Sometimes a patient is fortunate to have a cardiac arrest

Written by Pendell Meyers 

A man in his 60s presented with acute chest pain.

Here is his triage ECG:

What do you think?

There is sinus rhythm with clear LVH. Leads V5-6 are suspicious for upright, enlarged T waves that are possibly inappropriate for the QRS complex, especially V6. But without a baseline for comparison, it would be difficult for me to say that it is specific and diagnostic for OMI. The Queen of Hearts agrees, calling the ECG not specific for OMI.

Smith comment: V6 is very atypical for LVH and very suspicious for OMI.  There is a very high voltage R-wave without any S-wave (terminal QRS distortion) and with a concordant ST segment and T-wave, with convex ST segment.  It is essential to compare with old ECGs.  In the absence of old ECGs, one must record serial ECGs every 15 minutes.

He had several older ECGs on file, here are two examples:

6 days prior:

2 months prior:

In the context of ACS symptoms, and when able to compare the new vs. old ECG, the top ECG is DIAGNOSTIC of OMI until proven otherwise. 

Unfortunately, the ECG was interpreted as no significant change from prior, "no STEMI"!!

He was sent back to the waiting room, where he suffered a VF arrest. Defibrillation was performed, and ROSC was achieved. 

Approximately 5 minutes after ROSC, this ECG was obtained (about 45 minutes after arrival):

Obvious anterolateral OMI, and STEMI criteria positive for those who care or need it.

Smith comment: The patient was lucky to have a cardiac arrest.  Had he not had one, he would have sat in the waiting room until his entire myocardium at risk infarcted.  By undergoing an arrest, providers became aware of his OMI which had not been noticed on his diagnostic ECG, and he thus has a chance at some myocardial salvage.

Also: notice how the LAD Occlusion results in DECREASED S-wave amplitude, compared to the previous ECGs, in V2 and V3.  I have noticed that this nearly always happens, and is the reason that you rarely find an ECG that shows BOTH LVH with high right precordial amplitudes AND acute STEMI/OMI.

Total proximal LAD occlusion was found and stented at angiography soon after the ECG above. Here are some images:

Next morning ECG:

Reperfusion findings are clear..

There is some R-wave preservation, a good sign that some myocardium remains viable

Echocardiogram:

EF 15%

Severe global hypokinesis

Akinesis of basal-mid inferior and inferoseptal myocardium

Severe hypokinesis to akinesis of apical anteroseptal, anterior, and inferoseptal myocardium

An echo from 3 months ago showed an EF of 40% with global mild hypokinesis, without focal wall motion abnormalities.

Smith comment: the initial echo was so bad because even myocardium that was salvaged was "stunned" and it takes time to recover function.  Weeks later, the EF improved from 15% to 40%.  If this patient had not had ventricular fibrillation and thus not had a reasonably short door to balloon time, all of that stunned myocardium would instead be permanently infarcted, with permanent 15% EF.

Troponin I quickly exceeded the laboratory limit of reporting at 25,000 ng/L.

4 days later:

Continued reperfusion.

He was discharged home, but quickly bounced back 4 times within the next few months for worsening heart failure. Long term outcome is not available.

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MY Comment, by KEN GRAUER, MD (2/2/2025):

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We need to learn from cases like today's. Today's initial ECG is not an easy tracing to interpret. This is because (as per Dr. Meyers) — there is obvious LVH that complicates assessment for potential acute ST-T wave abnormalities.

• To Emphasize: Once again — the history is KEY. This patient is a man in his 60s who presented to the ED with new CP. As a result — without yet looking at the initial ECG, our "mindset" has-to-be awareness that this history alone places this patient in a higher risk category for having an acute cardiac event. 
• As a result — Our "mindset" has-to-be that we need to rule out an acute event, rather than the other way around. This means that if there is any uncertainty about the diagnosis (or about the initial ECG) — that we need to "dig further" until we arrive at more certainty in our diagnosis. Unfortunately, this was not done in today's case. I say this — because compared to an ECG done just 6 days earlier — there clearly has been significant ST-T wave change, that in this patient who presents to the ED with new CP — has-to-be recogized as an acute OMI until proven otherwise (See Figure-1 below — in which I place these first 2 tracings in today's case together).

