When ACS care is very delayed, "STEMI metrics" can be perfect. And how specific is Queen of Hearts?

 Written by Pendell Meyers, sent by anonymous, with additions by Smith

A man in his 40s had acute chest pain and called EMS.

EMS arrived and recorded this ECG:

What do you think?

Here is the PMcardio Queen of Hearts interpretation of the ECG:

STEMI equivalent detected. Inferior and posterior OMI without STEMI criteria.

If you think the Queen of Hearts is so sensitive because it sacrifices specificity, you would be wrong.

See this article, in which using the Queen would decrease false positives substantially:

Artificial Intelligence Driven Prehospital ECG Interpretation for the Reduction of False Positive Emergent Cardiac Catheterization Lab Activations: A Retrospective Cohort Study

There is much more data that shows that the Queen of Hearts is both more sensitive AND more specific (see 3 studies at the bottom)

Case Continued

The ED physician reviewed the prehospital ECG as "No STEMI” at triage and did not order a repeat.

The patient was placed in the waiting room. 

About an hour later another ECG was obtained:

Barely meets STEMI criteria in inferior leads, but obvious inferior and posterior OMI. Even lateral leads V5-V6 have HATW.

The cath lab was now activated for STEMI.

Cath done around 4 hours after first medical contact (symptom onset time uncertain) revealed an RCA occlusion requiring thrombectomy and PCI. 

Smith: How much does such a delay matter?  See this graphic here from JAMA 2005, by legendary authors Gregg Stone and Harvey White. You can read the abstract (or of course the entire article) at the link provided.  Very interesting.  

SUMMARY: From onset of symptoms, a 2 hours delay, from hour 2 to hour 4, results in loss of 60% of the mortality benefit of reperfusion

Gersh BJ, Stone GW, White HD, Holmes DR Jr. Pharmacological facilitation of primary percutaneous coronary intervention for acute myocardial infarction: is the slope of the curve the shape of the future? JAMA [Internet] 2005;293(8):979–86. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15728169   

The "STEMI metrics" for this patient reflect a "successful" time to cath within 90 minutes of the STEMI+ ECG. So the final diagnosis is STEMI, and there is no question or feedback about whether the acute coronary occlusion could have been identified sooner. 

If I were the patient, I would want intervention to be 2 hours earlier, wouldn't you?

What would you want? Does the disease only matter when it becomes easy enough to see on the ECG without any dedicated training? Is the disease the ST segment? or is the disease acute coronary occlusion?

In our study below, among patients who actually had STEMI at some point on the ECG, the PMCardio Queen of Hearts AI Model was able to detect OMI a median of 3 hours earlier than STEMI criteria. 

(And, in addition, she was able to detect many OMI that were never STEMI)

Herman, Meyers, Smith, et al. International Evaluation of an Artificial Intelligence-Powered Electrocardiogram Model Detecting Acute Coronary Occlusion Myocardial Infarction. EHJ DH. 2023.

https://doi.org/10.1093/ehjdh/ztad074

McLaren et al.  Missing Occlusions: Quality gaps for ED patients with Occlusion MI.  

More on Specificity of the Queen of Hearts:

1)

Perfect sensitivity and you can see the false positives at the bottom of the slide

2)

Look at the false positives on the right:  

For the cardiologist, none of the FP had a culprit.  

For the Queen, all 4 FPs had a culprit but the troponin was not high enough to qualify for this very strict OMI outcome definition requiring a peak hs troponin I of at least 5000 ng/L.

3)

https://herzmedizin.de/fuer-aerzte-und-fachpersonal/kongresse/dgk-jahrestagung-2025/-vor--kongressprogramm/wissenschaftliches-programm/koronare_herzerkrankungen/v1146.html

Artificial intellingence based detection of acute coronary occlusion compared to STEMI criteria - External validation study in a consecutive all-comer German chest pain unit cohort.

In ROC analysis the AI model had an area under the curve of 0.978 detecting ACO (see C). The model’s sensitivity was 70.2%, its specificity was 98.5%. This resulted in a negative predictive value of 99.2%. STEMI criteria reached an area under the curve of 0.92. The corresponding sensitivity was 28.8%, while the specificity was 93.7%. The negative predictive value of STEMI criteria was 98.1%.

In the subgroup of low risk patients ruled-out by hs-cTnT algorithm (n=2999) the AI model generated false positive results in 0.7% (n=20, specificity: 99.3%) of cases, compared to 5% (n=150, specificity: 95%) using STEMI criteria.

