Normal ACS care, everything by the book! But normal ACS care could be much better. This post explains everything.

Written by Willy Frick

A man in his 60s with a history of hypertension and 40 pack-year history presented to the ER with 1 day of intermittent, burning substernal chest pain radiating into both arms as well as his back and jaw. It has been stuttering, lasting 10 minutes at a time with associated diaphoresis. His ECG obtained around 8 AM is shown:

ECG 1

My guess is most blog readers will make this diagnosis without too much difficulty. The Queen of Hearts calls this OMI with confidence level 0.99, near maximal. In particular, we see:

• STE and hyperacute T waves in II, III, aVF (a good example of concave HATW)

• Reciprocal STD in aVL > I

• STD in V2 and V3

Easily diagnostic for inferoposterior OMI. Initial high sensitivity troponin I (hsTnI) was 41 ng/L (reference: ≤ 35 ng/L). The patient was given aspirin 325 mg and laboratory workup was initiated. While awaiting chest X-ray, the patient said the pain returned and was the worst he had ever had. It is not clear what was done in response to this, if anything. No medications were given. There was no repeat ECG. There was repeat troponin about an hour after that, and it trended down, from 41 ng/L to 30 ng/L, now within the reference range.

There is very scarce documentation, but the next ECG was obtained around 1 PM.

ECG 2

Diagnostic for inferoposterior reperfusion. Now we see:

• T wave inversion in III

• Biphasic T waves in aVF

• Reciprocal overly upright T waves in I and aVL

• Less STD V2 and V3 than before, with posterior reperfusion T waves

The patient was seen by cardiology who diagnosed him with NSTEMI, started heparin, and planned left heart catheterization the next day. The note says that the ECG has "no ST changes." 

One wonders whether they saw either ECG. 

Repeat hsTnI hours later was 568 ng/L (now reflecting the severe chest pain from hours ago, which was obviously an occlusion which reperfused). Overnight, troponin rose further, 1231 ng/L, then 2960 ng/L before trending back down.

Around 6:30 AM the following morning, the patient complained of severe chest pain and received nitroglycerin with improvement but not resolution. 

The next repeat ECG was not recorded until 8 AM!

ECG 3

Re-occlusion. Now, through the baseline artifact (which we can deduce originates from the left leg electrode given that lead I is spared), we see:

• Inferior STE and HATW

• Reciprocal depression in I and aVL

• STD V1-V5, probably maximal in V2-3

• Rising J point and HATW in V6

This ECG was positive for STEMI with the conventional machine algorithm, and cath lab was activated. Angiogram is shown below. First in slow motion with a freeze frame with annotated vessel anatomy, then at normal speed. As always I use the same color conventions for vessels as the rest of my angiography guide.

As you can see, the lesion is not very angiographically impressive, more on this below. Nevertheless, the operator performed intravascular ultrasound and saw erupted calcium nodule consistent with plaque erosion. Echocardiogram showed inferior hypokinesis. Troponin was rising when last checked, 8928 ng/L.

Discussion:

This case highlights many important points worthy of discussion, mainly because it represents very routine care for ACS but there are so many ways we could improve outcomes with tools we already have!

Limitations of registry data:

This patient presented with STEMI (-) OMI and developed STEMI the following day. The time that elapsed from first diagnostic ECG (ECG 1) to balloon was 24 hours and 54 minutes. But the time that elapsed from first STEMI (+) ECG to balloon was 57 minutes, and THIS is what will be recorded for reporting to the National Cardiovascular Data Registry for purposes of quality improvement. 

In other words, this is considered metric-satisfying care! 

In the world of STEMI, we are incapable of recognizing the first ECG as a false negative. As a result, the patient re-infarcted when that could easily have been prevented.

Think of all the countless similar patients. Just look at all the research based on this! How can any of that research be trusted when it classifies this as a success? How can we identify shortcomings in our current treatment paradigm? How can we prevent the next re-infarction?

The answer is obvious, revascularize OMIs. RIDDLE-NSTEMI already showed years ago that early intervention prevents reinfarction! 

Probably by enriching the trial population with reperfused OMIs (since new TWI was one of the inclusion criteria).