What Are the Oversights?

In my experience — many (if not most) clinicians do not compare serial ECGs by placing both ECGs that they are looking at side-by-side.

• I fully acknowledge that I miss important findings when I do not do this. I know this was not done in today's case — because if side-by-side comparison had been done — then the difference in ST-T wave appearance between leads V4,V5,V6 in ECG #1 and ECG #2 would not have gone unnoticed. 
• We have often remarked on the challenge that LVH may pose for recognizing acute ischemic changes. This is because LV "strain" often manifests straightened and elevated ST segments in anterior leads with deep S waves from marked LVH. For example, as an isolated finding — I would not necessarily interpret the ST segment straightening and elevation that we see in leads V2,V3 of ECG #1 (outlined in RED and light BLUE) as abnormal in a patient with marked LVH.
• The other challenge posed by the ECG of a patient with marked LVH with "strain" — is distinguishing between the ST-T wave inversion in one or more lateral leads due solely to LVH — vs that due to acute ischemia or infarction. This distinction is further complicated because marked LVH may at times mask the ST-T wave changes of acute ischemia. That said — the asymmetric ST-T wave depression in lead V6 of ECG #2 is classic for the ECG appearance of LV "stain". But 6 days later (ie, when ECG #1 was recorded) — there is not even a hint of ST flattening or depression in leads V4,V5,V6. This means that the ST-T wave appearance in ECG #1 clearly represents an acute change (compared to ECG #2) that would not be missed if there had been lead-to-lead comparison between these 2 tracings.

Figure-1: Comparison between today's initial ECG — with a prior ECG done just 6 days earlier.

How to Remember ECG Findings of LVH and LV "Strain"?

There are over 50 criteria in the literature for the ECG diagnosis of LVH. And — the ST-T wave appearance of LV "Strain" and "Strain Equivalents" is subjective, and can be confusing.

• To facilitate recall of these concepts — We've conveniently added a link in the menu at the top of every page in Dr. Smith's ECG Blog that takes you to My Comment in the June 20, 2020 post, in which I review a user-friendly approach to ECG recognition of LVH and "Strain" (See Figure-2).

Figure-2: Handy link to LVH Criteria (conveniently placed in the menu at the top of every page in Dr. Smith's ECG Blog).

WHY then is Today's Initial ECG So Difficult to Interpret?

The above said — I still found today's ECG incredibly difficult to interpret for the simple reason that there is marked overlap of QRS complexes in virtually all of the chest leads.

• Confession: I spent over half an hour staring at the QRS complexes in each of the chest leads, trying to distinguish between the limit of R waves from overlapping S waves. I am still not certain that my color-coding in Figure-1 is completely correct.
• KEY Point: Whereas the ST segment straightening and elevation that we see in leads V2 and V3 of ECG #1 does not necessarily look abnormal (because as noted earlier — LV "strain" from marked LVH may show this ST-T wave appearance in anterior leads) — the same is not true for leads V4,V5,V6.
• Lead V4 in ECG #1 (outlined in dark BLUE) — manifests an S wave that is only 13 mm deep. Doesn't the coved and elevated ST segment in this lead look disproportionate and abnormal?
• As noted earlier — LV "Strain" manifests as ST-T wave depression in lateral leads (or at least as ST-T wave flattening). LV "strain" does not manifest as ST segment coving and elevation, as we see in lead V5 and especially in lead V6 of ECG #1.

What Could Have Been Done to Facilitate Interpretation? 

• Rather than normal standardization — I would have immediately repeated today's initial ECG at half-standard voltage. Doing so would have minimized overlap — and facilitated appreciation of disproportionality by clarifying relative size of QRS complexes and ST-T waves.