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MY Comment, by KEN GRAUER, MD (3/23/2025):

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Although details from today’s case are limited — the “answer” should be obvious within seconds on seeing today’s initial ECG (TOP tracing that I have reproduced and labeled in Figure-1). This man in his 40s with acute CP (Chest Pain), severe enough to prompt him to call EMS — has had an infero-postero OMI that has-to-be assumed acute until proven otherwise.

• Learning more precisely when this patient’s CP began — and how severe his CP was at the time ECG #1 was obtained (as well as learning if this patient has a previous history of heart disease and what his “baseline” ECG looks like) — would help us to better determine the likely onset of his OMI.
• That said — there are a number of findings in this patient’s initial ECG that look recent, if not acute.

Why this Patient should NOT be sent to the Waiting Room:

After hearing the history and seeing the initial ECG in Figure-1 — today’s patient was sent to the Waiting Room. We are lucky this patient did not have a cardiac arrest while in the Waiting Room. Instead (as per Dr. Meyers) — worrisome ECG findings were evident on the initial ECG.

• My “eye” was immediately drawn to leads V2 and V3 (within the RED rectangle in ECG #1). In a patient with new CP — early transition (with a predominant R wave already in lead V2) — in association with loss of the normal slight, gently upsloping ST segment in leads V2,V3 (replaced by ST segment flattening — as highlighted by the RED arrows) is diagnostic of acute posterior OMI.
• Infarction Q waves are seen in each of the inferior leads (most notably in lead III). Considering the modest inferior lead QRS amplitudes — acuity is suggested by disproportionately "bulky" T waves in leads II and aVF (BLUE arrows in these leads). Even without reciprocal ST depression in lead aVL — in this patient with new CP, these findings are diagnostic of acute inferior OMI.
• KEY Point: If there was doubt about whether the above ECG findings are diagnostic — then ECG #1 should have been repeated within 15-20 minutes, rather than sending the patient to the Waiting Room, and not repeating the ECG for an hour. 

Figure-1: Comparison between the 2 ECGs in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

The Repeat ECG:

As per Dr. Meyers — lead-to-lead comparison of ECG #2 with ECG #1 leaves no doubt about the diagnosis of an acutely evolving infero-postero STEMI.

• Learning Point: The BEST way to improve our ability at recognizing less obvious but important subtle findings early on, is to go back to the initial ECG and compare lead-by-lead how the initial ECG evolved. That the disproportionately large T waves in leads II and aVF of the initial tracing were hyperacute is now proven by what the ST-T waves in these leads have become. Even the subtle ST segment straightening in lead III of the initial ECG was a harbinger of the marked ST elevation now seen in lead III of ECG #2.
• Similarly — the subtle-but-real ST segment straightening highlighted in lead V2 of ECG #1 — has now evolved to a more acute-appearing downsloping ST segment in ECG #2.
• Sombering Reality: Just as we saw in the recent March 17, 2025 post in Dr. Smith's ECG Blog — "quality control" of today's case will view physician recogition of STEMI criteria in ECG #2 as a "correct" interpretation — whereas STEMI criteria should never have developed because the cath lab should have been immediately activated as soon as the physician saw ECG #1. 

 

Is it possible that this patient with acute chest pain and this ECG does not need emergent intervention?

Case submitted by Andrew Grimes, Advanced Care paramedic, with additions from Jesse McLaren and Smith

 

An 84-year-old male with a notable cardiac history (CABG, multiple stents) woke at 0500hrs with pressure in his chest, diaphoresis, and light-headedness. He presented to a rural ED at approximately 0630hrs. Since he was recovering from a recent bout of Influenza-like illness and said yes to several ILI screening questions at triage, his chest tightness and diaphoresis were initially attributed to this. Still, an ECG was obtained at 0649hrs:

                (Digitized by PM Cardio)

McLaren: The patient has a high pretest probability based on age, risk factors and symptoms. Influenza-like illness can also trigger plaque rupture. Despite the baseline artifact there’s sinus bradycardia, convex ST elevation in III, reciprocal ST depression in aVL and possible anterior ST depression – indicating inferoposterior OMI. 

Here’s the Queen of Hearts interpretation, drawing attention especially to III and aVL: 

This patient does indeed need emergent intervention.  But, alas, as with so many patients, the ECG findings were not noticed and he did not get it.   

