A 40 year old man with chest pain since last night

Written and submitted by Ashley Mogul, with edits by Pendell Meyers and Steve Smith


A man in his 40s with recent smoking cessation but otherwise no known past medical history presented due to chest pain since the previous evening. The pain has been constant and associated with vomiting and diaphoresis. He decided to present the following day when the pain had not stopped.

Here is the presenting ECG (no prior available):

What do you think?

Relevant findings include slight STE in V1 with an upright T-wave, slightly large T-waves in V2-3 (possibly hyperacute if compared to baseline), and slight reciprocal depression in II, III, aVF, V4-V6.


Meyers: This ECG was texted to me with no clinical information, and my response was: "That looks like a very subtle LAD OMI. If clinical picture was anything compatible with ACS I would heart alert it [Ashley and I trained at Stony Brook where we call a "Heart Alert" on a situation/ECG that doesn't meet STEMI criteria but we are nevertheless worried about the need for emergent cath and emergent ACS workup] and get serial ECGs, unless I had access to an identical baseline (not likely in my opinion). Very very subtle one. What happened?"


These findings are very subtle but suspicious for LAD occlusion, as we have seen in many similar (but less difficult) cases on this blog:

A man in his sixties with chest pain at midnight with undetectable troponin

How long would you like to wait for your Occlusion MI to show a STEMI? Sometimes serial ECGs minimizes the delay.

What will you do for this patient transferred to you who is now asymptomatic?

Crushing Chest pain, but the ECG is not obvious; later there is both RBBB and LBBB

35 yo woman with LAD occlusion manifesting with only hyperacute Ts and inferior ST depression, also missed by computer

These findings were not initially recognized. Labs were sent and an initial Troponin I resulted at 2.14 ng/mL. At that time, the patient was given 324 mg ASA and sublingual NTG. Cardiology was called and the patient was taken for urgent catheterization with the time from ED arrival to cath about 1 hour and 45 minutes.

100% proximal LAD thrombotic occlusion with TIMI 0 flow was found and stented with excellent angiographic result and TIMI 3 flow. He also had non-acute CAD of the RCA (50%) and LCX (50%).

Cath images:

Before intervention.

Before intervention with arrows demonstrating the area of occlusion.

After intervention showing the site of prior occlusion.

After intervention.

ECG a few hours later:

Some leads with STD previously have now resolved. The T-wave in lead V1 is no longer upright, with terminal T-wave inversion which is likely due to reperfusion.

Echo showed akinesis of the anteroseptal and anterior walls as well as the apex with an LVEF of 45%. Troponin I elevated to 3.93 ng/mL but was not trended to peak.



Learning Points:

Not all OMI will present as STEMIs. Complete LAD occlusion can be incredibly subtle as in this case. Remember this case and the similar cases (links above) showing this patter of LAD occlusion including subtle STE with upright T-wave in V1-2 with reciprocal STD in lateral and inferior leads. When in doubt, record serial ECGs and watch out for signs of ischemia despite medical management.

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Comment by KEN GRAUER, MD (7/11/2019):

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Our thanks to Drs. Mogul, Meyers and Smith for this illustrative case.

• I focus my attention on the interpretation of the initial ED tracing ( = ECG #1 in Figure-1). Although the ECG findings are challenging — I feel they should not be missed.

Figure-1: The 2 ECGs in this case (See text).

My THOUGHTS on ECG #1 — The patient is a man in his 40s with a history of smoking — who presented with new chest pain that was ongoing through much of the night, and despite associated vomiting and diaphoresis — this patient would not go to the ED until the next day when chest pain persisted.

• This is a higher-prevalence History for acute coronary disease. By this, I mean that the onus is on us to rule out that even subtle ECG changes may be acute — rather than the other way around.

Descriptive Analysis of ECG#1:

• The rhythm is sinus at ~85/minute. The PR, QRS and QTc intervals are normal. The frontal plane axis is normal (about +40 degrees). There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• There are QS complexes in leads V1 and V2. There is notching on the initial part of the downslope of the S wave in lead V2. There may be tiny q waves in lateral chest leads.
• Transition (where the R wave becomes taller than the S wave is deep) occurs between leads V2-to-V3, which is normal. That said — R wave amplitude is minimal until lead V4 ...

The most remarkable finding in ECG #1 relates to the ST-T wave Changes:

• Looking sequentially, first at the 6 limb leads — and then at the 6 chest leads — what immediately caught my eye was that the T wave in lead V2 looked taller-than-it-should-be (that is, disproportionate) given the lack of any r wave in this lead.
• My eye was next “caught” by the appearance of the ST-T wave in lead V3. There is simply NO WAY that the ST-T wave in lead V3 is “normal”. A normal ST-T wave does not have a straight (ledge-like) ST segment as we see in ECG #1, that then abruptly rises to a disproportionately tall T wave (that is 1½ times the height of the R wave in this lead), and which manifests as wide of a T wave base.
• COMMENT: I will emphasize that despite my detailed, written descriptive analysis above — it literally took me less than 5 seconds to arrive at my ST-T wave assessment — and no more than 2-3 seconds more to assess leads V2 and V3. Even without looking at anything else on this ECG — in a patient with worrisome new chest pain, the ST-T wave appearance in lead V3 + the disproportionately tall T wave in neighboring lead V2 is enough (in my opinion), to say that while this may be subtle and we can’t be 100% certain — this patient merits prompt cath.

