85 year old with chest pain, STEMI negative, then normal troponin but with relatively large delta: discharge?

Written by Jesse McLaren, with comments from Smith

 

An 85 year old with a history of CAD presented with 3 hours of chest pain that feels like heartburn but that radiates to the left arm. Below is the ECG. What do you think?

There’s sinus bradycardia, first degree AV block, normal axis, delayed R wave progression, and normal voltages. There’s minimal concave ST elevation in III which does not meet STEMI criteria, so this ECG is "STEMI negative". But there are multiple other abnormalities that when combined are diagnostic of OMI and predictive of RCA occlusion:

1. sinus bradycardia, which is common in RCA occlusion
2. inferior hyperacute T waves (broad based, symmetric, tall relative to the QRS)
3. reciprocal ST depression and T wave inversion in aVL (and I), which is highly specific for inferior OMI
4. primary anterior ST depression, which is posterior OMI until proven otherwise
   

 

Here's the interpretation of the PMcardio AI trained in identifying OMI:

 

Below is the old ECG, showing the first degree AV block, delayed R wave progression and some of the precordial ST depression is old especially in the lateral leads. But the bradycardia and the infero-posterior OMI is definitely new: 

 

 Smith: this also has many abnormalities suggestive of ischemia: many leads have ischemic appearing ST depression

 

The emergency provider followed the sequential steps of the current paradigm:

1.     Use STEMI criteria to identify acute coronary occlusion: the ECG was STEMI negative

2.     Use troponin to rule out non-STEMI: two high sensitivity troponin I performed two hours apart were 4 and 16 ng/L, both in the normal range (upper limit of normal 16 in females and 26 in males).  The assay was Abbott Alinity, which is very similar to Abbott Architect high sensitivity troponin I.  See analysis below.

3.     Arrange follow up for chest pain patients who are “STEMI negative” with “normal troponin”: the patient was referred to outpatient cardiology

 

But 6 hours later the patient returned with recurrent chest pain: 

 

 

Again diagnostic of infero-posterior OMI, though this time it does STEMI criteria, albeit barely.  The cath lab was activated.

 

A repeat ECG was done on way to cath lab:

 

 

"STEMI negative" again. Hyperacute T waves are deflating, suggesting reperfusion but there is still reciprocal change in I/aVL and ST depression in V2, and the bradycardia is worse. On angiogram there was a 90% RCA occlusion. Troponin rose from 600 to 17,000 ng/L.

 

Discharge ECG showed resolution of bradycardia, inferior reperfusion T wave inversion, and baseline precordial ST depression.

 

 

Take home

1.     As the new ACC consensus states (citing the work of Smith/Meyers), "The application of STEMI ECG criteria on a standard 12-lead ECG alone will miss a significant minority of patients who have acute coronary occlusion. Therefore, the ECG should be closely examined for subtle changes that may represent initial ECG signs of vessel occlusion, such as hyperacute T waves...or ST-segment elevation <1 mm, particularly when combined with reciprocal ST-segment depression, as this may represent abnormal coronary blood flow and/or vessel occlusion."

2.     Using troponin for acute coronary occlusion is like relying on a rear-view mirror to navigate a car pile-up: it shows wreckage behind you that has already happened, but can’t see the road ahead and can give false reassurance when there's a head-on collision happening in real time. It’s common for acute coronary occlusion to present with troponin in the normal range, and the initial rise can’t predict the final damage. Even if the troponin on the first visit had been higher there still would have been delayed reperfusion because it would have been diagnosed as "non-STEMI"

3.     Using risk stratification tools like HEARTS or EDACS may have avoided the initial discharge, but shouldn’t be used if the ECG is already diagnostic of OMI. (See this other post: Chest pain, a ‘normal ECG’ a ‘normal trop’, and low HEART and EDACS score: discharge home? Stress test? Many errors here.) There’s also a hazard of relying on troponins that are in the normal range but above the level of detection. As this study from Dr. Smith concluded: “measurable hs-cTnI concentrations less than or equal to sex-specific URLs have important prognostic implications. Our findings underscore the importance of recognizing cTn as a continuous variable, with the higher the cTn, the higher the probability of MACE. We caution against the clinical use of the terms normal or negative among such patients.” (Clinical features and outcomes of emergency department patients with high-sensitivity cardiac Troponin I concentrations within sex-specific reference intervals.)