Summary of RIDDLE-NSTEMI:

RIDDLE-NSTEMI, JACC: Cardiovascular Interventions 2016

Limitations of conventional angiography:

This patient was very lucky that the interventional cardiologist who responded to the cath lab activation is evidence based and thorough. A recent meta-analysis by Stone et al. showed that use of intravascular imaging (intravascular ultrasound [IVUS] or optical coherence tomography [OCT]) reduces all cause mortality by 25% compared to angiography guided intervention.

Imagine a counterfactual circumstance where the patient in this case had a severe, stable LCx lesion. This could EASILY have resulted in wrong vessel PCI which happens very frequently. In fact, this incredible study by Heiter et al. found that wrong vessel PCI occurs in more often than 1 in 4 patients with NSTEMI! 

A shocking finding. Just see Hans's recent post.

This is why angiography can never serve as the gold standard for diagnosing OMI. The final report in this patient called the RCA 60-70%, which I think is generous and many might call this 50%. This is because conventional angiography is inherently limited even beyond inter-observer variability. OMI is a dynamic process, and understanding angiography requires clinical context, ECG, echo, intravascular imaging, and sometimes even more advanced imaging like MRI or CT.

Does anyone think that this is a "false positive" STEMI because the vessel was open? No! The final chart diagnosis assigned by the interventional cardiologist is STEMI.

In fact, in 33% of cases which everyone would call "STEMI", the artery is open; in 20%, the artery has TIMI-3 (perfect) flow.

But now imagine no ECG ever met STEMI criteria (which would have been the case had the patient failed to re-occlude). Naysayers would call OMI interpreters alarmist, and point to the TIMI 3 flow as evidence that delayed care was safe, and say that this was never going to be a big infarct.

Limitations of troponin:

This patient presented with very mildly elevated troponin which trended down into the normal range, falsely reassuring the clinicians. This is probably because there was only a very brief occlusion causing the presenting symptoms before he spontaneously reperfused. The timeline is as below:

• Brief occlusion with spontaneous reperfusion prior to arrival
• Initial troponin 41 ng/L and trended down to within the reference range

• Reocclusion around 9 AM (reporting the worst pain of his life) with spontaneous reperfusion
• Troponin did not peak until midnight at 2960 ng/L

• Reocclusion the next morning at 6 AM with STEMI and cath lab activation
• Repeat troponin at that time was actually down to 1965 ng/L and rose to 8928 ng/L 24 hours later reflecting the damage from reinfarction

Troponin is helpful, but it takes a back seat to history, ECG, and echo in the hyperacute setting.

Limitations of STEMI:

Because of TIMACS, the world of cardiology is convinced that delaying intervention in NSTEMI is safe. This blog has written exhaustively about why that is a mistaken understanding. In particular, TIMACS compared 16 hour intervention to 52 hour intervention, but most of salvageable myocardium infarcts within 6 hours.

Why would anyone expect to find a difference comparing two interventions that both occur after completion of the infarct? Once the house burns down, does it help if the fire department throws water on it 12 hours later vs a few days later?

This is the limitation of STEMI. Even though guidelines say that patients with high-risk features, refractory angina, instability, etc. should go for immediate angiography, it almost never happens. Less than 1 in 15 in fact.

Who can make the argument that waiting to revascularize this patient was a good idea? Who seriously believes that the portion of myocardium that infarcted did not matter? How is a patient permitted to infarct his inferior wall in a cath capable facility while being monitored for known myocardial infarction.

But all of this happens every day in cath labs across the world. This is a completely forgettable case for most cardiologists. This will not make it into any morbidity & mortality conferences. This patient reoccluded hours after aspirin and heparin were initiated and suffered a 100% preventable in-hospital myocardial infarction.

Key points:

• By design, the NCDR registry and existing quality improvement efforts systematically overlook opportunities for improvement

• Early intervention saves myocardium

• Coronary angiography has inherent limitations and evidence-based care requires intravascular imaging

• Troponin is a useful adjunctive test, but is delayed by many hours

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MY Comment, by KEN GRAUER, MD (3/17/2025):

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In today's thought-provoking case by Dr. Frick — probing questions are asked that need to be addressed by the medical community.

