Sometimes even ST Elevation meeting criteria is not enough to be convincing

Written by Emre Aslanger.  Emre is a new Editor of the Blog.  He is an interventionalist in Turkey.

A 50 something-year-old man with a history of newly diagnosed hypertension and diabetes, for which he did not take any medication, presented a non-PCI-capable center with a vague, but central chest pain. His vitals were normal and his first ECG was as shown below:

There is obvious ST segment elevation (STE) in anterior leads. STE in lead I and II are more subtle. The presence of J notch in V6 might have deceived the physician into thinking of early repolarization, but this can also be seen in anterior OMI. Note that QRS amplitudes are somewhat lower than expected and there is poor R wave progression. Add to these the slight reciprocal ST depression in lead III and aVF. 

   

There are tall and peaked T waves in anterior leads. Hyperacute T waves are generally described as such in many textbooks, but actually the majority of hyperacute T waves are “bulky” rather than being “peaked”, this is an example just happens to be both. Also not only the bulk of the T wave does matter, but also its proportion to the corresponding QRS complex is important. You can find many examples on this blog attesting that. Here, for example, T waves in lead II and aVF looks out of proportion to their respective QRS complexes in isolation.

 

Is this a subtle ECG ? I am sure that it is not for the readers of this blog. But I frequently witness that the diagnosis of OMI, especially anterior OMI, becomes much harder when there is no clear (although we have subtle ones here) reciprocal changes. This was a clearly diagnostic ECG that makes me think of a proximal left anterior descending artery (LAD) occlusion. 

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Smith: 

--Lead III is another giveaway.  You would not see this ST depression with a down-up T-wave in normal variant ST Elevation.

--How about the Formula for differentiating normal STE from Anterior OMI?

We do not see the computerized QTcB, but I measure it at 426 ms

RAV4 = 5.5 mm, QRSV2 = 12.5; STE60V3 = 3.5 mm

Formula = 22.51, all but diagnostic of LAD occlusion 

Dr. Aslanger performed the external validation of the formula. Full text here:

A tale of two formulas: Differentiation of subtle anterior MI from benign ST segment elevation

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This ECG was at 14:52. 

It is understood that the attending physician thought this ECG might have been more likely to be compatible with ‘early repolarization’ in the context of atypical chest pain and he ordered a hsTnT test, which turned out to be negative (11 ng/L, normal <14 ng/L). A second ECG was taken at 15:16.

If the first ECG was not diagnostic, the change between these two should have been. This is also a clear ECG for the readers of this blog, but may be hard for someone who is not used to seeing non-mainstream ECGs. There is STE in inferior leads now (The unfortunate thing about these leads is the conventional naming that labels them as inferior, which could not be more misleading in electrophysiological terms. See bibliography). STE in inferior leads is a frequent finding in distal LAD occlusions (not necessarily in “wraparound” LADs, which is already more or less a finding for many LADs that you will find if you look for), because apically directed ST segment vector is not pulled upwards by more dominant basal anterior segments. This is a bad ST vector orientation, because it causes widespread STE and one of the most important mistakes that needs to be avoided here is thinking of the diagnosis of pericarditis. 

Look at the STE in lead II, aVF. They are so out of proportion to their respective QRS complexes so that they are diagnostic even by themselves. Such an out-of-proportion STE is virtually never seen in pericarditis. Also note poor anterior R wave progression, again this is not a feature of pericarditis. I don’t even mention about the dynamic change between two ECGs. Also note how hyperacute T waves of proximal occlusion pattern changed into an apicolateral one. This ECG series shows many different examples of the findings bearing the same title. 

But why did the proximal LAD OMI pattern change into a distal LAD OMI pattern here ? Wait for the angiogram.  

With the false reassurance of negative troponin, confusing changes on ECG and atypical chest pain, a third ECG was taken much later (which was similar to the fourth taken at our institution, see below), at 17:40. I don’t know the reason why it took so long, but a second troponin turned out to be positive by then and the patient was referred to our hospital for “emergency PCI”. 