Smith comments on troponin:

I've done a lot of research on high sensitivity troponin, with colleagues including Fred Apple and Yader Sandoval.  We have published over 30 articles, most on high sensitivity troponin, mostly on Abbott Architect high sensitivity troponin I.  We have found that, to rule out myocardial infarction (and we mostly only studied Non-OMI), the 2-3 hour delta should be less than 3 ng/L.  This conforms with lots of other research done by the HIGH-STEACS group in Scotland and others.   In this case, the delta was 12 ng/L. 

A delta of 12 ng/L is highly likely to indicate acute MI, even if the value is below the 99th percentile.  How is that possible?  Because the 3rd or 4th troponin is highly likely to be ABOVE the 99th percentile if the 3 hour value has risen from 4 to 16 ng/L.

See this graphic from one of our papers:

The PPV is particularly low relative to the specificity because this was a very low risk population.  In a high risk situation, the PPV would be very high. 

Notice that these deltas are REGARDLESS of the initial value.  But if the initial value is very low, as in this case, a delta of 12 early in the course of chest pain is even more significant.

Conclusion:

This patient should NEVER have been ruled out by troponin.

And the ECG findings, which are diagnostic of OMI, were also missed.

Thus, this is the protocol Fred Apple and I developed for Hennepin for the Abbott Architect:

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My Comment by KEN GRAUER, MD (3/24/2023):

==================================

I like this case by Dr. McLaren — because it allows us to highlight a very important fault of the outdated STEMI paradigm that is all-too-often forgotten — namely, Being sure to obtain and clinically correlate at least 2 serial ECGs before you send the patient home! (with "clinical correlation" meaning lead-by-lead comparison of these serial ECGs — keeping in mind the presence and relative severity of CP at the time each ECG was obtained). 

• For ease of comparison in Figure-1 — I’ve reproduced the first 3 ECGs that were done in today’s case.

In reviewing events transpired in today's case — Obtaining a 2nd ECG and clinical correlation of symptom severity with each ECG that is recorded before discharging the patient was clearly not done on this patient's 1st visit to the ED (Emergency Department). I say this because:

• Considering that today's patient presented with new CP (Chest Pain) — the initial ECG is already diagnostic of an acute event until proven otherwise.
• As noted by Dr. McLaren, compared to the prior tracing — there are a number of new ST-T wave changes in ECG #1.
• There is no notation of whether CP was still present at the time ECG #1 was obtained (and if so, whether CP was increasing, remaining constant, or decreasing). Without this information — it is impossible to understand if the acute-looking ST-T wave changes in ECG #1 might indicate ongoing acute occlusion vs spontaneous reperfusion vs spontaneous reocclusion.
• 
  
• In addition to the above missteps — the Troponin Delta (ie, the increase in Troponin from 4-to-16 ng/L) that was interpreted as “negative” — is not a "normal" result (as discussed in detail by Dr. Smith). Therefore, even without the acute ECG changes seen in this case — full evaluation of this patient would be needed.

Challenging Aspects of Today's CASE:

Perhaps the most challenging aspect of today's case — is knowing HOW to interpret the initial ECG in light of obvious ECG abnormalities in the prior tracing. Addressing this issue raises the question of how to optimally compare serial tracings.

Regarding Comparison of Serial ECGs:

• I favor picking one of the 2 tracings that you are comparing — and systematically interpreting that tracing in its entirety before you look at the 2nd tracing.
• When comparing a current tracing with a prior ECG — we ideally should know the circumstances under which the prior tracing was done (ie, Was the patient stable and without symptoms? — or — Was the prior tracing obtained during chest pain or soon after an infarction?). Unfortunately — We do not know the circumstances under which the prior tracing in today's case was recorded.
• Are ECG parameters in the 2 tracings you are comparing similar? (ie, Is there a change in the frontal plane axis? Is R wave progression similar? Is the heart rate and rhythm in the 2 tracings the same?). Significant change in any of these parameters may result in ST-T wave changes that are not the result of ischemia or infarction.