• Dr. Frick exposes a series of errors of omission and commision that are embedded in the ongoing fallacy of the outdated, misleading and inaccurate STEMI paradigm. Specifically in today's case, as a direct result of overlooking an obvious acute coronary occlusion (an infarct that was initially STEMI(-) but clearly OMI(+) ) — the necessary cardiac cath with PCI was delayed for more than a day. 
• This needless delay allowed sufficient opportunity for the "culprit" artery to reocclude, this time resulting in a STEMI(+) ECG that finally "earned" the right to a cardiac cath with performance of PCI. But because written documentation of today's case will show PCI was performed less than 1 hour after STEMI criteria were satisfied — "quality control" will view this needlessly delayed intervention as "excellent care". In reality — this patient's STEMI could have (should have) been avoided if initial providers (including the initial consulting cardiologist) had simply been aware and paid attention to the importance of recognizing STEMI(-)/OMI(+) infarctions that merit prompt cath with PCI performed as soon as this is possible.

Dr. Frick goes on to ask, "How can any of this research be trusted when it classifies 'the time frame in today's case' as a success? (ie, in which PCI was done in <1 hour after STEMI criteria were satisfied — albeit this was more than 24 hours after acute OMI should have been diagnosed).

• The answer to Dr. Frick's question — is that current research performed by advocates of the outdated STEMI paradigm can not be trusted. Research regarding optimal management of acute MI should not be trusted until a preponderance of the medical (and cardiology) community finally accept that many acute coronary occlusions are missed by the outdated STEMI paradigm (and even when STEMI criteria are satisfied, as they eventually were in today's case — misguided adherence to STEMI criteria is responsible for loss of much viable myocardium because it all-too-often delays the indication for cath).

Among the Oversights ...

To recount just a few of today's oversights:

• As per Dr. Frick – there is ST elevation in each of the inferior leads in today's initial ECG (RED arrows in Figure-1). Reciprocal ST depression is clearly present in lead aVL. Regardless of whether the "required" millimeter-amount of ST elevation is present in ECG #1 to qualify as a "STEMI" — acute inferior OMI is confirmed in this high-risk 60-ish year old man with new CP (Chest Pain) by the ST-T wave appearance in these 4 limb leads.
• Acute posterior OMI is also clearly present in ECG #1 by the obvious abnormal ST depression in leads V2,V3. The order for cath lab activation should have been given within minutes of seeing this initial ECG.

Instead — It took 5 hours (!) for the ECG in today's case to be repeated:

• If any doubt existed in the mind of the providers after today's initial ECG regarding the need for prompt cath with PCI — the repeat ECG should have been ordered within no more than 10-15 minutes after the initial ECG was done.
• Instead — no repeat ECG was done for hours (not even after the patient's CP returned with even more severe intensity).
• Documentation regarding the severity of this patient's CP remained "scarce" — without any correlation of CP severity to the repeat ECG that was finally done.
• In Summary — It is difficult to imagine how the initial consulting cardiologist could have compared these first 2 ECGs that are shown in Figure-1 — and interpreted these 2 tracings as showing "no ST changes" — and assessed the case as a "NSTEMI" with no need for catheterization until the next day. (As per Dr. Frick — comparison of ECG #2 with ECG #1 clearly shows deflation of the inferior lead hyperacute T waves with reperfusion T waves now present in ECG #2 in the form of T wave inversion in leads III, aVF — and a now isoelectric ST segment with upright T wave in lead aVL).
• Additional oversights continued until STEMI criteria were finally satisfied and cardiac cath was performed.

BOTTOM Line: The events in today's case beg review and constructive feedback with thorough rethinking of the clinical approach. We must do better ...

Figure-1: Comparison between the first 2 ECGs in today's case.

What happens when you give morphine for chest pain in ACS? And what is pseudo-normalization of T-waves?

Written by Magnus Nossen, with edits by Smith

The patient in today's case is a 70-year-old farmer. He has a history of coronary artery disease and a STEMI two years prior that was treated with primary PCI. He contacted EMS due to acute onset chest pain and feeling unwell and fatigued. He was given ASA and sublingual NTG and taken to the ED. 

At the time of this initial ED ECG, his symptoms were improving

ECG #1 on admission to the ED

The patient was not seen quickly in the ED as it was a busy shift and the ECG did not meet STEMI criteria. 

He subsequently developed worsening chest pain. 

The below ECG was recorded. Does this repeat ECG shed any light on what is going on? 

ECG #2 repeat in the ED.

These two ECGs look similar at first glance. 

However, there are very important dynamic changes between the two recordings. 

The first ECG, taken after NTG administration and during pain relief, shows signs consistent with re-perfused lateral and posterior OMI. There are T-wave inversions in leads I and aVL. Also of note are tall T-waves in the right precordial leads. These anterior T waves are not hyperacute, but rather a result of posterior wall reperfusion. (Posterior reperfusion T-waves). The inferior T-waves are also large because they are reciprocal to the lateral reperfusion. 

