, from Norway

The patient is a 70 something male with a hx of hypertension and tobacco use disorder. He is otherwise healthy. The patient contacted EMS after a few hours of chest pain that started 5:30 AM. The pain was described as 6/10 radiating to the right shoulder. Vital signs were within normal limits, and the patient was not ill appearing. The chest pain was described as both sharp and pressure like. The ECG below was recorded and  electronically transferred to our PCI center for evaluation. 

What is your interpretation? Would you be worried? Be aware of the lead layout. Limb leads are presented in the Cabrera format. On the left 50mm/s (standard in Norway) On the right the image width has been reduced by 50%, effectively converting the image to 25mm/s.

ECG #1 

I think many providers might be reassured viewing this ECG. It does not meet conventional criteria for emergent cath lab activation. There is slight baseline wander on this ECG which does make the interpretation more challenging. There is however appreciable ST depression in leads II, III and aVF. There is slight but definite ST elevation with an inverted T wave in lead aVL. The findings are concerning for high lateral OMI, but without a prior ECG for comparison it is difficult to be certain. The patient was accepted for emergent evaluation in the cath lab based on the ECG and present complaint. 

Smith: I think this is diagnostic of high lateral OMI, though with reperfusion (aVL has very subtle STE, with Q-wave and inverted T-wave; reciprocal STD in inferior leads PLUS ischemic STD in V5, 6.  I am surprised that the Queen did not see it:

She usually sees these, but we have taught her mostly in a 3 x 4 format with 25 mm/sec. Supposedly, it should make no difference.  

Below is the second recorded ECG for this patient (ECG #2) — with the QoH interpretation below it. This ECG was recorded roughly 3 minutes after the first ECG. 

ECG #2

There are very slight dynamic ST-T changes when comparing with ECG #1. Most notably the ST depression in the inferior leads is slightly more upsloping. In other words, the inferior ST segments in the first ECG show more straightening which is more concerning for ischemia. The QoH interpretation however was the same for both ECGs.

QoH interpretation of ECG #2

Generally when patients are accepted for emergent evaluation in the cath lab, the EMS service keeps the patient connected to the twelve lead ECG during transport. The ECG is live fed to our institution. This is extremely helpful, as dynamic changes can be assessed continuously.

15 minutes after the decision to activate the cath lab and during transport to the PCI center ECG #3 was recorded. 

ECG #3 (Repeat ECG, done 15 minutes after the initial ECG)

Do you see any change? How would you interpret the ECG now?

The ECG above shows more obvious OMI findings. This is perhaps not easily appreciated unless you are trained in recognizing subtle ischemic changes. There is increasing ST elevation in lead aVL with more pronounced ST depression inferiorly. There also is slight straightening of the ST segment and slight ST elevation in lead I compared with the first ECGs. These changes confirm ongoing OMI with certainty. The changes also illustrate well the value of serial ECGs or continuous ECG monitoring in high risk patients. 

The QoH now recognizes the OMI with mid confidence. 

In the cath lab the patient was found to have a 100% occlusion of a small 1st marginal branch of the LCx. The culprit lesion was opened and stented. Initial high sensitivity Troponin T was 810ng/L, later peaking at 2333ng/L. 

Below is the post-PCI electrocardiogram.  

Post-PCI ECG

The ST elevation in lead aVL has disappeared. The T wave inversion in aVL is more pronounced. There are large T waves in the inferior leads. In this context, patient pain free — post-PCI and with the previous ECGs in mind— the large inferior T waves represent reciprocal change from lateral reperfusion T waves and are not hyperacute T waves of ischemia.

The videos files below show the occlusion and the flow following wiring of the culprit artery. 

DISCUSSION: This case nicely illustrates how subtle OMI changes really can be. The Queen of Hearts AI model did not identify OMI in the initial ECG. Below is the QoH explainability for the limb leads of the ECG #2 (left part of the image) and limb leads of ECG #3 (right side of the image). The sets of six limb leads are put next to each other for comparison. I've excluded the precordial leads as they didn't add much information in this case. 

You can look at each leads and compare the two ECGs. You then can appreciate the dynamic change and see what parts of the waveform the QoH identifies as ischemic findings. The AI model does find lead III and aVL somewhat suspicious on ECG #2, but not enough to give a diagnosis of OMI. The ST-T changes in the limb leads on the repeat ECG (#3) results in a correct diagnosis of OMI. 

Learning Points:  

• Serial ECG are very valuable when it comes to identifying a dynamic process such as ACS.
• This patient’s OMI was identified early due to expert ECG interpretation. Eventually with more training the QoH will outperform any human in the detection of acute coronary occlusion. 
• Incorporating the QoH interpretation into real time 12-lead ECG in high risk patients could greatly improve early diagnosis when it comes to OMI detection.

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MY Comment, by KEN GRAUER, MD (12/16/2023):

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Our THANKS to Dr. Magnus Nossen (from Fredrikstad, Norway) — who periodically contributes to Dr. Smith's ECG Blog with his impressive array of fascinating cases.

• In addition to educational insights — Dr. Nossen's contributions periodically serve as a source for review of the Cabrera Format, recorded at 50 mm/second — as is the customary ECG recording format in his country. 