Comparison of the 3 Tracings in Figure-1:

The first ECG we were shown in today's case is ECG #1:

• As per Dr. McLaren — there is marked sinus bradycardia and arrhythmia (ie, heart rate in the 40s) — with 1st-degree AV block (PR interval ~0.23 second).
• Regarding other intervals — the QRS is narrow — and the QTc is probably normal given the slow rate. The frontal plane axis is normal (about +70 degrees). There is no chamber enlargement.

Regarding Q-R-S-T Changes: There are artifactual undulations in the baseline of ECG #1 — but this does not prevent interpretation of this tracing. 

• There are no significant Q waves (ie, The QS in lead V1 is not abnormal per se). A tiny-but-present initial r wave is seen in lead V2 — with this R wave progressively increasing across the precordium. Transition (where the R wave becomes taller than the S wave is deep) — is slightly delayed (to between leads V3-to-V5).
• ST segments are straightened in multiple leads. In the inferior leads, this is associated with slight J-point ST elevation and clearly hyperacute T waves (that are disproportionately tall, "fat" at their peak — and wider than expected at their base).
• Reciprocal changes (ie, a mirror-image opposite ST-T wave picture) — are seen in lead aVL, and to a lesser extent in lead I. Considering how tiny QRS amplitude is in these high-lateral leads — these have to be considered acute changes until proven otherwise!
• 
  
• In the Chest Leads — ST-T wave changes are equally concerning. There is ST segment coving with T wave inversion in leads V1,V2. We see a distinct straightening with downsloping of the ST segment in leads V3-thru-V6. This is followed by terminal T wave positivity in these leads — with T waves in leads V3,V4,V5 being clearly "hypervoluminous" ("fatter"-at-their-peak and wider-at-their-base than they should be — as well as disproportionately tall in leads V3,V4 considering R wave amplitude in these leads).
• 
  
• IMPRESSION of ECG #1: As per Dr. McLaren — Especially in view of the marked bradycardia, the above ECG findings are diagnostic of acute infero-postero OMI until proven otherwise! The ST segment coving in leads V1,V2 suggests possible acute RV involvement — with acute occlusion of the RCA as the presumed "culprit" artery. Given the history of new chest pain — prompt cath is clearly indicated on the basis of this initial ECG.

Comparison of ECG #1 with the Prior Tracing:

As alluded to earlier — ECG #2 is not a normal tracing. Instead — there is ST segment straightening in multiple leads, sometimes with slight ST depression. T waves look disproportionately large in a number of leads (potentially hyperacute IF the patient was having new chest pain at this time). There is ST segment coving with shallow T wave inversion in lead aVL.

• Several differences in ECG parameters make comparison of ECG #1 with ECG #2 challenging. These include: i) The much faster heart rate in the prior tracing; and, ii) Little change in the frontal plane axis — but clearly increased QRS amplitude in the prior tracing.

Looking first at the Limb Leads: 

• Although straightening of ST segments is not a new finding in ECG #1 — there should be no doubt that the subtle ST elevation in leads III and aVF is real — since if anything, there was slight ST depression in these leads on the prior tracing. Similarly, the hyperacute T wave appearance in these inferior leads is markedly increased in ECG #1.
• Reciprocal ST-T wave depression with T wave inversion is similarly markedly accentuated in leads I and aVL of ECG #1.

In the Chest Leads:

• Although ST segment straightening with prominent T waves was present in the prior tracing — lead-by-lead comparison suggests that the T waves in leads V3-thru-V6 in ECG #1 are relatively taller (considering QRS amplitude in each respective lead) — and definitely "fatter"-at-their-peak and wider-at-their-base (ie, more hyperacute) than they were in the prior tracing.
• 
  
• IMPRESSION: In this 85-year old patient with new chest pain — comparison of the prior tracing with ECG #1 should remove all doubt about the acuity of ECG changes on this initial tracing. Prompt cath is clearly indicated — especially in view of the worrisome bradycardia in ECG #1. The patient should not have been sent home.