Another MUST know ECG, and why its notoriety annoys Dr. Smith

Written by Magnus Nossen

The ECG below was obtained from 50-something male with a history of hypertension and tobacco use. The patient contacted the ambulance service after he experienced sudden onset chest pain and diaphoresis that had started 20 minutes prior. The ECG below ECG was recorded on the scene.

What is the cause of the ECG changes here? How will you manage this patient?

ECG #1

The ECG shows sinus rhythm with a narrow QRS complex. The frontal plane axis is about 0 degrees. Heart rate is 85 beats per minute. There are significant and widespread ST-segment and T wave changes. The ST-segment in lead V1 has upward convexity. Throughout the precordium (V2-V6) there is ST depression followed by bulky, hyperacute T waves. 

• This ECG pattern was described by de Winter et. al in 2008, and is eponymously named after the main author. The de Winter ECG pattern (sometimes referred to as de Winter's T-wave pattern) consists of an ST-segment upsloping depression at the J point of 1 to 3 mm in leads V1 to V6, associated with tall, bulky or "hyperacute" T waves. 

The de Winter electrocardiogram pattern is an infrequent presentation, reported to occur in 2% to 3.4% of patients with anterior myocardial infarction (1). Below I have marked the J-point on the limb leads and the precordial leads showing the upsloping ST depression in leads V2-V6. There is a de Winter T- wave pattern also in lead I.

This ECG is diagnostic of a proximal LAD occlusion. This ECG pattern is my favorite example of how the STEMI criteria are fundamentally flawed. I was handed this ECG while caring for another OMI patient, and I immediately recognized this ECG pattern and activated the cath lab. If you have seen this pattern once — the diagnosis is obvious to you. The ECG-to-balloon time was short, only 35minutes. At cath there was a 100% proximal LAD occlusion, which was opened and stented.

• This patient received optimal care. Troponin T peaked at 9378 ng/L. Echocardiography showed septal and apical hypokinesis, with a left ventricular ejection fraction of 35-40%. 
• The hypokinesis was transient. Echocardiography 3 months following the infarct showed a normal ejection fraction of 55% without apparent hypokinesis! 
• Due to the rapid treatment — much myocardium was saved, and the initial hypokinesis was due to myocardial stunning (see below). Peak troponin may be very high following rapid reperfusion. 

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Smith: This is a classic case and well managed, as it should be.  However, I get annoyed by the attention devoted to de Winter's T-waves because they are a TINY minority of subtle hyperacute T-waves that result from LAD Occlusion (LAD OMI).  They are the most recognizable of all the hyperacute T-waves because of the depressed ST takeoff.  This means that the less recognizable HATW are not recognized and so many patients get ignored!  Moreover, de Winter stated that the morphology was "persisent."  First, de Winter T-waves are NOT always persistent (in fact, frequently are not), but, more importantly, the same can be said for standard hyperacute T-waves: they very frequently do not evolve to ST Elevation.  We have a series of 20 TIMI-0 LAD Occlusions that do meet STEMI criteria.  17 have HATW.  None evolved to ST Elevation.  Under Review.

See all the other manifestations of HATW in LAD Occlusion: Ten (10) Examples of Hyperacute T-waves in Lead V2 (a few in V3), due to acute LAD occlusion

In addition, these hyperacute T-waves with a depressed ST takeoff were first described by Soo in 1995, but he gets little credit for that.  De Winter did not reference Soo.  I have referenced Soo 3 times.

Soo CS. Tall precordial T waves with depressed ST take-off: an early sign of acute myocardial infarction? Singapore Med J 1995;36(2):236–7.

 CS Soo, Lecturer and Cardiologist, Department of Medicine, Universiti Malaya, Malaysia
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Myocardial stunning is a state of cardiac dysfunction that can occurs in a portion of myocardium without necrosis after a brief interruption in perfusion. This typically occurs in the setting of a rapidly reperfused coronary artery following a myocardial infarction. In this situation, even after the ischemia is relieved and myocardial blood flow is restored — myocardial contractile function remains impaired for a variable period of time (usually days to a few weeks).