The more additional leads that we can identify in ECG #1 that show ST-T wave abnormalities — the greater the likelihood that our suspicion for an acute cardiac event (based on this history + the ST-T wave appearance in leads V2 and V3) is correct:

• The ST-T wave in neighboring lead V1 of ECG #1 is abnormal. It is not normal to see ≥1.5 mm of ST elevation in lead V1 — and, given the ST-T wave appearance in leads V2,V3 — there is little doubt that the ST elevation that we see in lead V1 is part of this process!

Other findings in ECG #1 are more subtle. I probably would not have thought much of them IF the ST-T wave appearance of lead V3 was not so flagrantly abnormal, with associated ST-T wave findings in neighboring leads V1 and V2 (as described above).

• Considering the hyperacute T wave appearance in lead V3 — it is almost certain that the slight-but-real scooped ST depression and prominent T wave in lead V4 is part of the process. Doesn’t the shape of the upper part of the T wave in lead V4 (if not also in V5 and V6) look a lot like the shape of the T waves in leads V3 and V2 that we now know are hyperacute?
• ST-T wave changes in the limb leads are much less marked. But in the context of chest lead findings just described — the T wave in lead III looks hyperacute (it equals R wave height in lead III, with an extremely wide base considering this tiny R wave). Finally, while there is no ST depression in lead aVL — the ST-T wave flattening we see in this lead is not the normal response when the R wave in aVL is upright.

Taking another look at R wave progression in the chest leads:

• Notching of the downslope of the S wave of a QS complex (as we see in lead V2 of ECG #1) — increases the likelihood that this QS complex reflects an infarction Q wave.
• Although a predominant R wave does develop in lead V3 of ECG #1 — this R wave is barely 3 mm tall. This adds further support that the QS in leads V1,V2 (with notched S wave downslope in V2) + the abnormal ST-T wave changes in lead V1-thru-V4 described above are all part of the same ongoing acute process!

BOTTOM Line: While ECG #1 does not satisfy the definition of a STEMI — as per Dr. Meyers, it really looks like acute LAD OMI. And in a patient with this worrisome of a history — I don’t see how one can justify not calling a heart alert.

Additional LEARNING Points: Among the best ways to enhance appreciation of subtle acute changes — is to compare the initial ECG to one or more post-reperfusion ECGs ( = ECG #2 in Figure-1).

• To be sure comparison of serial tracings is valid — one must always ensure that frontal plane axis, R wave progression, and QRS morphology are all comparable. And, there are slight differences in this regard when comparing ECG #1 with ECG #2. Thus, several leads (most notably leads I, III; aVR,aVL,aVF) show baseline artifact in ECG #2 that was not present previously. In addition, the frontal plane axis in ECG #2 is a little more vertical (about +75 degrees, compared to an axis of +40 degrees in ECG #1). That said, I believe that for the most part — comparison of ST-T wave appearance between these 2 tracings is valid.
• There is a difference in QRS appearance of lead V3 between the 2 tracings. Although impossible to prove — I suspect the return of a predominant R wave in lead V3 of ECG #2 is due to reperfusion of the LAD, rather than to any change in precordial lead placement.
• Note after reperfusion (ie, in ECG #2) — that: i) there is now no more than trace (if any) ST elevation in lead V1; ii) the T wave in lead V2 does not look nearly as disproportionate as it did before PCI; iii) even accounting for the changed QRS appearance in lead V3 — the ST-T wave in V3 of ECG #2 now looks benign; and, iv) the very subtle suggestion of hyperacute T wave changes in leads V4, V5, V6, as well as lead III — is no longer present in ECG #2. The ST segments in these leads also look better.
• Final Pearl: I find it ever-so-helpful to look for those 1 or 2 leads in the initial tracing that without doubt are abnormal. Once you find such leads (such as leads V3 and V2 in ECG #1) — it becomes much easier to identify other leads that show more subtle, but clearly abnormal findings.

EXTRA Credit: Go back to ECG #2. Note the artifact in 5 of the 6 limb leads. From which extremity is the problem causing the artifact arising?

ANSWER: There is no artifact at all in lead II of ECG #2. Bipolar lead II is derived from the difference in electrical potential from the foot (F) and the right arm (RA) electrodes. But the left arm (LA) electrode is not involved in derivation of lead II. In contrast, the LA electrode is involved in derivation of both leads I and lead III (which are the leads that show the artifact). That the left arm (LA) is the “culprit” extremity is supported by the fact that in the augmented leads, the amount of artifact is greatest in lead aVL, and approximately half this amount in leads aVR and aVF. CLICK HERE — for a brief article by Rowlands et al that explains these concepts in more detail.