The Repeat ECG:

As per Dr. McLaren — the patient was unfortunately discharged from the ED — but returned 6 hours later with a recurrence of chest pain. Millimeter-based STEMI criteria are finally attained.

• Comparison of ECG #3 with the initial ECG done 6 hours earlier — and with the "baseline" (prior) tracing, provides insight into the sequence of ECG changes correlated to patient symptoms.
• There is now definite ST elevation in all 3 inferior leads in ECG #3 — in association with T-QRS-D (Terminal-QRS-Distortion — as the S wave in leads III and aVF has been lifted from the baseline) + an even greater increase in relative size of the hyperacute inferior T waves (The T waves in leads III and aVF now tower over the R waves in these leads — whereas they were approximately the same height as the R waves in ECG #1).
• Reciprocal ST-T wave depression/T wave inversion in high-lateral leads I and aVL has increased a comparable amount to the inferior lead ST elevation.
• 
  
• In contrast — ST-T wave changes look less prominent in ECG #3 than they were on the initial tracing. The evolution of sequential ECG changes during an acute ongoing event is not always homogeneous.

Figure-1: Comparison between the initial ECG in today's case — with a prior tracing — and with the repeat ECG (done 6 hours after ECG #1).

Watch what happens when you teach others how to find OMI

 Submitted by Dr. Caio Aguiar from Brazil, written by Pendell Meyers

It is immensely rewarding to receive these emails, like I received from Dr. Aguiar last week:

"Last year I had a couple of lessons with you while on my internship.

I finished my residency of Emergency Medicine and I’m working at a great Emergency Department here in Brazil.

Since then, I started looking for OMI EKG findings and not just STEMI.

So, I'm a follower of your blog, and I think I have a interesting case that I attended yesterday."

Case

"Male, 43yo, come to ED with Epigastric Pain started 3 hours ago. Risk Factors: High Cholesterol. Vitals Signs: Normal."

Here is his initial ECG:

PM Cardio standardized version below:

What do you think?

Here we have enlarged it for easier viewing, with limb leads on the left and precordial leads on the right:

Dr. Aguiar diagnosed posterolateral OMI based on hyperacute T waves and slight STE in aVL, with its reciprocal STD and reciprocal negative hyperacute T waves in II, III, aVF, as well as the STD proportionally maximal right on the border of V4/V5.

Here is PM Cardio's Queen of Hearts interpretation of the ECG. Confidently diagnoses OMI.

He contacted the interventional cardiologist who was not convinced and cancelled the cath lab, stating that he wanted to see the first troponin result.

Meyers note: In a case like this, when the cardiologist cannot see the posterior OMI, posterior leads may have shown STE, which might be more understandable for them. Remember: these findings above are included as STEMI equivalent findings in the 2022 ACC Expert Consensus Decision Pathway on ACS Patients in the ED.

The troponin I resulted at about 2-3 hours after arrival (I am not sure why it took this long), at 700 ng/L (upper reference limit 40 ng/L).

A repeat ECG at this time is below:

The repeat ECG shows more STE (but still not 1.0 mm in lead I, thus not STEMI criteria) and was finally understood by the cardiologist.

Angiogram soon after (around 4 hrs after presentation) showed multi vessel CAD, with culprit lesion total occlusion of the first obtuse marginal branch (OM1), which was stented.

No more troponins were obtained.

Unfortunately the echo was not available.

 

Here is his ECG several hours after reperfusion:

Resolving HATW/STE/STDmaxV1-V4, and new terminal T wave inversion in aVL, all suggesting effective reperfusion.

Learning Points:

To take optimal care of ACS patients, the initial providers who see the patient (hopefully assisted by AI soon) must be able to recognize subtle OMI findings. If only the cardiologist also had such training in this case, the 3-4 hour delay could have been avoided. If Dr. Aguiar hadn't seen it, the patient might have been labelled "NSTEMI" and forced to wait until the next day.

Speed and frequency of repeat ECGs and troponins can help distinguish some OMIs that are not yet understood.

Teaching is rewarding! Go teach some OMI findings.

