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).

 

"Anterior" ST Depression: Which Lesion is the Culprit?

Written by Hans Helseth

Hans is an EKG tech who is applying to medical school. EKG interpretation skills have little to do with one's level of education. In fact, much of what passes for EKG education can actually harm one's interpretation skills.

A 62 year old man with hyperlipidemia presented to a rural emergency department with 7 hours of 3/10 chest pain. Here is his triage EKG:

With ST depression maximal in V2-V4 and resolved by V5-V6, this is diagnostic of posterior OMI, as shown by Meyers et al. (https://www.ahajournals.org/doi/10.1161/JAHA.121.022866)

_________

Smith: Although many writers state that the tall R-wave is essential to the diagnosis of posterior OMI, that is a false statement: we showed in the above study that the R-wave is irrelevant. A large R-wave is analogous to a Q-wave and only shows that the infarct has progressed to involve a large territory. ACUTE posterior OMI does not have a large R-wave. (We also showed that an upright T-wave is not required, and that many have a negative or biphasic T-wave). The pain has been present for 7 hours, which corresponds to a long duration of infarction and the presence of "Q" waves (in this case tall R-waves)

_________

With inferior ST depression and possible ST segment straightening in aVL there is also suggestion of high lateral involvement, meaning the likely culprit artery is the left circumflex or one of its branches.

Here is the QoH interpretation:

The ED provider described the T waves in V2 and V3 as “hyperacute”. It is not clear by her note what she meant by this (whether or not she recognized this EKG as diagnostic of transmural ischemia, and if so, of what territory) but emergent reperfusion therapy was not pursued.

At 1022, a troponin I (ref range <0.034 ng/mL) resulted at 4.437 ng/mL. This was the only troponin measured during this case. The patient was diagnosed with NSTEMI and placed on a heparin drip.

[Smith: this high initial troponin confirms that this is a subacute OMI and that one should expect Q-waves (tall R-waves)].

Another EKG was recorded after almost two hours. The status of the patient’s pain at this time is unknown:

It remains mostly unchanged. 

At 1210, the case was discussed with a cardiologist at a PCI capable facility, who accepted the patient for transfer, noting the ST depression in anterior leads as “consistent with ischemia” but “not a STEMI”. The patient arrived to the ED of the PCI facility where this EKG was recorded:

The ST depressions have almost completely resolved, which suggests reperfusion of the posterior wall, although again, the patient’s pain status at this time is unknown.

At 1547 the patient was taken for angiography:

The cath report by the interventionist describes:

• 80% Ostial LAD (green arrows)

• 95% Mid LAD (blue arrows)

• 100% First Obtuse Marginal (red arrows)

Some may prefer to call the occluded vessel the second obtuse marginal, as a small branch with the same course can be seen originating proximally to it (see Terminology and Semantics of Willy Frick’s cardiac cath guide).

Based on the EKGs, which lesion is most likely the culprit?

In this case, the interventionist called the mid LAD lesion the likely culprit. The proximal and mid LAD stenoses were stented and the OM 2 was left alone. It is unclear by the note whether or not the OM lesion was interpreted as CTO, but it was not touched.

An EKG was recorded after cath:

The ST depression has worsened. There is no restoration of flow through the likely true culprit lesion in the second obtuse marginal, so the EKG continues to show transmural ischemia of the posterior and high lateral walls.

Another EKG was recorded the day after PCI:

The ST depression has worsened further. There is still no restoration of flow past the lesion.

An Echo performed the day after PCI showed an EF of 51% and hypokinesis in the mid posterior, mid lateral, and basal lateral segments. This distribution of wall motion abnormality is more consistent with a culprit in the obtuse marginal rather than the mid LAD. Had more troponins been measured, it is likely they would have continued to climb as the patient’s artery remained occluded.

The patient was discharged the day after PCI. There is no follow up.

It is still widely believed that ST depression localized to a certain territory on the EKG is indicative of subendocardial ischemia of that territory. In this case, it is possible that the physicians interpreted the ST depression in anterior leads as subendocardial ischemia of the anterior wall, and the mid LAD stenosis as the culprit of that ischemia.

Subendocardial ischemia does not localize. It manifests with an ST elevation vector towards lead aVR, causing ST depression maximal in apical leads (II, V5-V6). See this exemplified many times on this blog. Localized ST depression, as in this case, is indicative of transmural ischemia of the opposite territory. Anterior ST depression = posterior ST elevation. 