He arrived to our hospital one hour later. The ECG in ER is shown below:

ECG is still diagnostic but we are watching the natural course of myocardial infarction here. I have trouble understanding the chain of events that resulted in the unacceptable delay and cost the patient’s anterior wall.

Here is the angiogram: 

There is a thrombotic ostial LAD lesion in addition to widespread atherosclerotic involvement, fortunately reperfused by itself. You may see a filling defect in distal LAD, most probably due to an embolization from proximal lesion. Also note that LAD does not extensively wrap-around apex and supply inferior wall. The lesion was successfully stented, but it was unfortunately done after a significant myocardial loss. 

Fortunately, peak troponin was only 1090 ng/L and next day EF was 45-50% with apical and mid anterior hypokinesia. The patient was (and we, his caregivers were)  really lucky to get away with such a limited damage.        

Take home messages:

• Any coronary occlusion may present with vague symptoms, but when ECG is clear, there should not be any suspicion. ECG hardly ever tells lies! Many times it is more prudent to count on ECG than the patient’s history.
• Troponin can never compensate your limited ECG reading skills or the complete lack thereof.
• Anterior OMI may, and frequently does, present without reciprocal changes.  
• The leads showing STE should not be assumed to be the ones overlying the infarcting segments. It is all about the orientation of ST vector. Because of it the occlusion pattern on ECG may change during the course of OMI.
• Despite a prolonged ECG findings, the damage can rarely be less than expected, due to spontaneous open-and-close cycles, ischemic preconditioning, and the presence of collaterals.

References 

1. Aslanger EK. Considerations on the naming of myocardial infarctions. J Electrocardiol. 2022 Mar-Apr;71:44-46. doi: 10.1016/j.jelectrocard.2022.01.006. Epub 2022 Jan 31. PMID: 35124348.
2. Bozbeyoğlu E, Yıldırımtürk Ö, Aslanger E, Şimşek B, Karabay CY, Özveren O, Değertekin MM. Is the inferior ST-segment elevation in anterior myocardial infarction reliable in prediction of wrap-around left anterior descending artery occlusion? Anatol J Cardiol. 2019 Apr;21(5):253-258. doi: 10.14744/AnatolJCardiol.2019.09465. PMID: 31062754; PMCID: PMC6528511.
3. Aslanger EK, Meyers HP, Smith SW. Recognizing electrocardiographically subtle occlusion myocardial infarction and differentiating it from mimics: Ten steps to or away from cath lab. Turk Kardiyol Dern Ars. 2021 Sep;49(6):488-500. doi: 10.5543/tkda.2021.21026. PMID: 34523597.

 

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MY Comment by KEN GRAUER, MD (11/13/2022):

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Highly interesting case by Emre Aslanger. Among the important points brought out by Dr. Aslanger's discussion are the following: 

• Despite the history of a "vague" type of chest pain and negative initial troponin — extensive infarction nevertheless occurred.
• Anterior OMI is not always accompanied by inferior lead reciprocal changes (Many cases on Dr. Smith's Blog show this same phenomenon).
• ST elevation in both anterior and inferior leads does not necessarily indicate an LAD "wraparound" lesion (Bozbeyoğlu reference documenting this cited by Dr. Aslanger below — with Dr. Aslanger as one of the co-authors).
• The "occlusion pattern" on ECG may change during the course of evolution (in today's case — from a proximal LAD OMI to a more distal LAD OMI pattern, presumably due to embolization from a proximal lesion).
• Extensive atherosclerotic involvement (with multi-vessel disease) — may produce confounding changes on ECG. 
• Spontaneous "open-and-close" cycles of the "culprit" artery may similarly produce confounding ECG changes — with an unpredictable picture of how much myocardial damage is ultimately produced (Many cases of this same phenomenon on Dr. Smith's ECG Blog).

I focus my comment on one additional aspect that led to confounding ECG changes in today's case.