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My Comment by KEN GRAUER, MD (3/21/2023):

==================================

Today's case provides one more example of an acute OMI not initially recognized by the On-Call interventionist. The OMI was immediately recognized by the emergency physician who was trained by Dr. Meyers

• Dr. Meyers' suggestion for when the interventionist does not initially recognize a posterior OMI because "there is not enough ST elevation" — is a good one: Do posterior leads.
• 
  
• To EMPHASIZE (as we have previously done in Dr. Smith's ECG Blog — as per My Comment at the bottom of the page in the September 21, 2022 post) — QRST amplitudes (and therefore the amount of ST-T wave elevation) in posterior leads is often modest at best — simply because posterior placement of leads V7,V8,V9 situates these leads in a position from which electrical activity must pass through the thick musculature of the back before being recorded on the ECG. That said — sometimes there will be ST elevation in posterior leads. This may be beneficial if it serves to convince an interventionist who otherwise was not going to cath the patient.

MY Suggestion:

It is difficult to understand why so many clinicians still have difficulty recognizing acute posterior OMI. As noted above — Even when there is posterior OMI, the amount of ST elevation that is seen in posterior leads is most often modest.

• In contrast to posterior leads — the amplitude of ST-T wave deviations that is seen in anterior chest leads is not attenuated by the thick musculature of the back before being recorded on the ECG. As a result — the mirror-image of anterior chest leads provides a more readily visible picture of ongoing ST-T wave deviations in the posterior wall of the left ventricle.
• 
  
• I've called application of this principle the "Mirror Test". This is simply a visual aid that I've used for decades to facilitate recognition of acute posterior OMI. (I've added LINKS to a series of other cases in this September 21, 2022 post that illustrate the utility of the Mirror Test). 
• 
  
• As Drs. Smith and Meyers have emphasized on many occasions — ST depression that is maximal between leads V2-to-V4 in a patient with new chest pain should be assumed to be posterior OMI until proven otherwise. The shape of this ST-T wave depression indicative of posterior OMI is often quite distinctive — in that its mirror-image "looks like" an acute STEMI.

Application to Today's CASE:

The patient in today's case is a 43-year old man who presented to the ED with new symptoms (ie, Not chest pain — but epigastric pain, that can be a mimic at times for an acute cardiac event).

• For clarity in Figure-1 — I've reproduced the initial ECG in today's case, together with the mirror-image of the chest leads to the right in this Figure.

Dr. Meyers has drawn attention to the abnormal limb lead findings in ECG #1. These include: i) Hyperacute T waves with slight ST elevation in lead aVL; and, ii) Equally acute-looking reciprocal ST-T wave depression in each of the inferior leads.

I wanted to focus on Chest Lead findings:

• Normally, there is gentle upsloping and slight ST elevation in leads V2,V3. Instead — the ST segment is abnormally straightened, with no more than tiny T waves in these leads. Note the distinct shelf-like ST segment in lead V2.
• ST depression begins in lead V4 — and is maximal in leads V5 and V6.
• 
  
• Because of marked overlap of the QRS in multiple leads — I've outlined in RED the QRS complex in leads V4 and V5.
• 
  
• LOOK at the mirror-image picture of the chest leads ( = ECG #1a, to the right of the initial ECG in Figure-1). Doesn't the mirror-image of the ST-T waves in leads V4,V5 look like an acute MI?

COMMENTS:

• Limb lead findings in ECG #1 are strongly suggestive of acute high-lateral OMI.
• Typically with isolated posterior OMI — ST depression will be maximal between leads V2-to-V4. This is not quite what we see in ECG #1. Instead — we see abnormal ST-T waves beginning with the ST-T wave flattening that begins in leads V2,V3 — with a positive Mirror Test in lead V4.
• Significant ST depression extends out to leads V5,V6. Of note — there is also ST elevation in lead aVR.
• 
  
• IMPRESSION: I thought ECG #1 conveyed a "mixed" picture. The very acute-looking ST-T waves in the limb leads strongly suggests high-lateral OMI. The abnormally straightened ST segments in leads V2,V3 (shelf-like straightening in V2) — with positive Mirror Test in lead V4 suggests posterior OMI — which together with the hyperacute and elevated ST segment in lead aVL, is consistent with acute occlusion of a branch of the LCx. But ST depression is present in multiple leads, with ST elevation in lead aVR — a picture consistent with diffuse subendocardial ischemia from multi-vessel disease. (Alas, this is precisely what cardiac cath showed = multi-vessel disease with a "culprit" vessel in the 1st Obtuse Marginal branch of the LCx).