If you look closely at the two ECGs side by side, you can see the dynamic change.  Below, I have placed the ECGs side by side for comparison  

On the repeat ECG, the T-waves in aVL are not nearly as negative as they were on the admission ECG. The T-wave amplitude in the inferior and anterior leads is decreasing. This, in the context of worsening chest pain, is evidence of reocclusion of the infarct-related artery and active OMI in development. 

Chest pain was increasing at the time of ECG #2 which prompted evaluation by the physician caring for the patient. 

The patient was placed on an NTG drip and given morphine. 

The subtle ECG changes were not recognized. 

After NTG and morphine, the patient's symptoms improved. The ECG below was recorded. What do you think?

ECG #3 while on NG drip and after morphine

At this point, the patient reported less severe symptoms, although he still had chest pain. The improvement in symptoms was attributed to the NTG drip. The following was noted in the patient's chart. "Pain is improving and ischemic T-wave inversions are no longer present". 

This assessment is incorrect. The ECG clearly shows worsening ischemic changes. ECG #3 shows evolution of reocclusion, now with upright T-waves in I and aVL (this is called pseudonormalization), inferior reciprocal ST depression in inferior leads (with down-up T-waves), and increasing STD in precordial leads with decreasing T-wave amplitude (also due to reocclusion to blood supply to the posterior wall).  This is all diagnostic of active (not reperfused) acute posterior  OMI.  

These are obvious OMI findings that do not meet STEMI criteria. 

Pain improvement cannot be due to NTG with the above ECG. 

It must be a result of the morphine that was administered. 

These findings were not recognized, and because the patient (after morphine) reported improved symptoms, urgent coronary angiography was not performed. 

The troponin I on admission was 54ng/L. The repeat troponin I the following morning returned at 27.890ng/l.  This has become a very large infarction.

Below is the Queen of Hearts (QoH) interpretation for each of the ECGs in today's case. For ECG #1 she sees reperfused OMI, for ECG #2 she sees reperfused OMI but with low confidence (as the artery is re-occluding). ECG #3 is easily recognized as OMI and the AI model recommends immediate revascularization

The patient in today's case received suboptimal care and suffered a substantial myocardial infarction. He eventually underwent CAG, where a circumflex occlusion was stented. Despite the delayed therapy, the patient did well clinically.

This case highlights how T-waves are very important in the assessment of ischemia and dynamic changes in acute coronary syndrome. 

T-wave inversions in the acute phase of ACS are usually a welcome finding, indicating reperfusion. 

If TWI disappears or reverses, always consider re- occlusion (pseudonormalization)! 

I have often seen colleagues worry about T-wave inversions as a sign of ongoing ischemia.  But T-wave inversion in leads overlying the infarcted territory is a good sign: a sign of reperfusion. 

If there is persistent (not decreasing) chest pain and T-wave inversions, there is usually some type of secondary cause of inverted T waves such as LVH or wide QRS complexes. 

Here is an old (2015), but still very relevant, lecture on T-wave inversion by Dr. Smith: 

40 minute lecture on T-wave inversion

Learning points: 

• T-waves are often dynamic in ACS and may hint at reperfusion and re-occlusion before the ST-segment does. 
• In a patient with ACS symptoms disappearing TWI should be considered re-occlusion of the infarct related artery. 
• Be careful before administering morphine as it will improve pain. 
• T wave inversions are often caused by reperfusion.

Smith: Never give opiate pain relief unless you are committed to the cath lab!!  You will obscure the symptoms and think that your medical management is working to relieve ischemia, when it is only relieving pain!!

Here is evidence for this:

Opiates are associated with worse outcomes in Myocardial Infarction.

See this case: A man his 50s with chest pain. What happens when you treat with morphine rather than with reperfusion?

----See this study showing an association between morphine and mortality in ACS:
Use of Morphine in ACS is independently associated with mortality, at odds ratio of 1.4. Meine TJ, Roe M, Chen A, Patel M, Washam J, Ohman E, Peacock W, Pollack C, Gibler W, Peterson E. Association of intravenous morphine use and outcomes in acute coronary syndromes: Results from the CRUSADE Quality Improvement Initiative. Am Heart J. 2005;149:1043–1049.