• I initially suspected LA-LL Lead Reversal in the first 2 tracings in today's case. Having been "burned" by this subtle form of lead misplacement on several occasions in the past — my attention was captured by the presence of a P wave in lead I larger than the P wave in lead II. This is virtually never seen with sinus rhythm, given the orientation in the frontal plane of the SA Node with respect to the AV Node.
• 
  
• Alas — I was wrong. There is no lead reversal in today's case. The fact that the P wave in lead I remains larger than the P wave in lead II for all 3 tracings confirms that instead of lead reversal — there is an ectopic atrial rhythm!

I'll add a "shifting" frontal plane axis to the confounding ECG changes seen over the course of the 3 ECGs in today's case (ie, lead aVF evolving from a tiny but isoelectric QRS in ECG #1 — to an all positive QRS in ECG #2 — to a predominantly negative QRS in ECG #3). The explanation for this axis shift brings us back to the series of important findings highlighted by Dr. Aslanger:

• Cardiac cath showed widespread coronary disease (and this may produce confounding ECG findings).
• The infarction that ultimately evolved was extensive! (essentially wiping out all positive forces in the chest leads of the last tracing).
• The "occlusion pattern" on ECG changed during the course of OMI evolution (with resultant frontal plane axis shift and dramatic QRST morphology changes over the course of the 3 tracings).

P.S. — Lead reversals do occur! Prior to my "high intensity exposure" on the internet to confounding ECG pictures worldwide — I didn't realize how common lead reversals are in practice. I suspect this is because clinicians aren't as attuned to looking for them.

• It is usually easy to recognize the most common cause of lead reversal — which is mixup of the LA-RA electrodes. But other forms (especially LA-RA lead reversal) — can be far more subtle, and are easily overlooked.
• 
  
• There was no lead reversal in today's case.
• 
  
• For those interested in examples of Lead Reversal (and HOW to recognize this when it occurs) — Please check out My Comment at the bottom of the page in the August 17, 2022 post in Dr. Smith's ECG Blog. I work through a case of LA-RA lead reversal — and link to 11 other examples of lead reversal that we've published in recent years. 

A woman in her 30s with several days of chest pain and an episode of altered mental status.

Written by Pendell Meyers, reviewed by Smith, Grauer, McLaren

A woman in her early 30s with history of diabetes had 2-3 days of gradual onset nonradiating chest pain with associated nausea, malaise, and shortness of breath. Then she had an "abrupt change in her mental status and became more somnolent and less responsive" at home in front of her family. Her family called EMS, who found the patient awake and alert complaining of worsening chest pain compared to the prior few days.

En route to the ED, they recorded this ECG and transmitted it, asking whether the cath lab should be activated:

What do you think?

There is sinus rhythm at just under 100 bpm. The QRS has high leftward voltage consistent with LVH more than simple healthy young voltage. There is large STE in V1-V3, as well as aVL. There is STD in V5-6, II, III, and aVF. The T waves are questionably hyperacute in V1-V4, but the QRS is also very tall and dramatic. We have very few cases of LVH with large voltage present simultaneously with anterior hyperacute T waves, but the concern is that this could be one of them. A baseline ECG would help greatly (available below).

The subtle LAD OMI vs. normal variant STE formula is not applicable due to the presence of inferior reciprocal STD and lateral STD, and because it was not trained on LVH patients. 

If you had erroneously applied the formula, it would be falsely reassuring due to the large QRS voltage present in this case:

A prior baseline was available (though I doubt it was at hand when EMS asked for a prehospital decision on the ECG above):

Baseline (assuming baseline, no clinical info available) from last year.

With the baseline (just LVH with some normal variant STE), it is obviously easy to see that the initial ECG above is LAD OMI.

Here is her ECG immediately on arrival to the ED:

Obvious STEMI(+) OMI.

An ED echo reportedly showed an anterior wall motion abnormality and grossly depressed EF.