Figure-1: The initial ECG in today's case — with the mirror-image view of the chest leads to the right. (To improve visualization — I've digitized the original ECG using PMcardio).

A 50-Something Male with 2 hours of Chest discomfort

This ECG was texted to me in real time, but I did not notice the message until about an hour after it came. 

"50 + yo. Concerning history, known CAD"

Recorded 2 hours after pain onset:

What do you think?

This was my response:

"This looks like a worrisome EKG. It looks like an Occlusion MI (OMI), but I am not 100% certain. But by now you must have a repeat ECG.  Can I see it?"

Pendell Meyers had an identical response when I sent it to him.

PM Cardio AI algorithm said "OMI with high confidence"

Explanation: There is subtle ST Elevation in inferior leads, with a hyperacute T-wave in III, reciprocal STD in aVL with an inverted T-wave in aVL, as well as an inverted T-wave in V2, and up-sloping ST segments in V5,6 with a biphasic (up-down) T-wave.

The first hs troponin I was barely detectable at 4 ng/L.

He sent me an old one from 2 years prior:

The STE is now known to be new.  

This makes the first one diagnostic.

There is some LVH vs. Benign T-wave inversion in V3-V6.

A repeat ECG was recorded 80 minutes after the first, at 200 minutes after pain onset:

There are dynamic changes.  Confirms that the first one is diagnostic.

The cath lab was activated.  The interventionalist asked for another troponin, which shortly returned at 66 ng/L.

Another ECG was recorded while waiting for the cath team (it was nighttime). This was at 140 minutes after presentation, or 260 minutes after pain onset:

Similar to the 80 minutes ECG.

Angiogram:

Culprit for the patient's inferior ECG changes and non-ST elevation myocardial infarction is a 100% acute thrombotic occlusion of the proximal RCA.

It was opened and stented.

Formal bubble contrast echo:

The estimated left ventricular ejection fraction 57%.

Regional wall motion abnormality-inferolateral.

Regional wall motion abnormality-inferior.

No further troponins were measured.

Here is a next AM ECG:

Now there are new inferior Q-waves.  

There is deeper T-wave inversion in V3-V6 than on the baseline ECG above.

The patient was diagnosed with a"Non-STEMI."

To me, that is a meaningless diagnosis.  

Here is the main learning point:

The infarct was due to an occluded artery (Occlusion MI, OMI).  In 30% of OMI, there is no significant ST Elevation.  They should be called Occlusion MI.

Traditionally, Occlusion MI (OMI) myocardial infarctions that are not STEMI are called NonSTEMI.  They have large infarcts and high mortality.

Likewise, Non-Occlusion MI (Non-OMI, or NOMI) (artery is not occluded) myocardial infarctions are given the same name (Non-STEMI) even though they are qualitatively different: they have small infarct size and FAR lower mortality that NonSTEMI-OMI.  

Calling BOTH of these very different pathologies by the same name ("Non-STEMI") simply because of one very inaccurate ECG characteristic (presence of absence of ST elevation) obscures the reality of the underlying pathology and its danger.

Call these what they are:  Occlusion MI!

Other Learning Points:

1. Learn to recognize subtle OMI

2. Door to opening is dependent upon recognition of these subtle findings.

3. The first troponin is not helpful to allay your concerns

4. The PM Cardio Bot (AI ECG OMI interpretation) is amazingly accurate and we hope it will be available to all soon.

5. RCA occlusion can (and often does) affect the lateral wall, manifesting in V5 and V6.  

6. In fact, when inferior OMI does manifest in V5,6, there is still always STD in aVL (in our study, this was true in 33/33 cases; this is because aVL is high lateral and V5,6 are more inferior)

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My Comment by KEN GRAUER, MD (3/19/2023):

==================================

Interesting case presented above by Dr. Smith — that emphasizes important points about the OMI Paradigm. I focus My Comment on some additional aspects of this approach.

