Our patients deserve better than the "STEMI criteria"

Written by Pendell Meyers, of the Stony Brook class of 2019, with edits by Steve Smith

Two Cases

Imagine that two patients present simultaneously to your Emergency Department with moderately concerning chest pain and the following ECGs (no priors available).

The first patient has this ECG:

The second patient has this ECG:

Do either of them, neither of them, or both, require emergent reperfusion therapy?



















STEMI guidelines (and therefore most clinicians) provide you with a clear answer. Clear and yet perfectly wrong in these two cases.


Let's take them one at a time.


Case #1

A woman in her 50s presented with 2 weeks of fatigue and chest heaviness that started several hours prior to arrival. She stated that she had been diagnosed with influenza 2 weeks ago and had felt worse today with new chest heaviness, so she went to an urgent care facility where she was sent to the ED for an abnormal ECG.

Here is her initial ECG on arrival, complaining of active chest heaviness:

What do you think?

The ECG shows sinus bradycardia with deep wide Q waves and a large amount of ST elevation in the  inferior leads, with reciprocal depression and T-wave inversion in aVL and I. There are also Q waves in V4-V6 with ST elevation and relatively large T-waves. There is no ST depression in V2-V3, but there is a biphasic T-wave in V2.

I showed this ECG to Dr. Smith with no other information. He immediately replied: "normal variant or LVH." We knew this was not acute coronary occlusion, despite the features listed above. I thought the Q waves might be indicative of prior completed inferior MI, but I did not think the morphology looked consistent with even subacute MI. I felt that there was absolutely no evidence of acute coronary occlusion on this ECG.

Why we can say that it doesn't look like ACO despite these objective features is difficult to explain. 

The best answer is that you simply have to see thousands of ECGs and correlate which ones turn out to be ACO and which are false positives. When you do that, you will have seen this ECG many times. The first few times you will be fooled, and then you will learn why it's not ACO.

For those that want a less accurate but more concrete explanation, here are a few points to consider:

1) When there is ST elevation in inferior leads with reciprocal ST depression in aVL, inferior MI is all but diagnosed, unless this STE and STD is preceded by an abnormal QRS! (no LVH, no LBBB, no paced rhythm, no WPW, and no abnormal Q-waves)

Any abnormal depolarization causes abnormal repolarization. Here there is markedly abnormal depolarization with large and deep Q waves inferiorly. No matter what the cause of these Q waves, whether it be old MI, LVH, or a normal variant, they all cause abnormal repolarization. Usually this manifests as ST and T-wave deviation in the opposite direction of the largest/widest abnormality in the QRS ("appropriate discordance"). Such deep Q waves will frequently generate ST elevation and reciprocal changes in the opposite leads.

2) Another important feature that makes it NOT look like MI is the extreme concavity of the ST segments, such that the base of the T-wave is narrow, causing some peaking of the T-wave.

3) There is a small slurring of the end of the QRS complex in some leads, consistent with a J-wave. This is not a perfect rule, but it is very rarely found in true ACO.



The clinicians were alarmed by the ECG findings (as is recommended by all available guidelines), and activated the cath lab. Here are the cath images:

Normal left main, LAD, and LCX.

Normal RCA.

Her catheterization showed completely normal coronary arteries. She had three consecutive negative troponins. Echo was completely normal, no evidence of LVH or any wall motion abnormalities. Extended viral panel was negative.

This is always the most interesting part of the chart review for me, when the clinicians struggle to reconcile normal results with the intense mobilization of resources used and an ECG that they cannot bring themselves to consider a possible normal variant: The clinicians concluded that the patient has "viral myocarditis."

Smith comment: this is NOT myocarditis.  First, the ECG is a normal variant.  Second, myocarditis will always have a positive troponin.

I find it highly unlikely (but not impossible) that the patient has viral myocarditis causing her chest pain and ECG abnormalities without any troponin elevation, wall motion abnormalities, coronary artery abnormalities, or pericardial effusion. It is much more likely that this unfortunate woman simply has a very scary normal variant baseline ECG. Unless she presents to the same institution or carries a copy of her ECG for the rest of her life, this problem will recur. We have many similar cases on this blog.

Her post-cath ECG is unchanged:

This is more proof that is is a normal variant. Acutely abnormal ECGs, whether due to ischemia or myocarditis or takotsubo, will evolve. There is no evolution of the ST segments or T-waves in II, III, aVF, or aVL.

Case #2

A male in his 50s presented with episodic chest pain over the past few days, which recurred and became worse 1 hour prior to arrival. At the time of presentation his pain was 4/10 and decreasing.

Here is his initial ECG:

What is your interpretation?

I sent this ECG to Dr. Smith without any clinical information and he immediately replied "inferior MI."

Congratulations if you see the subtle but important abnormalities here. There is a very tiny amount of ST elevation in lead III which is proportionally significant given a small normal QRS complex. The T-waves are borderline large for their QRS complexes, and alone could not be called hyperacute. However, there is a tiny amount of ST depression and (more noticeably) T-wave inversion in lead aVL which is far out of proportion to the very small QRS complex. The findings in aVL are not appropriate for or explained by the normal QRS complex, and therefore confirm that the subtle findings in lead III are new and indicative of ACO.