And Another that we wrote:

----Bracey, A.  Meyers HP.  Smith SW.  Wei L. Singer DD.  Singer A.  Association between opioid analgesia and delays to cardiac catheterization of patients with occlusion Myocardial Infarctions. Academic Emergency Medicine 27(S1): S220; May 2020.  Abstract 556.

Main result: STEMI(-) OMI Patients

65 (23.9%) patients were found to have STEMI(-) occlusion myocardial infarction (OMI) at the time of cardiac catheterization. The 45 patients with STEMI(-) OMI without pre-cath opioids had a door-to-balloon time of 75 minutes, vs. 684 minutes for the 25 STEMI(-) OMI with pre-cath opioids.

High Risk ACS guidelines are only followed in 6% of patiients:

Lupu L, Taha L, Banai A, Shmueli H, Borohovitz A, Matetzky S, Gabarin M, Shuvy M, Beigel R, Orvin K, Minha S ’ar, Shacham Y, Banai S, Glikson M, Asher E. Immediate and early percutaneous coronary intervention in very high-risk and high-risk non-ST segment elevation myocardial infarction patients. Clin Cardiol [Internet]. 2022;Available from: https://onlinelibrary.wiley.com/doi/10.1002/clc.23781

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MY Comment, by KEN GRAUER, MD (3/14/2025):

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Today’s case is marked by an important and fundamental oversight that significantly delayed optimal treatment.

• This all-too-commonly occurring oversight stems from a failure to appreciate the sequential ECG changes that should be expected during the course of an acute evolving infarction.
• The Theory is Simple: Depending on the area of the heart involved — ST segments will elevate with inferior, lateral or anterior OMI when the "culprit" artery occludes — and return to baseline on the way toward T wave inversion when the culprit artery reopens (regardless of whether the artery is reperfused by PCI or thrombolysis — or opens spontaneously).
• The opposite occurs with posterior OMI (ie, there is ST depression with acute occlusion, that is maximal in leads V2,V3,V4 — with return of ST segments to baseline on the way toward developing tall, peaked chest lead T waves that are maximal in leads V2,V3,V4 when the occluded RCA or LCx reopens).
• KEY Point: Correlating each serial ECG to the presence and relative severity of CP at the time each each is done (ie, by a CP "scale" from 1-to-10 that is noted on the chart) — provides an important clue to the state (open or closed) of the "culprit" artery. For example, if posterior reperfusion T waves become less tall and less peaked with a sudden increase in CP severity — this could be a worrisome sign that the "culprit" RCA or LCx is once again occluding (and that ischemic ST depression will soon follow). This fundamental oversight occurred in today's case.

Reviewing the History:

The history in today's case immediately places this 70-year old man in a higher-risk group for an acute event simply because: i) The patient has known coronary disease; and, ii) He experienced the onset of new CP severe enough to call EMS.

• While delays happen in a busy ED when there are more acute patients than clinicians to care for them — delay should not happen for a higher-risk patient because, “STEMI criteria are not met".
• Along the way — Morphine should not be used to determine if prompt cardiac cath is indicated (as it apparently was in this case). Morphine could have been given early on in today's case — because sudden onset of new CP in a patient with known coronary disease and an obviously abnormal initial ECG is already indication for prompt cath. 
• Once you know that prompt cath is needed (because history, ECG findings and troponin indicate acute coronary occlusion) — chest pain relief assumes high priority. But relieving CP before you establish the diagnosis of acute OMI masks symptoms, and only serves to delay the needed PCI (as occurred in today's case).

Reviewing the Serial ECGs:

For clarity and ease of comparison — I’ve put representative complexes from each of the 3 tracings in today’s case together in Figure-1.

• As noted by Dr. Nossen, although the initial ECG does not satisfy millimeter-based STEMI criteria — this tracing is markedly abnormal. It is diagnostic of acute postero-lateral OMI. Consistent with the clinical history of reduced CP at the time ECG #1 was recorded — this initial tracing already suggests spontaneous reperfusion because: i) There is deep T wave inversion in lead aVL; ii) The reciprocal of this lead aVL finding is seen in the form of terminal T wave positivity in each of the inferior leads; and, iii) Chest leads show overly tall, T wave peaking that is maximal in leads V2,V3,V4. 

KEY Point: As emphasized by Dr. Nossen — unless you place the serial ECGs you are assessing side-by-side — it is all-too-easy to overlook the "tell-tale" dynamic ST-T wave changes that become obvious when looking at Figure-1.