This was likely a case of wrong-vessel PCI. This is surprisingly common. Heitner et al found that in 14% of patients with NSTEMI, a blinded interventional cardiologist interpreting coronary angiograms identified a different culprit artery than CMR (https://www.ahajournals.org/doi/10.1161/CIRCINTERVENTIONS.118.007305). This is a case which demonstrates the importance of OMI findings on the EKG in the job of the interventionist. 

Learning Points:

• ST depression maximal in V1-V4 is posterior OMI, not anterior ischemia, not subendocardial ischemia

• This should have undergone emergent angiograph and PCI of the correct vessel

• Wrong-vessel PCI is not uncommon in “NSTEMI”

• Serial troponins and EKGs can be a useful tool for confirming the success of PCI.

Smith: here is a post with many ECGs which compares and contrasts the ST depression of posterior OMI from that of deWinter's T-waves:

De Winter's T-waves are Not a Stable ECG condition. Upright T-waves in Posterior OMI are Distinct from de Winter's waves.

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MY Comment, by KEN GRAUER, MD (3/10/2025):

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I wrote the following in My Comment in the September 21, 2020 post of Dr. Smith's ECG Blog: 

"I wish those cardiologists who continue to strictly adhere to STEMI millimeter criteria would read Dr. Smith’s ECG Blog. IF they don’t — they will continue to overlook obvious OMIs that deserve to undergo prompt cardiac catheterization for optimal care." 

5 years later (now in 2025) — the problem remains.

• The posterior wall of the LV is not directly viewed by any of the 12 leads on a standard ECG. As a result — ST elevation will not be seen in any of the standard 12 leads in an isolated posterior OMI.
• Posterior leads (ie, leads V7, V8, V9) — have been suggested as a way to enhance ECG visualization of the posterior wall. With acute posterior MI — these posterior leads will sometimes manifest ST elevation not seen on the standard 12 leads.
• That said, as we have often emphasized in Dr. Smith's ECG Blog — the amount of ST elevation you are likely to see with posterior leads in acute posterior MI is limited. As a result, the diagnostic utility of posterior leads is limited (See My Comment in the September 21, 2022 post).
• Most of the time when there is acute posterior OMI — there will be associated acute inferior and/or lateral MI. But when the OMI is isolated to the posterior wall — there simply won't be any ST elevation in any of the standard leads.

Among the problems in today's case were the following:

• Cardiac cath was delayed for nearly 6 hours — because none of the ECGs that were done showed ST elevation. 
• Meanwhile — acute coronary occlusion causing an isolated posterior OMI was not recognized by several providers, including the consulting cardiologist. This, despite the diagnostic initial ECG that was done at the time the patient first arrivd in the ED.
• The initial Troponin came back markedly elevated — but because there was no ST elevation, the infarction was labeled a NSTEMI. This outdated (useless) term ignores the clinical reality that many acute coronary occlusions do not manifest ST elevation.
• And, because the concept that acute coronary occlusion causing isolated posterior OMI is readily recognized by ST depression that is maximal in leads V2,V3,V4 — when cath was finally done, it was performed on the wrong coronary artery (whereas ECG recognition of isolated posterior OMI on the initial ECG immediately pointed to the LCx system as the "culprit" artery — as is shown below in Figure-3).

As I lamented in 2020 — Rather than taking the extra time to obtain another ECG with posterior leads (that at best — provides limited information) — I favor GETTING GOOD at using the Mirror Test as an aid for recognizing acute posterior MI.

• The Mirror Test is a simple visual aid: It helps the clinician recognize acute posterior infarction. It is based on the premise that the anterior leads provide a mirror image of electrical activity in the posterior wall. By simply inverting a standard 12-lead ECG, and then holding it up to the light — you can easily visualize the “mirror-image” of leads V1, V2, V3 (See Figure-2 below).
• I’ve previously discussed application of the Mirror Test on many occasions (in My Comment at the bottom of the September 13, 2020 post and the February 16, 2019 post, among others).
• In Figure-1 — I apply the Mirror Test to leads V2,V3 in today's initial ECG. As shown in the mirror-image RED insert — Isn't it now obvious that there is acute coronary occlusion causing isolated posterior OMI?

Figure-1: Application of the Mirror Test to leads V2,V3 in today's initial ECG.

Figure-2: Illustration of the rational for the Mirror Test (Figure excerpted from Grauer K: ECG-2014 Pocket Brain ePub).

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In Figure-3 — We see the rationale for anatomic localization of the "culprit" artery to either a non-dominant LCx or an Obtuse Marginal branch of the LCx — when there is isolated posterior OMI.

Figure-3: KEY points in the recognition of isolated posterior MI (adapted from my ECG-2014-ePub — with addition of Figure from Vince DiGiulio).