Image reproduced from Kloner, R.A. (2020) 

If you are a regular reader of this blog — this diagnosis will be easy for you, and you will manage this type of patient correctly with immediate revascularization. Unfortunately, for providers not familiar with this type of LAD OMI presentation — the diagnosis will likely be delayed, as will appropriate treatment.

Learning to recognize ECG findings consistent with OMI takes time and practice. Artificial intelligence can assist providers in detecting patients in need of emergent revascularization. The Queen of Hearts was not used in the management of today's patient. Had the AI model been used it would have identified the ECG as OMI with high confidence. Below you can see the QoH interpretation of the initial ECG in today’s case. 

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Two Additional Examples: ECG interpretation is pattern recognition — and pattern recognition takes practice both for humans and AI models. Below I have added ECGs from two other patients. Both cases below show a textbook de Winter ECG pattern. Originally recorded with a paper speed 50mm/sec ECGs — below these ECGs are compressed by 50% on the X-axis to "look" like they where recorded at 25mm/sec.

The above ECG is from man in his 80s with crushing chest pain. This patient suffered V-fib arrest soon after this ECG was recorded. Sadly, he could not be resuscitated. This ECG and patient outcome is a reminder of why it is so important to recognize this ECG pattern. 

• Below is the Queen of heart explainability chart. The overall interpretation was OMI with high confidence.

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This 2nd Example shows the ECG from a 50-year old male with sudden onset typical chest pain. This is another example of the de Winter ECG pattern. At cath there was a subtotally thrombotic occlusion of a proximal LAD with TIMI 2 flow. Peak troponin T 5933 ng/L.

Again I have added the QoH explainability feature below. Overall interpretation was OMI high confidence. 

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Discussion: The de Winter ECG pattern is seen in about two percent of patients with LAD OMI. The pattern is mostly described with LAD OMI, but has been reported in other coronary distributions as well. This ECG pattern is seen in the acute phase of OMI and it these patients need to be taken immediately to the cath lab or, if primary PCI is not available they should be given thrombolytic therapy as a conventional STEMI. 

It was previously thought that the de Winter ECG pattern represents ECG changes when there is a minimal trickle of blood reaching the downstream myocardium. However, many patients with de Winter ECG pattern have TIMI 0 at angiography and the ECG pattern does not necessarily progress to STEMI.

See this page for more ECG cases involving de Winters pattern

Learning points:

• The de Winter ECG pattern may remain unchanged never developing to STEMI. 
• Time is myocardium and prompt revascularization improves patient outcomes.
• Transient ischemia may lead to "stunning". Stunned myocardium will regain its function after a period of days to weeks.

References: 

Kloner, R. A. (2020). Stunned and hibernating myocardium: Where are we nearly 4 decades later? Journal of the American Heart Association

Vilela, E. M., & Braga, J. P. (2024, January 31). The de Winter ECG Pattern. StatPearls - NCBI Bookshelf

De Winter, R. J., Verouden, N. J. W., Wellens, H. J. J., & Wilde, A. a. M. (2008). A new ECG sign of proximal LAD occlusion. New England Journal of Medicine.. 

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MY Comment, by KEN GRAUER, MD (1/26/2025):

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"Some patients read the textbook. Others don't". I offer this quote as my reflection on today's case. The 50-something year old man presented by Dr. Nossen certainly "read the textbook" regarding deWinter T waves in the initial ECG from today's case.

From the original description by deWinter et al (N Engl J Med 359:2071-2073, 2008) — There is a “new ECG pattern” without ST elevation that signifies acute occlusion of the proximal LAD (Left Anterior Descending) coronary artery.

• The authors recognized this pattern in ~2% of patients with acute anterior MI (ie, in 30/1532 patients studied). Cardiac cath confirmed LAD occlusion in all cases — with ~50% of patients having a "wraparound" LAD. Left mainstem occlusion was not present.
• This was the authors’ original description of the new ECG pattern: “Instead of the signature ST-segment elevation — the ST segment showed 1-3 mm of upsloping ST depression at the J point in leads V1-to-V6 — that continued into tall, positive symmetrical T waves”.
• The QRS complex was usually not widened (or no more than minimally widened).
• Most patients also manifested 1-2 mm of ST elevation in lead aVR. 