"Given patient's change in mental status, CTA of the chest was ordered to rule out dissection." 

Meyers note: I think CT angio for dissection is unnecessary in this case, as it is in almost all OMI cases. As Jesse McLaren pointed out to me, STEMI or OMI secondary to dissection is very rare (https://pubmed.ncbi.nlm.nih.gov/28511806/), so looking for it in the absence of compelling reasons (eg focal neuro or pulse deficit) will just delay reperfusion (https://pubmed.ncbi.nlm.nih.gov/22534052/).

"While at CT scanner, the patient lost pulses and appeared to have polymorphic VT cardiac arrest, then she achieved immediate ROSC with one defibrillation."

The initial high sensitivity troponin I returned at 34 ng/L.

The CT showed no dissection.

She proceeded to cath where they found total thrombotic proximal LAD occlusion (see images below).

ECG hours after PCI:

Next day ECG:

Troponin peaked at 23,591 ng/L.

Cardiac MRI done 5 days later:

EF 35%. Severe hypokinesis of the entire septum, anterior wall, and distal/apical segments. No LV thrombus. 

Learning Points:

LVH can make OMI interpretation more difficult. It is rare to see high LVH voltage in the same leads as OMI. But this one is an excellent example.

The first troponin is minimal when the benefit of reperfusion is maximal.

Comparison to baseline, and serial ECGs, can make a difficult interpretation easy. 

Sudden syncope or "seizure" in sick patients should be assumed to be cardiac arrest until proven otherwise.

Young people and women have OMI, and like other populations they may have delayed recognition.

OMI always evolves on ECG, if you have the ECGs to see it.

Young Women do suffer from thrombotic coronary occlusion!!

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MY Comment by KEN GRAUER, MD (8/15/2022):

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I saw the initial tracing in today’s case ( = ECG #1) — knowing only that the patient was a woman in her 30s on her way to the ED. I presumed she must have been having chest pain — but didn’t know how worrisome the history was (or was not) for a new cardiac event. I focus my comment on this initial tracing — which for clarity I’ve reproduced below in Figure-1. My thoughts on this initial ECG were the following:

• The rhythm is sinus at ~90-95/minute. Intervals (QR, QRS, QTc) and the frontal plane axis are normal (about +20 degrees).
• QRS amplitudes are greatly increased — especially in the chest leads, where there is significant "lead overlap" of complexes.

Regarding Q-R-S-T Changes:

• There are small and narrow Q waves in lateral leads (I,aVL,V5,V6) — which are almost certain to be normal septal q waves.
• R wave progression is normal (with transition appropriately occurring between leads V2-to-V3).

The KEY Question is whether ST-T wave appearance in ECG #1 is (or is not) suggestive of an acute cardiac event.

Figure-1: The initial ECG in today’s case.

Should the Cath Lab Be Activated?

As emphasized by Dr. Meyers — assessment of the initial ECG in today’s case was complicated by the presence of LVH. It is simply not common to see the picture of markedly increased QRS amplitude, in association with hyperacute T waves in the anterior leads.

• Dr. Meyers also emphasized that on occasion — finding a baseline tracing on the patient for comparison can be diagnostic. This was the case with today’s patient — as a quick comparison with the previous ECG left NO doubt that the chest lead ST-T wave peaking in ECG #1 was a new (and therefore acute) finding. Unfortunately, baseline ECGs are not always available at the time they are needed for initial triage decision-making of whether or not to activate the cath lab. So HOW to proceed?

I’d point out the following.