• Prove to yourself that there have been dynamic ST-T wave changes. Look lead-to-lead — and compare the relative size of ST-T waves in ECG #1 vs those in ECG #2. 
• If you look carefully — Isn't there a difference in ST-T wave appearance in no less than 10/12 leads? 
• Although the amount of change in ST-T waves between these 2 tracings may not be great in some leads — the consistency in the direction of these changes is unmistakeable (ie, T wave inversion and T wave peaking are clearly more accentuated in ECG #1 at the time the patient arrived in the ED and CP was decreasing after NTG).

Now look lead-by-lead and compare ST-T wave appearance in ECG #2 (at which time CP was increasing) — with ECG #3 (when CP was reduced by IV NTG and morphine).

• Isn't there a difference in ST-T wave appearance in virtually all leads?

BOTTOM Line: Lead-by-lead comparison between today's 3 serial tracings, when correlated to this patient's coming-and-going of CP — tells a convincing story of acute LCx occlusion.

• Relief of this patient's CP at the time ECG #1 was recorded — is consistent with the above described ECG signs of spontaneous reperfusion of this postero-lateral OMI.
• These reperfusion ST-T wave changes lessened in association with ECG #2 — because this repeat tracing was recorded at a time when CP had returned (ie, on the way toward developing high-lateral lead ST elevation and anterior lead ST depression from postero-lateral OMI).
• ECG #3 reflects further progression of "culprit" artery reocclusion — with ST elevation now clearly beginning in lead aVL — with more acute-looking reciprocal ST depression in inferior leads — and more acute-looking changes across the chest leads.
• Even allowing for failure to recognize acute OMI after ECG #1 — and failure to recognize acute OMI after ECG #2 — awareness of the fundament concept of sequential ECG changes discussed above is essential for the goal of optimizing salvage of viable myocardium (and at least recognizing acute OMI and the need for timely cath from ECG #3). 
• The lesson from today's oversights needs to be learned. 

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

 

Chest pain and computer ‘normal’ ECG. Wait for troponin? And what is the reference standard for ECG diagnosis? Cardiologist or outcome?

Written by Jesse McLaren

A 50 year old presented to triage with one hour of chest pain, and the following ECG labeled ‘normal’ by the computer (GE Marquette SL) algorithm. 

 

What do you think?

There’s normal sinus rhythm, first degree AV block, early R wave, normal voltages. There’s hyperacute T waves in I/aVL with reciprocal inferior ST depression, diagnostic of high lateral occlusion MI.

Here’s the Queen of Hearts interpretation (OMI with high confidence):

But many small studies have concluded (erroneously) that triage ECGs labeled ‘normal’ by computer algorithm don’t need to be interrupted by a physician.(see reference below)

 

What’s the gold standard for ECG interpretation: is it cardiologist interpretation?

The latest is Langlois-Carbonneau et al. Safety and accuracy of the computer interpretation of normal ECGs at triage. CJEM 2025. They concluded, "Our findings increase confidence in the normal automated GE Marquette 12 SL ECG software interpretation to predict a benign outcome. Our data corroborate that immediate management of a patient with a normal automated triage ECG reading is not modified by real-time ED physician ECG interpretation."

But like many similar studies, the study was small (one year at one centre with no indication of the incidence of acute coronary occlusion), and it used as the gold standard the final cardiologist interpretation of the ECG - not the patient outcome! 

(Smith comment: this is a very stupid outcome measure)

What if we use that methodology for the ECG above?

The final blinded cardiologist interpretation was only non-specific “ST and T wave abnormality”. If we took this as the gold standard, we would conclude that the computer interpretation was safe and accurate – at least accurate enough to not miss “STEMI”, and that physicians should not be interrupted to interpret it, because there would be no change in patient management.

If this advice had been followed, then the patient would have remained in the waiting room, waiting to be seen by a provider. The first troponin was normal (6ng/L, just barely above the level of detection of 2ng/L, and below the upper limit of normal of 26ng/L). But troponin is a rear-view mirror which shows damage that has already occurred, and is often within the normal range within only 2 hours of onset of acute coronary occlusion. So waiting for serial troponin would have further delayed reperfusion.

Smith comment: we showed that the first troponin, even in full-blown STEMI, is negative 25% of the time.