In their original 2008 manuscript — deWinter et al went on to describe the following additional features:

• “Although tall, symmetrical T waves have been recognized as a transient early feature that changes into overt ST elevation in the precordial leads — in this group of patients, this new pattern was static, persisting from time of the 1st ECG until the pre-cath ECG.”
• Hyperkalemia was not a contributing factor to this ECG pattern (ie, Serum K+ levels on admission were normal for these patients).   

 

NOTE: Technically speaking — the deWinter T wave pattern as described in 2008 by deWinter et al differs from the finding of simple "hyperacute" anterior T waves — because ECG findings with a strict deWinter T wave pattern persist for an hour or more until the "culprit" LAD vessel has been reperfused.

• As suggested from the 8 example ECGs taken from the deWinter manuscript (labeled A-thru-H, as shown in Figure-1) — there should be involvement in all 6 chest leads with the strict deWinter pattern, with most leads showing several mm of upsloping J-point ST depression and giant T waves.

Figure-1: Comparison of ECG findings in today's case (LEFT panel) — with the deWinter T Wave Pattern, as first described by Robbert J. de Winter et al (N Engl J Med 359:2071-2073, 2008). ECGs for the 8 patients shown here from the original deWinter manuscript (labeled A-thru-H ) — were obtained between 26 and 141 minutes after the onset of symptoms.
=  =  =  =  =
NOTE: I have corrected in Figure-1 for an error that I believe was made by the authors in their original manuscript ( = Leads I and aVL were switched in Patient C in the original manuscript from what I show above. That original mounting of those 2 leads would make for an impossible frontal plane axis and unlikely ST-T wave picture. I believe what shows above in my Figure-1 is now correct).

Today's Patient "Read" the Textbook ... 

• The initial ECG from today's patient clearly manifests the "Can't Miss!" typical deWinter T wave picture of marked, upsloping J-point ST depression — that continues into tall, positive symmetric T waves (seen here in 5/6 chest leads — with coved ST elevation in the remaining chest lead V1). 
• And, as if to say, "Don't dare delay my PCI!" — there is also the "Can't Miss" picture of marked reciprocal ST depression in the inferior leads.

Is Inferior Lead ST Depression a Part of deWinter T Waves?

For as many cases as I have seen of this entity — I had to go back and look at the representative figure from the original manuscript to answer this question.

• The ANSWER: As shown in Figure-1 — 6/8 of the representative ECGs from the original manuscript manifest inferior lead reciprocal ST depression in association with the deWinter T wave pattern in the chest leads.
• The 2 representative ECGs that did not manifest reciprocal ST depression are from Patient B and Patient E. On the contrary — T waves in the ECGs from these 2 patients were prominently upright (perhaps with the slightest amount of ST depression in a couple of leads).
• Bottom Line: While common to see inferior lead reciprocal ST depression with deWinter T waves — this is not an invariable finding.

Additional Observations from Figure-1:

• The original manuscript notes that most patients in their study of deWinter T waves had ST elevation in lead aVR. This is seen in all 8 representative ECGs in Figure-1.
• Finally — I found the variable ST-T wave picture in lead aVL highly interesting. One of my "Go To" leads when assessing for the likelihood of proximal LAD occlusion — is to look for ST elevation in lead aVL. Yet among the 8 representative ECGs in Figure-1 — the ST-T wave picture in lead aVL ranged from hyperacute ST elevation (in A and C) — to a flat ST-T wave (in E) — to T wave inversion (in B and H).
• Bottom Line: Even among these 8 "representative" tracings (from the 30 patients identified as manifesting deWinter T waves) — there is variability in the ECG picture of this entity.