STEMI criteria are only 43% sensitive for OMI.  Many arteries in NSTEMI-OMI will open up by next day angiogram, after the damage is done.  But in 34% there is persistent occlusion at next day angiogram.  And they have nearly double the mortality of NSTEMI with an open artery in spite of being younger and healthier at baseline.  This means that, in the United States alone, of 500,000 NSTEMI, 170,000 do not get the care they deserve.  They end up with high mortality and needless heart failure.

Hung C-S, Chen Y-H, Huang C-C, et al. Prevalence and outcome of patients with non-ST segment elevation myocardial infarction with occluded “culprit” artery - a systemic review and meta-analysis. Crit Care [Internet] 2018;22(1):34. Available from: https://link.springer.com/article/10.1186/s13054-018-1944-x   

Vitals were grossly normal. He was treated with MDIs, but when this did not provide any improvement, a cardiac workup was ordered. The initial hs-cTn was negative (11 ng/L). He was given two separate sprays of nitroglycerin sublingually, neither of which improved his pain but did cause him to become briefly hypotensive (<90mmHg SBP).

McLaren: it is not unusual for troponin < 2 hours after symptom onset to be in the normal range, which is falsely reassuring in the presence of an ECG showing acute coronary occlusion.  

Smith: The ECG is diagnostic of occlusion.  Do not wait for troponin!!

Several hours later, the repeat troponin returned at >600 ng/L. 

Smith: now there is absolutely no doubt about the diagnosis, even if you have no idea how to read an ECG.  The patient has acute persistent refrectory chest pain and elevated troponin.  There is no need for another ECG.  Just go to the cath lab!  Unfortunately, only 6% of patients with very high risk NSTEMI needing the cath lab now get managed appropriately.

Cardiology at a larger center was consulted and a repeat ECG was obtained at 1119hrs:

Smith: there is evidence of reperfusion on the ECG: less STE, more T-wave inversion in inferior leads and loss of T-wave size in V4-6.  But the patient still has pain.

The cardiologist was concerned about a posterior MI and suggested a 15-lead ECG, which was obtained at 1210hrs:

 

Smith: there is no need for a posterior ECG!  The right precordial leads V1-V3 tell you all you need to know.  ANY ST depression in these leads is OMI until proven otherwise.  See our article here.  When you have a diagnosis of posterior OMI, posterior leads may be falsely negative.  

The posterior lead V9 is clearly misplaced, as it should be relatively reciprocal (opposite) in morphology to V2.
 

McLaren: The inferior T wave inversion suggests either reperfusion (if resolved symptoms) or subacute refractory ischemia – and from the previous description of pain refractory to nitro it is likely the latter. Despite no posterior ST elevation there is still anterior ST depression, and an enlarging R in V2 wave from posterior infarction.

Case Continued

NSTEMI protocol was ordered, and the patient was given ASA, enoxaparin, and ticagrelor. A stat transfer to the cardiology center was ordered. The transfer was uneventful and serial ECGs showed no appreciable further evolution. The patient maintained a 4/10 "pressure" but insisted he was quite comfortable. On arrival at the cardiac care unit, the patient soon underwent PCI. He had a 100% RCA occlusion which was stented. His LCx was open but small, and perfused only a small portion of his posterior wall. The cardiologist described him as a "challenging" case.

 

I thought this case was interesting with several learning points, including:

1.     The initial misdirection to ILI

2.     Unrecognized ECG signs of occlusion

3.     Queen of Hears has no trouble diagnosing OMI

4.     Treatment as "NSTEMI" despite a 100% RCA occlusion and ongoing pain.

5.     Use of posterior leads can be falsely negative

6.     Posterior leads can be placed erroneously

           7.     Regarding the ECG, this case shows inferior ST elevation with reciprocal depression in aVL that does not quite meet STEMI criteria, ST depression maximal in V2-V3 (>97% specific for posterior MI), and an increasingly anterior R wave progression indicating posterior wall infarction.

Beware confusing the diagnosis of posterior STEMI by using posterior leads...

7 steps to missing posterior Occlusion MI, and how to avoid them

Interventionalist at the Receiving Hospital: "No STEMI, no cath. I do not accept the transfer."