Today's case illustrates a cath-proven OMI that might be all-too-easy to overlook because: i) ECG changes on the initial tracing are subtle, and do not satisfy STEMI critieria; ii) The initial ECG was recorded using the Cabrera format, which many clinical providers are not familiar with (especially when 50 mm/sec. recording speed is used) — and — iii) The modest ST elevation that is present in today's initial tracing, is only seen in a single lead ( = lead aVL).

• For those in search of brief review of the Cabrera Format for ECG recording — Please check out My Comment at the bottom of the page in the October 26, 2020 post in Dr. Smith's ECG Blog.
• As I periodically “confess” whenever I am presented with an ECG recorded at 50 mm/second — I routinely reduce the width of the ECG before me prior to beginning my interpretation. This is because my brain is “programmed” to interpreting 12-lead ECGs and rhythm strips at the 25 mm/sec. speed that is standard in the United States. After 4+ decades of interpreting tens of thousands of tracings — there is an instant (automatic) process of "pattern recognition" that immediately occurs in my brain, even before I initiate systematic assessment of any given tracing. This process is invalidated by the unfamiliar presence of different-sized complexes that result when a 50 mm/second recording speed is used.
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• NOTE: Certain countries (such as Germany) frequently use a 50 mm/sec. recording speed, even when not using the Cabrera format. Usually it will be obvious on sight when a 50 mm/sec. speed is used — but sometimes it won’t be. This is especially true when assessing narrow QRS rhythms for heart rate (ie, a narrow QRS rhythm may appear widened and excessively slow if you fail to recognize a 50 mm/second recording speed). Therefore — it’s important to always be aware of the recording speed (and to BE SURE to clarify IF the tracing you are interpreting is from a foreign country — especially if the recording speed isn’t marked at the bottom of the ECG). 

The 3 ECG Formats in Figure-1:

To facilitate appreciation of the KEY concepts in today's case — I thought it would be helpful to show the 3 ways I chose to illustrate today's initial ECG in Figure-1.

• In the upper left of Figure-1 (light BLUE border) — is the original ECG viewed by Dr. Nossen (ie, in Cabrera Format — recorded at 50 mm/sec. speed). As I indicate in my introduction above — I fully acknowledge my insecurity in interpreting a 12-lead ECG recorded at 50 mm/second speed — which is why I immediately reduced width of this tracing by 50% (upper right tracing in Figure-1 — with the RED border).
• Both of these upper tracings in Figure-1 are recorded in Cabrera format — which as per My Comment at the bottom of the page in the October 26, 2020 post — entails inversion of lead aVR (to negative aVR = -aVR) — with a more logical sequential display of frontal plane leads, beginning with lead aVL (at -30 degrees) — and extending by equally spaced 30 degree intervals until arriving at the most distant right-sided lead ( = lead III at +120 degrees).
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• For readers preferring a format they are most familiar with — I converted today's initial ECG into the 12-lead orientation most commonly used in the U.S., including width reduction by 50% to expedite visual recognition (lower tracing in Figure-1 — with the GREEN border).

Figure-1: I've reproduced the initial ECG in today's case in 3 different formats: i) In the original Cabrera Format (recorded at 50 mm/sec.); — ii) Cabrera Format, but with the width reduced by 50%; — and, iii) Converted to standard USA 12-lead format (with width reduced by 50%).

WHY is Today's Case Challenging?

Regardless of which of the formats in Figure-1 you favor — assessment of today's initial ECG presents a challenge. That said, in a 70s man with risk factors (hypertension; smoking) who is awakened by new CP (Chest Pain) — ECG #1 should be interpreted as suggestive of acute OMI until proven otherwise.

• Lead aVL is the "highest" of the high-lateral leads (corresponding to a -30 degree vantage point in the frontal plane — compared to a 0 degree location for lead I). As per Dr. Nossen — although slight, there is even if not elevation — an abnormal coving of the ST segment in lead aVL, that terminates in frank T wave inversion. Considering small amplitude of the R wave in this lead — the Q wave in aVL is abnormally wide.
• Support that the abnormal appearance of lead aVL is a "real" finding — is forthcoming from unmistakeable straightening (if not slight depression) of the ST segments in each of the inferior leads ( = leads II,III,aVF) — with that "magical" mirror-image opposite picture of the ST-T waves in lead aVL vs lead III that is so characteristic of either inferior OMI (if there is ST elevation in lead III) — or of high-lateral OMI (if there is ST elevation in aVL, as there is in today's case). 
• (For more on this mirror-image opposite ST-T wave relation in leads III vs aVL — See My Comment in the March 8, 2019 and August 9, 2018 posts in Dr. Smith's ECG Blog).
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• COMMENT: It is relatively uncommon for there to be ST elevation in only lead aVL — without there being at least some ST elevation in other lateral leads (ie, in leads I, V5 and/or V6). In addition — acute high-lateral OMI is most commonly accompanied by suggestion of posterior involvement — yet there is no ST depression in either lead V2 or V3. There is slight ST depression in lateral chest leads V4,V5,V6 — but I thought this to be nonspecific.
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• BOTTOM Line: As per Dr. Nossen — ECG findings in today's initial tracing are subtle. That said — in this older man with risk factors and new CP, ST-T wave changes in leads aVL and in the inferior leads suffice to suggest acute OMI until proven otherwise. Isolation of ST elevation to only lead aVL is consistent with acute occlusion of a marginal branch in the LCx, which is precisely what was found on cardiac catheterization.