• There are many ECG criteria for the diagnosis of LVH. I list those that I favor in Figure-2 — and discuss in detail my approach to the ECG diagnosis of LVH at THIS LINK.
• Note addition of the patient’s age to the criteria I suggest in Figure-2. The reason for including age — is that younger adults often manifest increased QRS amplitudes on ECG without true chamber LVH. While there is no universally-agreed-upon discrete “maximal age dividing point” — I’ve found ~35 years of age to work well clinically in my experience over decades.
• 
  
• This number “35” facilitates recall — because, of the 50+ criteria for LVH in the literature — by far the most sensitive and specific criterion in my experience also involves the number “35” (ie, Sum of deepest S in V1 or V2 + tallest R in V5 or V6 ≥35 mm satisfies voltage criteria for LVH in adults ≥35 years of age).
• 
  
• Assessment of LVH in the pediatric population is problematic — because of the difficulty determining reliable diagnostic voltage criteria for each age group (complicated further by technical issues of ensuring precise chest lead electrode placement in these smaller body frame patients). As a result — I routinely refer to tables for assessing maximal expected amplitudes for each specific age group.
• 
  
• To “simplify life” when assessing for LVH in younger adults (ie, patients in their late teens, 20s and early 30s) — I’ve found over the years that reversing the number “35” provides a quick “ballpark” assessment criterion as to whether there is sufficient voltage on the ECG of a younger adult (ie, who is under 35yo) to qualify for “LVH” (ie, Sum of deepest S in V1 or V2 + tallest R in V5 or V6 ≥53 mm).

Figure-2: Criteria I favor for the ECG diagnosis of LVH. (NOTE: I’ve excerpted this Figure from My Comment at the bottom of the page in the June 20, 2020 post in Dr. Smith’s ECG Blog).

Is there Voltage for LVH in Figure-1?

The patient in today’s case was a woman in her 30s — therefore more likely to manifest increased QRS amplitude not necessarily the result of LVH. Given the challenge of confusing “amplitude overlap” in the chest leads of Figure-1 — I clarify the limits of QRS deflections by coloring the complexes in Figure-3.

• Note that even accounting for the fact that today’s patient is a younger adult — the 53 mm criterion threshold is attained, suggesting true voltage for LVH in this younger age group patient.
• 
  
• Remember: The ECG is an imperfect tool to assess LVH. If true chamber size is needed — then an Echo (which also provides information on cardiac function) is far superior to ECG for assessment of chamber enlargement. That said — “pre-ECG interpretation likelihood” for LVH is clearly increased in today’s patient because of longstanding diabetes.

Figure-3: I’ve colored the QRS complex in 5 of the chest leads — to illustrate the actual size of the QRS complex in each of these leads. The deepest S wave is in lead V2 ( = 27 mm, as shown in RED) + the tallest R wave in lead V5 ( = 27 mm, as shown in GREEN) exceeds 53 mm. Note that the S wave in lead V1 is also unusually deep ( = 26 mm) — and the R wave in lead V4 is of unknown amplitude, since it is cut off by the top of the ECG paper (See text).

A Final Look at the ECG in Figure-1:

I fully acknowledge that I was not at all certain from seeing the initial ECG in Figure-1 whether this patient was (or was not) having an acute event. Against an acute event was the following:

• The patient has LVH on ECG — and as we have mentioned, it is uncommon to see hyperacute anterior T waves in association with marked LVH. Among the types of benign repolarization variants is T wave peaking that is often surprisingly tall in anterior leads in which there are deep S waves.
• There is excellent R wave progression — with an extremely tall R wave in lead V3 (R wave amplitude is typically reduced when there is anterior OMI).
• The QTc is at most no more than minimally prolonged (whereas acute infarction often produces significant QTc prolongation).

On the other hand — In Favor of an acute event until proven otherwise are the following:

• Although the patient in today's case is a young adult — this woman in her 30s has diabetes mellitus (presumably for some period of time) — therefore she clearly is at greater risk of myocardial infarction at an earlier age.
• Even accounting for LVH — the T wave in anterior chest leads is taller than is usually expected. This is especially true in lead V3 — where the 15 mm tall T wave is nearly as tall as the R wave in this lead. The "shape" of LV "strain" when seen in anterior leads tends to be the mirror-image opposite of the slow downslope-faster upslope ST depression typically seen in leads V5,V6 with LVH. It would be unusual to see such a tall, pointed T wave with narrow base from LVH as we see in lead V3.
• Neighboring leads V2 and V4 also appear taller and pointier than is usually seen with either LVH or depolarization variants.
• Finally, while the ST-T wave may normally be negative in lead III when the QRS is predominantly negative — there usually is not the J-point depression seen in Figure-3 (RED arrow in lead III).