Fortunately, the emergency physician was immediately shown the ECG and immediately identified high lateral occlusion. So they modified patient management in real-time despite the false reassurance of the 'normal' ECG. A 15 lead was done, which was similar and had the same final blinded cardiology interpretation. Despite serial ECGs being "STEMI negative", the cath lab was activated.

What is the gold standard for ECG interpretation: patient outcome!!!

On angiogram there was a 99% first diagonal occlusion with TIMI 1 flow. Repeat troponin was 4,000ng/L and not repeated afterwards, and there was no follow up ECG. Because of rapid cath lab activation, the discharge diagnosis was “STEMI” even though no ECG met STEMI criteria by cardiology interpretation.

Smith comment: we have a paper under consideration that shows that the only independently significant factor in final diagnosis of STEMI vs. Non-STEMI is time to treatment, not presence of STE millimeter criteria, nor presence of occlusion!

But according to Langlois-Carbonneau et al., even a final interpretation of STEMI does not change their conclusion that computer ‘normal’ ECGs are safe and accurate. 

Case 2 in this same paper

They included the following case (different from the one above!):

A 68 year old woman presented to the ED with a history of "atypical" chest pain (Smith: "atypical" is a garbage description of chest pain). Here is her ECG:

What do you think?

Smith: this is diagnostic of acute inferior posterior lateral OMI

Here is the description in the paper:

“The 68 years old female with a final STEMI diagnosis presented to ED with a history of atypical chest pain. The ED physician’s ECG interpretation of her first ECG was “ST elevation in II-aVF and V5-V6,(…)concave, no reciprocal changes.” When troponins came back positive, the emergent catheterization procedure was activated. The complete cardiology consult was done the next day and the initial ECG was analyzed as ‘slight ST elevation in II-aVF-V4-V5-V6.’ The patient’s final diagnosis remained STEMI but this is contentious as the patient did not actually fulfill STEMI criteria on the initial ECG. Moreover, this patient’s ECG was read as “normal” by the blinded attending cardiologist.”

So even in hindsight, these authors concluded that the computer interpretation on the ECG paper is more reliable for the final diagnosis than an actual acutely occluded coronary artery!

Smith comment: this is even more stupid.

Here's the PMCardio AI OMI Model Queen of Hearts interpretation:

This confirms that computer ‘normal’ ECGs are neither safe nor accurate, that physicians can identify subtle OMI in real time (enhanced by AI), and that the gold standard should be patient outcome. 

 

Take home

1.     Computer ‘normal’ ECGs are not safe or accurate. See > 50 cases on Dr. Smith’s EGC Blog. We’ve also published the largest study on this question: Emergency Department Code STEMI patients with initial electrocardiogram labeled ‘normal’ by computer interpretation: a 7-year retrospective review. Using patient outcome (Code STEMI with culprit lesion) we found 4% had had a triage ECG labeled ‘normal’ by the computer – a third of which were identified in real time by the emergency physician. This underestimates computer false ‘normal’ ECGs because we only included code STEMIs, not Non-STEMIs with OMI.
2.     The gold standard should be patient outcome. See our letter to the editor in response: McLaren, Meyers, Smith, Chartier. What is the gold standard for ECG interpretation: computer, cardiologist, or patient outcome. CJEM 2025 March 10
3.      The initial troponin is not reliable in OMI, and can be in the normal range with acute  symptoms

References concluding erroneously that if the conventional algorithm says "normal" that the triage ECG does not need to be reviewed by the physician.

1. Winter LJ, Dhillon RK, Pannu GK, Terrazza P, Holmes JF, Bing ML. Emergent cardiac outcomes in patients with normal electrocardiograms in the emergency department. Am J Emerg Med. 2022; 51: 384-387.

2. Villarroel NA, Houghton CJ, Mader SC, Poronsky KE, Deutsch AL, Mader TJ. A prospective analysis of time to screen protocol ECGs in adult emergency department triage patients. Am J Emerg Med. 2021; 46: 23-26.