New Observations regarding deWinter T Waves:

The "good news" — deWinter T waves are now accepted as a "STEMI Equivalent", even when there is no ST elevation (Ricci, Smith, et al — Ann Emerg Med, 2025 in Press). Emergency angiography is needed and indicated for this ECG pattern.

• This Ricci, Smith et al manuscript add that deWinter T waves, "are in fact just a small but more easily recognized subset of hyperacute T waves" — and that most such patients with hyperacute T waves do not manifest the originally described deWinter T wave feature of a depressed ST segment takeoff.
• Finally, Ricci, Smith et al acknowledge that while deWinter T waves were initially described as indication of acute coronary occlusion in the LAD distribution — that the deWinter T wave pattern may occur in any coronary distribution!
• 
  
• Grauer Note: Having now observed literally hundreds of cases in numerous international ECG-internet Forums of deWinter-like T waves in patients with new cardiac symptoms — many (if not most) of these cases do not fit the strict original definition of "deWinter T waves" — in that fewer than all 6 chest leads are often involved — J-point ST depression is often minimal (if present at all) in many of the chest leads — and, the number of leads that manifest giant T waves is limited.
• In addition — ECG changes in many of the cases I have observed are not “static” until reperfusion (as had been initially reported in 2008 by deWinter et al.). Neveretheless, cath follow-up has routinely confirmed LAD occlusion in almost all cases.
• My Impression: In large part, the ECG findings seen depend greatly on when during the ongoing process of acute coronary occlusion the ECG is taken. 
• Finally — hyperacute T waves with similar clinical implications as strictly defined deWinter T waves — appear to be a much more frequent occurence among patients with acute anterior OMI, than the 2% incidence initially cited by the deWinter group authors in their original manuscript.
• 
  
• Sobering Closing Note: Although the word is spreading that the deWinter T wave pattern is a STEMI-equivalent that merits prompt cath with PCI — all-too-many interventionists still deny (and delay) this initial treatment "because STEMI-criteria are not met". This needs to change. 

A 34 yo Man with chest pain and Zero ST Elevation

Written by Hans Helseth

A 34 year old man with no known medical history presented to the ED after an hour of chest pain. He described the pain as a mid sternal "burning sensation" and rated it 8.5 out of 10 at onset, but on presentation to the ED, reported that the pain had improved to 4.5. His first EKG is shown below, with a lead II rhythm strip:

EKG 1, 1645

A provisder who is looking for STEMI would not see much in this EKG. 

Despite zero ST elevation, however, the T waves in the inferior leads are symmetrical and large in proportion to their QRS complexes. This is the classic morphology of hyperacute T waves. This EKG coupled with the patient's story is highly suggestive if not diagnostic of inferior OMI.

I interpret this as manifesting active inferior OMI, although the patient's improving pain suggests at least some reperfusion. It is possible that the T waves in this EKG are of an intermediate morphology between full-blown STEMI and inferior reperfusion. It is also possible for hyperacute T waves to remain somewhat stable during either a sustained period of occlusion or partial reperfusion.

Here is the interpretation of the PMCardio Queen of Hearts AI Model:

Smith: The Queen does not know if the patient has active pain, resolving pain, or pain completely gone.  Although to me this is diagnostic of Acute ACTIVE Inferior OMI, I think the Queen says "reperfused" OMI because she thinks that there are reperfusion T-waves in aVL, with reciprocally hyperacute upright inferior T-waves.

Nevertheless, as you can see, she recommends cath lab activation if there are ongoing symptoms.  Patient has 4.5/10 chest pain.  So he needs the cath lab.

Case Continued

This EKG was interpreted as normal by the clinicians overseeing this patient's care.

A high sensitivity troponin I resulted at 336 ng/L (Upper limit: 76) after which the clinical suspicion changed from reflux/gastritis to "NSTEMI". The patient was given nitroglycerin, but his blood pressure dropped to 70 systolic, he became dizzy, and he still had chest pain. An EKG was repeated about an hour after the first:

EKG 2, 1745

The inferior T waves have inflated tremendously. 