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MY Comment, by KEN GRAUER, MD (3/19/2025):

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Perhaps the most commonly overlooked infarction pattern — is posterior OMI. The reason for this is simple: Because of the relative location of electrical activity with acute infarction of the LV posterior wall — there is no ST elevation on a standard 12-lead ECG.

• Failure to recognize posterior OMI is not a problem IF, as often happens — there is clear evidence of associated inferior wall MI (which is common because both the RCA and LCx usually supply both the posterior and inferior walls of the LV). But when infarction is either localized to the posterior wall — or when ECG signs of inferior wall involvement are subtle (as in today’s case) — it becomes easy for the “unaware” provider to overlook posterior OMI.
• Many providers address the lack of ST elevation on a standard ECG by turning to posterior leads. But as we've shown many times in Dr. Smith's ECG Blog — having to pass through the thick back musculature significantly reduces ECG waveform amplitudes, such that the sensitivity of posterior leads for picking up posterior OMI is lacking. 
• Posterior leads are not needed to recognize posterior OMI. In a patient with chest pain — the finding of maximal ST segment depression in lead V2 and/or V3 and/or V4 indicates posterior OMI — especially when the shape of such ST segment flattening/depression is consistent with a positive "Mirror" Test (See My Comment in the September 21, 2022 post).

Today's CASE is illustrative:

• Because today's patient presented with "ILI" symptoms (ie, of an Influenza-Like Illness) — his chest tightness and diaphoresis was attributed to a viral illness. But all patients who present to an ED with chest discomfort have an ECG — and the initial ECG in today's case (that I've reproduced and labeled in Figure-1) — is diagnostic of acute posterior OMI.
• Today's patient is 84 years old — he has known severe coronary disease (prior CABG; multiple stents) — and he was awakened from sleep because of chest pressure, diaphoresis and light-headedness. Considering this history — any ECG abnormalities have to be assumed acute until proven otherwise.
• Considering this history — my "eye" was immediately drawn to the 2 leads within the RED rectangles. The ST-T wave in lead III is "bulky", coved, ever-so-slightly elevated, and with a hint of terminal T wave inversion. In support that this lead III finding is indicative of acute inferior OMI — is reciprocal ST depression in lead aVL.
• The 2 leads within the BLUE rectangles confirm associated posterior OMI — by the presence of ST segment straightening in lead V2 — and flattened ST depression in lead V3 (whereas normally — there should be slight, gradually upsloping ST elevation in these 2 leads). Especially abnormal are the peaked T waves in these 2 chest leads, with size of the T wave in lead V2 clearly disproportionate to QRS amplitude in V2.
• Other leads (ie, leads II and V6) also manifest T waves that look hyperacute — but despite the artifact — it is the ST-T waves in the 4 leads within the colored rectangles that should indicate acute infero-postero OMI until proven otherwise.

Figure-1: Comparison between the first 2 ECGs in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

Additional Lessons to be Learned:

• Despite the presentation of new severe chest pressure in a high-risk patient — today's initial ECG was not repeated for over 3 hours. Especially when the initial tracing manifests ECG findings of potential concern — the initial ECG should be repeated within no more than 15-30 minutes. Additional serial ECGs should be obtained often until you can be confident of the diagnosis.
• As per Dr. McLaren — a initial negative Troponin does not rule out an acute event, as some time may be needed before Troponin values increase.
• Today's patient became hypotensive following nitroglycerin. Especially when considering acute inferior infarction — NTG-induced hypotension should be a prompt to obtain right-sided leads to rule out significant RV involvement (See My Comment in the July 19, 2020 post).
• Comparison of serial ECGs is best accomplished by placing the 2 tracings being looked at side-by-side. This is done in Figure-1 — and lead-by-lead comparison suggests some of the hyperacute T waves are now not as prominent in the repeat ECG (ie, ST segments have deflated some in leads II,III,aVF) — there is less ST depression in lead aVL — and there has been progression of reperfusion T waves (T wave inversion is now clearly seen in leads III and aVF — and the T wave in lead V2 is taller). If the patient's symptoms were less in association with the development of these reperfusion T waves in ECG #2 — this would be further evidence of acute infero-postero OMI in need of prompt cath.
• BOTTOM Line: If, in a patient with new chest pain — the visual "picture" of ST-T wave flattening-depression in the 2 leads within the BLUE rectangle in Figure-1 is seen — Think acute posterior OMI until proven otherwise. There is no need for posterior leads to arrive at this conclusion.

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.