• For ease of comparison in Figure-1 — I’ve reproduced the first 3 tracings in today’s case.

What Is It About the 1st ECG?

WHY was the initial ECG in today’s case immediately recognized by Drs. Smith and Meyers as “worrisome”? My thoughts on seeing this tracing  ( = ECG #1 in Figure-1) — were as follows:

• The “final diagnosis” in today’s case was a "Non-STEMI" — despite a cardiac cath that showed a proximal RCA occlusion. As per Dr. Smith — diagnosing today's case in that way indicates a misunderstanding of the pathophysiology involved. The reason the initial ECG is so concerning — is that it already suggests high likelihood of OMI ( = Occlusion-based MI) in this 50-ish year old man who presents with a 2-hour history of new chest pain.
• To realize — Assessment of ECG #1 is complicated by knowing: i) That today’s patient has a history of documented CAD; and, ii) The lack of a prior tracing for comparison at the time the initial ECG was interpreted. That said — the 1 lead in ECG #1 that has to be assumed acute until proven otherwise — is lead aVL (within the RED rectangle in ECG #1). Today’s patient is having new chest pain — the R wave in lead aVL is tiny, but it is preceded by a disproportionately deep Q wave (considering the small amplitude of the R in aVL) — the ST segment in lead aVL is coved, and the inverted T wave in this lead is clearly hypervoluminous (and disproportionate compared to the small size of the QRS in this lead).
• In support of our presumption that ST-T wave changes in lead aVL are acute in this patient with new chest pain — is the mirror-image opposite ST-T wave picture in lead III (ie, There is slight-but-real ST elevation — straightening of the ST segment takeoff — and a “fatter”-than-it-should-be hyperacute T wave in this lead).
• 
  
• To EMPHASIZE: ST-T wave abnormalities are also present in most other leads in ECG #1 — but they are clearly more subtle, and difficult to declare as “acute” in this patient with known coronary disease in the absence of a prior ECG for comparison.
• 
  
• Editorial Comment: As per Dr. Smith — It is encouraging to see that the PMcardio AI interpretation of ECG #1 was made with high confidence for the diagnosis of acute coronary occlusion (because the PMcardio AI program was able to recognize the hyperacute findings in leads III and aVL). This signals tremendous improvement in the ability of computerized programming using Artificial Intelligence to “learn” when properly “taught” (ie, programmed) — how to detect acute coronary occlusion at an early point in the process, even without ST elevation.

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

What We Learn from the Prior Tracing?

As per Dr. Smith — as soon as a prior ECG from today’s patient became available — the diagnosis of an acute (presumably ongoing) cardiac event was confirmed. 

• To EMPHASIZE: We are not told the circumstances under which ECG #2 was obtained. As a result — we do not know if ECG #2 represents a stable “baseline” tracing — or whether it might have been obtained during a period of ischemia in this patient with a history of known coronary disease. That said — we do know that ECG #2 was the last ECG on file prior to this patient’s presentation to the ED on the day of admission. As a result (as per Dr. Smith) — this confirms that the ST-T wave changes in the limb leads of ECG #1 are new since the last ECG was recorded.

Looking Closer at ECG #1 vs ECG #2:

Sinus rhythm is present in both ECG #1 and ECG #2, albeit the heart rate is slightly slower in ECG #1. It’s important to note that both the frontal plane axis, as well as the sequence of R wave progression and QRS amplitudes — are different in the 2 tracings. That said — I completely agree with Dr. Smith that compared to the prior tracing — acute changes are seen on ECG #1:

• The change in frontal plane axis between the 2 tracings should not be expected to result in the disproportionate, hypervoluminous T wave inversion that we see in lead aVL of ECG #1. It should also not result in the hyperacute-appearing upright T waves seen in leads III and aVF of ECG #1, that were so flattened in the prior tracing.