BOTTOM Line: This young woman in her 30s has diabetes mellitus — and presented with a history of "worsening chest pain". While I was uncertain from her initial ECG if an acute process was ongoing — the worrisome history and questionable ECG features described above combine to clearly merit diagnostic cath to clarify the anatomy.

• To Emphasize: Once the prior ECG became available for comparison — there no longer was any doubt that the ECG findings highlighted above were acute!

What happens when you don't recognize an OMI?

This was sent by an "avid reader."  The case was from his hospital, which does not have a cath lab.

Case

A 60-something male was sent in from a cardiologists' office after presenting there with chest pain.  The office ECG is unavailable.

The pain had been intermittent for a few days, but worse on the day of admission.

Here was the initial ECG:

To me, and to him, this is an obvious acute LAD occlusion.
There are hyperacute T-waves, especially in V2, plus other more subtle findings.
If you use the 4-variable formula:STE60V3 = 2.5
QTc = 398
RAV4 = 3
QRSV2 = 15
Value = 20.28, confirming LAD occlusion (18.2 is the most accurate cutoff).

The Emergency physician and the cardiologist concluded: "No STEMI.  Admit here.  Do not transfer."

At a minimum, this patient needs ECGs recorded every 15 minutes.  This was not done.  The next ECG was recorded 90 minutes later:

Now it is an obvious anterior STEMI.
The ST Elevation even meets "criteria" now.
Why does the computer not diagnose it?

The first troponin I returned at 1.5 ng/mL.  A repeat returned at 2.5 ng/mL.  Still no 3rd ECG recorded.

At this point, the patient developed cardiogenic shock, and another ECG, at 270 minutes (3 hours after the 2nd ECG), was recorded:

Now there is massive ST elevation.
There are multiple PVCs.
There is clear STE in aVL, with inferior reciprocal ST depression.

The patient was transferred by helicopter to a PCI facility.

Cath: "Entire left system occluded." (including left main).  Ejection fraction 10%.  Too ill for CABG surgery.

I do not have further outcome, but his chances of survival are not good.


Learning point:

Do not wait for STEMI if you find an OMI.

We all have much to learn.  Hopefully this physician will learn from this one, so that future similar patients will not be similarly doomed.

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Comment by KEN GRAUER, MD (5/7/2019):

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This tragic case is one to learn from. Unfortunately, those in need of the most learning ( = those close-minded colleagues of the “avid reader” who sent in this case) are the least likely to profit from mistakes made. Dr. Smith has already emphasized many KEY points about this case. 

• I’d add the following thoughts regarding the initial ECG obtained on this 60-something man with new-onset chest pain (Figure-1):

Figure-1: The initial ECG in this case, obtained in the ED on this patient with chest pain. I’ve copied the computerized interpretation of this tracing (See text).

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Thought #1:

• I would wager that the Emergency physician who read the ECG in Figure-1 did not use a Systematic Approach. If he/she did — they would surely have noticed that in addition to lead V2 (which as per Dr. Smith — shows an obviously much-taller-and-fatter-at-its-base-than-it-should-be, therefore hyperacute T wave) — there is NO way that lead V1 can be “normal” in a patient with new-onset chest pain. There is at least 2 mm of ST elevation in lead V1 (RED arrow) — and that is virtually never “normal”.
• There are many systems in use for ECG interpretation. Regardless of whether you use mine, or another one that you prefer — the KEY is to always go through each of the essential parameters to assess in the identical sequence, so that you never forget to assess them all. This entails looking at each of the 12-leads on the ECG.
• Advantages of Using a Systematic Approach: i) With just a little bit of practice — it will speed up your interpretation! (because you have a step-by-step approach — and will no longer go back-and-forth to reassess things you’ve already looked at); and,  ii) A systematic approach will improve your accuracy (because you no longer leave things out …).