A small amount ST elevation has developed, although still not enough to meet STEMI criteria. There is also diagnostic evidence of posterior OMI in V2 and lateral OMI in V6.

Cardiology was consulted at a PCI-capable hospital. The cardiologist agreed to accept the patient for transfer, but did not accept the patient for direct admission to the cath lab because the EKG was not felt to represent "STEMI".

Smith: This was a cardiologist who made this statement!!!  Hans has not even been to medical school.  

One's training has NOTHING to do with one's OMI ECG interpretation skills.

The QoH now correctly sees active OMI:

A CT scan to rule out aortic dissection was performed (Smith: why???) before transferring the patient to the cath facility. It was without evidence of dissection. When the patient finally arrived to the PCI-capable hospital, his pain had reportedly improved, but not resolved. Another EKG, shown with a V1 rhythm strip, was recorded in the emergency department:

EKG 3, 1930

There appears again to be some reperfusion since the last EKG, as the T waves in inferior leads have deflated slightly. The Q waves in the inferior leads have deepened. 

This EKG was interpreted as showing "T wave inversion in aVL, otherwise no significant ST elevation or depression." 

The patient waited another three hours in the ED until the cath lab was ready to accept him.

6 hours after his initial presentation, he went to the cath lab:

There is a filling defect consistent with thrombus in the distal RCA. There was TIMI 2 flow distal to the thrombotic occlusion. The thrombus was aspirated and the distal RCA was stented. 

The rest of the patient's hospital stay was uneventful. A formal echo the next day showed an estimated EF of 55-60% with no definite regional WMA.

Learning Points:

• Hyperacute T waves can be present for a long period of time, especially if serial EKGs are not recorded frequently enough to observe their evolution.
• Hyperacute T-waves frequently NEVER progress to diagnostic ST Elevation
• Patients with ACS and pain refractory to anti-ischemic therapy should be sent emergently for catheterization, regardless of the ECG.
• Some OMI have zero ST elevation
• OMI can happen in young patients with no known medical history

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MY Comment, by KEN GRAUER, MD (1/28/2025):  

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There is a lot to be learned from today's post. In Figure-1 — I facilitate comparison of the 3 ECGs in today's case by putting them together.

• Although tempting to seek false reassurance from the relatively young age (34yo) of today's previously healthy patient — the history of new CP (Chest Pain) lasting an hour of sufficient severity to prompt an ED visit does place this patient in a higher risk category, pending other factors.

As per Hans Helseth — the initial ECG is clearly worrisome:

• My "eye" was immediately drawn to the inferior leads (within the RED rectangles) — each of which show disproportionately enlarged T waves that exceed R wave amplitude in the same lead (The huge T wave in lead aVF literally dwarfs the tiny QRS in this lead). In a patient with cardiac-sounding CP — T waves that are clearly taller-than-they-should-be — "fatter"-at-their-peak and wider-at-their-base than expected — have to be interpreted as hyperacute T waves until proven otherwise.
• Removal of any doubt that these inferior lead ST-T wave changes are significant — is forthcoming from the abnormal ST segment coving and surprisingly deep T wave inversion in lead aVL ( = reciprocal ST-T wave change). 
• NOTE: The T wave in lead aVL may at times be normally inverted. The physiologic reason for this finding — is that the T wave axis in the limb leads generally follows the QRS axis. As a result: i) The QRS complex will typically be predominantly negative in lead aVL when T wave inversion is benign; — ii) The ST segment in this lead should not be coved; — and, iii) The appearance of the inverted T wave should not be nearly as "bulky" as it appears to be in Figure-1.
• Impression: In this patient with new CP — ST-T wave findings in these 4 limb leads are diagnostic of acute inferior OMI until proven otherwise. 

Other findings in ECG #1 are more subtle. 