In the Chest Leads of ECG #2:

• Voltage criteria for LVH are satisfied in lead V6 (R wave in V6 ≥18mm). R wave amplitude is also unexpectedly tall in leads V4,V5. ST-T waves especially in lateral chest leads V4,V5,V6 — manifest the typical appearance of LV “strain” (ie, slight J-point ST depression — with asymmetric, slowly downsloping ST segment that terminates in a more rapid rise back to the baseline). [For more on "My Take" regarding the ECG diagnosis of LVH and "strain" — Please see My Comment at the bottom of the page in the June 20, 2020 post of Dr. Smith’s ECG Blog].
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• NOTE #1: While LVH does not generally result in the slight J-point depression, ST segment flattening, and down-up terminal T wave seen in lead V3 of ECG #2 — this could still be a longstanding finding from LVH in a patient with surprisingly tall R waves beginning in lead V3.
• NOTE #2: The ST segment coving with shallow but symmetric T wave inversion in leads V2-thru-V6 — does represent some ST elevation that has occurred in leads V3-thru-V6 of ECG #1, when one considers that there was slight-but-real ST depression on the prior tracing!
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• PEARL: New ST-T wave elevation or depression is often much harder to assess when a baseline tracing shows ST-T wave abnormalities from LVH with “strain” and/or in a patient with ECG abnormalities from preexisting coronary disease (and today’s patient had LVH and known coronary disease).

What Do We Learn from ECG #3?

As per Dr. Smith — the repeat ECG in today’s case ( = ECG #3 — done 80 minutes after ECG #1 when chest pain returned) — confirmed the diagnosis of acute coronary occlusion because of dynamic ST-T wave changes compared to ECG #1.

• Q waves are now present in each of the inferior leads in ECG #3. 
• The ST-T waves in leads III and aVF of ECG #3 — are now clearly more hyperacute than they were in ECG #1 (ie, there is now definite ST elevation — with T waves that are obviously much “fatter”-at-their-peak than they were in ECG #1 ).
• Support that these changes in leads III and aVF are real — is forthcoming from the equally dynamic change in the ST-T wave in lead aVL of ECG #3 (that now shows J-point ST depression — with a “fatter” T wave at its nadir).
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• NOTE #3: I thought ECG #3 localized the “culprit” artery to the proximal RCA because: i) ST-T wave elevation and hyperacuity were now pronounced in leads III and aVF — but lacking in lead II; — ii) Reciprocal ST-T wave changes were equally marked in lead aVL (more so than in lead I); — and, iii) There was now slight ST elevation with a prominent upright T wave in lead V1 — which in a patient with RCA OMI suggests that there may be acute RV involvement.
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• Elsewhere in the chest leads — artifact precludes drawing conclusions about ST-T wave changes in leads V4,V5 of ECG #3 — but the ST coving and sharp T wave inversion in lead V3 (compared to the appearance of lead V3 in ECG #1) — is another dynamic change in this repeat ECG.

BOTTOM LINE regarding Today’s CASE:

In 2023, given the current state of our knowledge — the discharge diagnosis that was given for this case (ie, that of a Non-STEMI) — is meaningless and misleading. Instead — Cardiac cath proved there was acute occlusion of the proximal RCA. 

• In context with the presenting history — the diagnosis of acute OMI was strongly suggested as soon as the initial ECG was recorded. 
• The need for prompt cath and PCI was firmly established as soon as this initial ECG was compared with the prior tracing ( = ECG #2).
• The follow-up ECG (done 80 minutes after ECG #1, when chest pain returned) — was diagnostic of acute OMI, removing doubt about acute occlusion until proven otherwise by prompt cath.
• The normal initial troponin is not unexpected, and does nothing to dissuade the diagnosis of acute OMI.
• Multiple serial ECGs should have been obtained long before 80 minutes after the initial ECG was recorded (Doing so would have established the diagnosis of acute occlusion that much sooner).
• There is no “magic” to prompt diagnosis of OMI in cases such as today’s — since even AI (by use the PMcardio interpretation program) is now able to establish “with high confidence” from the initial ECG that OMI is occurring.
• I don’t understand continued use by all-too-many clinicians (including cardiologists) — of the outdated, meaningless and misleading term “Non-STEMI” — even after cardiac cath proof that acute occlusion did occur.