There is also ST depression in V3-V6, maximal in V4. This should be assumed to indicate posterior wall involvement of ACO.


These findings were not appreciated. The patient received nitroglycerin and the pain resolved. He was planned to undergo coronary CT angiography for further risk stratification. First troponin was negative.

Repeat ECGs were appropriately obtained, while the patient was completely pain free:





These show (incomplete) resolution of prior abnormalities, confirming that they are dynamic findings and also confirming reperfusion. There is also a change in heart rate which could affect the ST segment and T-waves.  The vessel is open at the time of this ECG.

While waiting for CTCA, his second troponin T turned positive at 0.020 ng/mL. CTCA was cancelled. The third troponin returned at 0.030 ng/mL.

At this point the notes state that the patient had a recurrence of chest pain, was given one dose of sublingual nitroglycerin, followed by lightheadedness with sinus bradycardia in the 30s. Unfortunately there is no mention of an ECG being performed at this time, and no ECG on file. The patient was admitted to cardiology with plans for an urgent cath the next morning. No further troponins were measured.

The next morning, cardiac cath revealed the following:

 This was called a 99% proximal RCA thrombotic stenosis, however I don't see any distal flow. This appears to be 100% occlusion. Thrombectomy and stent was performed with the following angiographic result:

After stenting, the full course of the RCA is now visible.

Unfortunately no more troponins were ordered, so the peak troponin value is unavailable. Echo performed 8 hours after cath did not show any wall motion abnormalities but was suboptimal quality.

Both patients did well.



Great comments by Pendell Meyers:

These two selected cases demonstrate a critically important problem with the current paradigm of MI management. The patients who benefit from emergent cath are those with acute coronary occlusion or near occlusion with insufficient collateral circulation to a substantial portion of the myocardium - this is the anatomic substrate of the entity we are supposed to call "STEMI."

Unfortunately, the term "STEMI" itself and all the guidelines for the past 30 years have restricted our minds into thinking that acute coronary occlusion is diagnosed only by "STEMI criteria." As we have shown countless times on this blog, acute coronary occlusion (ACO) is a complex and dynamic process, and cannot be simplified to measuring millimeters of ST elevation. Numerous studies have documented the STEMI criteria missing at least 25% of ACO. Conversely, we all know there is an unacceptably high rate of false positives using the STEMI criteria, which distracts the clinician from a patient's actual dangerous pathology, causes premature closure, puts the patient at risk of unnecessary procedures and their complications, as well as unnecessary mobilization of scarce resources.

Expert ECG interpretation is almost certianly superior to STEMI criteria in every way. If we are to progress in the management of acute MI, we have no choice but to break the current paradigm. The term "STEMI" cognitively inspires you to think that only the ST segments matter, and that the ST segment deviation is the reliable marker of ACO. To combat this problem we have invented other terms such as "subtle STEMI," "STEMI-equivalent," or "semi-STEMI" in attempt to convey that there are other ECG findings that indicate the same pathology as classic true positive STEMI, but these have not produced widespread change in the knowledge or perception of optimal ACO management, except among the readership of this blog and other similar resources. We have tried too long to keep the term "STEMI" in the name to pay homage to the breakthroughs in the 1970s-1990s which pulled us into the reperfusion era. Eugene Braunwald and others have suggested a requiem for the term "unstable angina," yet we have shown repeatedly on this blog that unstable angina is alive and well. But perhaps the time has come for a requiem for the term "STEMI." While it is true that using STEMI criteria in the 1980s and 1990s was proven better than flipping a coin to decide who needs emergent reperfusion therapy, it is no longer our best option and is actually inhibiting us from discovering that we already have better options. Too long has it restricted our thinking and prevented further research from showing who actually benefits from emergent reperfusion. Experts routinely perform better, and hopefully one day neural networks or the like will make all this a moot point.

The next available step is to formally show that experts can recognize ACO with more accuracy than STEMI criteria and current practice. We are planning a retrospective study now, which will be designed as the first study in an arc of research aimed at evaluating whether expert ECG interpretation can cause better outcomes for patients by more accurately predicting who needs emergent reperfusion therapy. If retrospective studies can show that expert ECG interpretation may have led to faster reperfusion of ACO, then prospective studies may one day be justified in cases where there is otherwise clinical equipoise. If such an ECG were reviewed by an expert, prospectively at the moment of the decision to emergently reperfuse or not, I believe that we could show patient-important outcome improvements correlating with increased accuracy of ACO detection and emergent reperfusion.

Perhaps most importantly, please remember that ACO sometimes manifests with completely normal serial ECGs. The ECG is an accurate surrogate marker of ACO in the hands of experts, but can never be perfect. Some patients deserve immediate diagnostic cath even without ECG abnormalities.

See this lecture by Dr. Smith:
"The False STEMI-NonSTEMI Dichotomy"