• There appears to be an IRBBB (Incomplete Right Bundle Branch Block) pattern in the form of an rsr' in lead V1 with terminal S waves in lateral leads I and V6. That said — typical IRBBB should not manifest ST segment coving with slight ST elevation in lead V1 (BLUE arrow in lead V1). Instead — there should be slight ST depression in association with IRBBB. In this patient with suspected inferior OMI — this raises suspicion of acute RV involvement.
• The ST-T wave in leads V2 and V3 normally manifest gently upsloping, slight ST elevation in leads V2,V3. Although the ST-T wave in lead V3 looks unremarkable in ECG #1 — the ST segment in lead V2 is isoelectric with a suggestion of ST segment flattening. In addition, the R wave in lead V2 is significantly taller-than-expected (given the tiny r wave in neighboring lead V1) — which in a patient with suspected inferior OMI — raises suspicion of associated posterior OMI.
• Finally, while not taller than the R wave in the same lead — the peak of the T wave in lead V6 appears "fatter"-than-expected — which in this patient with suspected inferior OMI, suggests this is a hyperacute T wave.
• 
  
• To Emphasize: These findings in leads V1,V2 and V6 of ECG #1 are subtle — and in isolation would be nondiagnostic. But in the setting of a patient with new CP and suspected acute inferior OMI — these findings add concern for an acute evolving event. The cath lab should be activated.
• At the least — ECG #1 should be repeated within 15-20 minutes after the initial tracing.
• Failing that — return of the initial significantly elevated Troponin value given new CP and this abnormal ECG should have sufficed for activation the cath lab.

NOTE: This patient's BP dropped to 70 systolic on receiving NTG. He continued to have CP.

• In a patient with suspected inferior OMI — a marked hypotensive response to NTG strongly suggests acute RV involvement.
• Right-sided chest leads should be obtained to assess for acute RV MI, especially given suggestion of ST segment coving with slight elevation in lead V1.

The repeat ECG is the MIDDLE tracing in Figure-1:

• As per Hans Helseth — the inferior T waves in ECG #2 appear even more hypervoluminous than they were ECG #1. In addition — there are now Q waves in leads III and aVF — whereas there previously was an rSRs complex in ECG #1 in these leads.
• Support that the increase in inferior lead T wave hyperacuity is real — is forthcoming from the deeper T wave inversion in lead aVL of ECG #2, along with subtle-but-new ST depression in lead I. 
• There has been little change in the chest leads.
• KEY Point: It would be easy to miss these subtle-but-real changes in limb lead ST-T wave appearance in the repeat ECG if these 2 tracings were looked at separately. This highlights the importance of putting both tracings you are looking at together — and comparing both tracings lead-by-lead.
• The fact that this patient still has ongoing CP — and now demonstrates "dynamic" ST-T wave changes compared to the initial ECG is but one more indication of the need for prompt cath.

As noted by Hans Helseth — the patient was finally transferred to a PCI-capable facility.

• Cardiac cath was delayed a number of additional hours because, "the ECG did not show a STEMI". This unfortunately is faulty reasoning. As per Dr. Smith (See his comments in the January 24, 2025 post, among many other cases on Dr. Smith's ECG Blog): i) Up to 40% of OMIs do not meet STEMI criteria despite TIMI-0 flow. Delay in reperfusion of such patients by as little as 1-2 hours may reduce potential benefit from myocardial salvage by as much as 50%; — and, ii) The findings of new and now ongoing CP in association with localized hyperacute T waves — and now with "dynamic" ST-T wave changes is diagnostic of an acute ongoing cardiac event — especially in association with already significant Troponin elevation.

The 3rd ECG in today's case was obtained on arrival at the PCI center — and is the BOTTOM tracing in Figure-1. 

• Although there is not a lot of ST-T wave change since ECG #2 — what is new (and what once again is BEST noticed by comparing serial tracings when put next to each other) — is a significat increase in heart rate. While not quite "tachycardia" (ie, the rate in ECG #3 is ~90/minute) — in association with evidence of ongoing CP and acute infero-postero-lateral OMI, possibly with RV involvement — a significant increase in heart rate should prompt reassessment to ensure that the patient is not developing shock.

Figure-1: Comparison of the 3 ECGs in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).