3. Hughes KE, Lewis SM, Katz L, Jones J. Safety of computer interpretation of normal triage electrocardiograms. Acad Emerg Med [Internet] 2017;24(1):120–4. Available from: https://pubmed.ncbi.nlm.nih.gov/27519772/ 

4. Deutsch A, Poroksy K, Westafer L, Visintainer P, Mader T. Validity of computer-interpreted “normal” and “otherwise normal” ECG in emergency department triage patients. West J Emerg Med [Internet] 2024 [cited 2024 Aug 26];25(1):3–8. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10777178/ 

5. Langlois-Carbonneau V, Dufresne F, Labbé È, Hamelin K, Berbiche D, Gosselin S. Safety and accuracy of the computer interpretation of normal ECGs at triage. CJEM [Internet] 2024;26(12):857–64. Available from: https://link.springer.com/article/10.1007/s43678-024-00790-5

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MY Comment, by KEN GRAUER, MD (3/12/2025):

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Today’s case by Dr. McLaren once again raises the question of, “What is a ‘normal’ ECG?” (Please see My Comment at the bottom of the page in the January 15, 2025 post for "My Take" on what constitutes a "normal" ECG). 

Regular readers of Dr. Smith’s ECG Blog are well familiar with the following facts:

• A “normal” ECG is not an ECG that is called “normal” by any computerized ECG interpretation program other than QOH (Queen Of Hearts). 
• A “normal” ECG is not an ECG that is called “normal” by a cardiologist who does not yet accept and believe in the OMI Manifesto (See the July 31, 2020 post — and — McLaren, Meyers & Smith: J Electrocardiol 76:39-44, 2023 — and — Meyers, Weingart, Smith: The OMI Manifesto, 2018).
• As per Dr. McLaren — a normal initial hs-Troponin in no way rules out the possibility of an acute OMI. To quote Dr. Smith, "Using Troponin to diagnose 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 not see the road ahead." As a result — "A normal initial Troponin can give false reassurance, when there's a head-on collision happening in real time!" (from the March 24, 2023 post).
• Up to 1/3 of patients with an "NSTEMI" turn out to have an acute coronary occlusion that could benefit from PCI — and — More than 1/2 of patients with acute coronary occlusion do not manifest ST elevation (Statistics from McLaren, Meyers, Smith et al: JACC Adv 3:101314, 2024).
• BOTTOM Line: Correlating the history with the relative severity of CP associated with each ECG (and with serial Troponins) — is far more accurate for rapid recognition of acute coronary occlusion than waiting until “enough” ST elevation develops to qualify as a STEMI (and all-too-often with acute OMIs — this "required" amount of ST elevation never occurs).

The Computer Can Not be Trusted:

Returning to today's case — I have labeled in Figure-1 the initial ECG from this 50-year old patient who presented to the ED for new-onset CP (Chest Pain) of 1 hour duration.

• Amazingly — the GE Marquette SL computer program labeled the ECG in Figure-1 as "normal".

As per Dr. McLaren — ECG #1 is diagnostic of acute coronary occlusion. In this patient with new CP — failure to at least note the obvious ST-T wave abnormalities in 5/6 of the limb leads serves to immediately discredit any validity that this ECG computer algorithm might have.

• Considering the modest QRS amplitude in each of the limb leads — the amount of ST elevation in high-lateral leads I and aVL is significant. More than this — the T waves in these 2 leads are clearly hyperacute (ie, much "fatter"-at-their-peak and wider-at-their-base than they should be given how small the R waves in these leads are).
• Equally impressive reciprocal ST-T wave changes in each of the inferior leads instantly confirms acute coronary occlusion until proven otherwise (ie, leads II,III,aVF showing downsloping ST depression with widening of the lowest ST segment point and terminal T wave positivity).

Although ST-T waves in the chest leads are not as acute-appearing — there are diffuse abnormalities in these chest leads that made me wonder about posterior OMI or multi-vessel disease:

• The already tall R wave in lead V2 is a common finding with posterior OMI.
• The gently upsloping slight ST elevation that is normally seen in leads V2,V3 is absent.
• ST segments are uncharacteristically flattened in leads V3,V4,V5.
• Especially considering the hyperacute T waves with ST elevation that we saw in lateral limb leads I and aVL — I thought the broadened T wave peak in lead V6 (if not also in lead V5) represented hyperacute lateral chest leads.

To Emphasize: Computerized ECG reports other than QOH (Queen Of Hearts) simply can not be trusted.

• The above said — the fault does not lie with these computer programs. These programs simply have never been programmed with sufficient outcome data to enable accurate ECG assessment in patients with CP. We need to know this!
• Fortunately — the ECG in today's case was promptly shown to the ED physician who correctly identified the acute abnormalities.

Figure-1: I've labeled the initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).