My SYSTEM:  ( — CLICK HERE — )

Beginning with Descriptive Analysis:

• Rate & Rhythm — The rhythm is sinus at ~60/minute. There is one late-cycle PVC ( = the 2nd beat in the tracing).
• Intervals — The PR interval is normal; the QRS complex is not wide; and the QTc is not prolonged.
• Axis — There is a slightly leftward frontal plane axis (the QRS is all positive in lead I — and probably a little more negative than positive in lead aVF).
• Chamber Enlargement — None.
• Q-R-S-T Changes — There is a Q wave in lead aVF. We only see 1 sinus-conducted beat in lead III — and it’s hard to be certain if there is or is not a tiny initial r wave in this lead. There definitely is a small initial r wave in lead II. Otherwise there is a QS complex in lead V1 — but definite precordial lead R waves have formed by V2. R Wave Progression — shows slightly delayed transition (the R becomes taller than the S wave is deep between lead V4-to-V5). ST-T Waves — There are sagging ST segments in each of the inferior leads. The most remarkable finding is the ST elevation in leads V1 and V2 (and probably also a small amount in lead V3) — with T waves that look taller-and-fatter-than-they-should-be given relative amplitude of the QRS complex in leads V1-thru-V4.

Putting this Together in your Clinical Impression:

• The rhythm in Figure-1 is sinus at ~60/minute — there is 1 late-cycle PVC — and, there is evidence of a probable prior inferior MI (ie,a Q in lead aVF [if not also in lead III] — but with inferior lead ST-T waves that do not look acute). Of most concern — there is ST elevation in V1 & V2, and hyperacute T waves in leads V1-thru-V4. Given that this man in his 60s has new-onset chest pain — one has to assume an acute cardiac syndrome (presumed OMI) until you prove otherwise.
• P.S. — QRS complexes are fragmented (at least in leads V4, V5 and V6) — which strongly suggests there is underlying heart disease.

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Thought #2:

• Think “Patterns of Leads”. The experienced interpreter saves time and increases accuracy by “taking in” several leads in a given lead area at the same moment in time. For example, the “theme” in the inferior leads is that there has been prior inferior infarction — even though there is definitely no Q wave for the sinus-conducted beat in lead II. And, the reason I think there is slight ST elevation with a hyperacute T wave in lead V3 — is that there is NO doubt about these findings in neighboring leads V1 and V2. This is why the T wave in the next neighboring lead ( = lead V4) is probably also hyperacute (taller-and-fatter-than-it-should-be given the small QRS complex in V4).

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Thought #3:

• What about the Computerized Interpretation? It is hard to believe that the computer is calling chest lead ST-T waves in Figure-1 “probable early repolarization”. This just goes to show How Wrong the computer can be! But we should never be depending on the computerized interpretation to begin with!
• I happen to like computerized ECG interpretations — because I know how best to use them (CLICK HERE — for My Approach for Using the Computer). I realize many clinicians do not like computerized interpretations. It’s a matter of personal preference and clinical experience with computerized interpretations.
• The BASICS: Never look at the computerized interpretation until after you have made your own independent assessment! In general — the computer is great for calculating rates, axis, and intervals. In my experience — it is terrible for assessing any rhythm other than sinus! The computer usually does OK for assessing normal tracings — but it may overlook certain findings (such as the ST elevation and hyperacute T waves, as well as the prior inferior MI in Figure-1). BOTTOM Line: The computerized report may help by suggesting certain findings that you may not have thought of — BUT — you must always overread what the computer says. IF you disagree with what the computer says — then cross out those parts in the computer report that you disagree with! In this particular case — I suspect that the computer reading of, “probably early repolarization” may have led one or more of the clinicians astray ...