Acute chest pain and an abnormal ECG. Do precordial leads show benign T-wave inversion or ischemia?

Written by Willy Frick

A 51 year old man with hypertension presented with three hours of acute onset, severe midsternal chest pain associated with two episodes of nausea and vomiting.

ECG 1

What do you think?

Smith: Inferior leads have subtle ST Elevation with reciprocal STD in aVL.  The end of the T-wave in all of II, III, aVF has a rapid downturn, suggesting early T-wave inversion.  

In V3-V6, there are slightly upsloping ST segments with terminal T-wave inversion in V3-V6 which is classic for benign T-wave inversion.  This ST-T is associated with a tall R-wave and a small S-wave.  Benign T-wave inversion is most commonly seen in young African Americans, and less so over age 50, so one must be careful--they might be ischemic T-waves, but if they are ischemic they would most likely represent reperfusion T-waves.  Since the patient has active pain, that is less likely.  In any case, I would call this diagnostic of inferior OMI and it requires cath lab activation.  

Is this:

1) inferior OMI with benign T-wave inversion in precordial leads? or

2) Inferior and lateral OMI that is beginning to reperfuse, even though the patient still has chest pain?

• Benign T-wave Inversion -- Countless Examples (1)

The Queen of Hearts Active OMI model (aOMI) is shown below:

Willy: My initial impression looking at this ECG was that it was not ischemic. The morphology of the ST-T in leads V3 and V4 struck me as very similar to benign T wave inversion cases I have seen in the past.

I sent the ECG to Dr. Meyers and he said "might be a difficult BTWI, but I would have to figure out if there is inferior OMI immediately." He went on to point out that aVL is unusual for BTWI. In particular, there is STD and ischemic down-up T waves.

He concluded by saying that "History and concern should win regardless of EKG." He asked for any old recordings for comparison, but none were available at the time.

Even though this blog is devoted to understanding the nuances of EKG, we always need to remember that an EKG is only a single test. It is imperfect. Maybe the imperfections are entirely a function of fallible human readers (like me), and maybe some of it is inherent to the nature of the test. In this case, the context is a 51 year old man with risk factors presenting with acute onset substernal chest pain with nausea and vomiting. The pre-EKG probability for OMI could hardly be much higher! So an equivocal (or even normal) EKG is not enough. (It's the opposite of this case.)

Fortunately, the patient underwent immediate angiography. There was an 80% lesion in the mid to distal RCA with TIMI 3 flow (meaning normal flow). The operator performed intravascular ultrasound and visualized acute plaque rupture with thrombus formation and placed a stent. Repeat ECG the following morning is shown below:

ECG 2

This ECG shows clear biphasic reperfusion T waves in the inferior leads. To me, V4-6 show pretty convincing reperfusion T waves. But V3 is still hard to interpret, especially in the context of the presenting ECG. There is one final ECG 2 days after cath.

ECG 3

A few months later, I was finally able to track down a prior ECG, obtained during an office visit for hypertension management. This is shown below:

Prior baseline

For convenience, I have put leads from baseline, active OMI, and post PCI tracings side by side to help understand the differences.

Serial comparison makes the inferior leads quite obvious. Compared to baseline tracing, the ECG on presentation shows obviously new STE and HATW. The axis change makes serial comparison of aVL trickier. Still, it is a very bland looking lead in baseline, and therefore much more sinister when viewed through the lens of serial comparison.

The precordial leads are admittedly harder to make sense of. Here is my take:

• Baseline shows non-specific TWI.

• Post-PCI shows reperfusion TWI.

• Therefore, presentation ECG (obtained during active OMI) is the result of layering STE and HATW on top of non-specific TWI.

Smith: I agree with this.  There was reperfusion ischemia superimposed on benign T-wave inversion.

Fortunately, the patient had both spontaneous reperfusion and very rapid treatment. His high sensitivity troponin I peaked at 2974 ng/L (ref. <35). His echo showed ejection fraction > 70% with normal wall motion. He is very lucky that he spontaneously reperfused and was stented before he had the chance to re-occlude. He did well.

Learning points:

• In acute chest pain, STE in inferior leads with reciprocal STD in aVL is inferior OMI until proven otherwise.

• As always history is the most important diagnostic test.

• Serial ECG comparison remains undefeated.

• Benign looking features (precordial TWI from ECG 1) can co-exist with OMI findings

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MY Comment, by KEN GRAUER, MD (11/17/2024):

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The wonders of medicine keep us humble and honest. When I first saw today's initial ECG without knowing the history — I had the same impression as Dr. Frick, namely that the ECG was not ischemic. I thought so because:

• A fairly similar ST-T wave shape was present in multiple leads — and resembled that of certain repolarization variants.
• There is excellent R wave progression (with early transition showing abrupt transition to a predominant R wave already by lead V3).
• R waves are tall in V3,V4.
• The QTc appears to be relatively short.

The above said — I didn't feel so bad on learning that cardiac cath revealed an RCA "culprit" — because as emphasized by Drs. Frick and Meyers, "History and concern should win regardless of the ECG".

• When you do get fooled (as we all do at least some of the time) — GO BACK and review the tracing. Credit again to Dr. Meyers for his focus on the shape of the ST-T wave in lead aVL of ECG #1 — that simply does not look consistent with a repolarization variant.
• Considering the ST-T wave appearance of lead aVL — Lead I also demonstrates an uncharacteristically flat ST-T wave, that typically is not seen with repolarization variants.
• And — the History is that of a 51 yo man with 3 hours of new severe CP, associated with nausea and vomiting. So regardless of whatever your impression might have been on seeing today's initial ECG — prompt evaluation is indicated until a definitive answer is forthcoming.

Additional "Take-Home" Points from Today's CASE:

• We've reviewed ECG features of BTWI (Benign T Wave Inversion) on many occasions in Dr. Smith's ECG Blog. As per My Comment in the June 30, 2023 post (in which I review the 9 Criteria derived over the years by Drs. Wang and Smith as suggestive of BTWI) — Today's initial ECG deviates from these criteria because: i) J-point notching is absent, especially from leads V3,4,5,6 which are the chest leads with T wave inversion; — ii) Right-sided chest lead V2 shows ST segment straightening instead of a gently upsloping ST segment; — and, iii) Leads V3,V4 that manifest the most T wave inversion lack the usual amount of ST elevation that is typically seen with BTWI.
• When in need of a "Refresher" on what BTWI may look like — I suggest periodically checking out Dr. Meyers' March 22, 2022 post — in which he shows a series of cases illustrating BTWI in "all of its flavors".
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• Although telltale reperfusion T waves may be seen very soon after spontaneous or PCI reperfusion — it often takes a day or two for "the Answer" to become obvious (Witness comparison between ECG #1 vs ECG #3 done 2 days later).
• As per Dr. Frick — Confusion may result from the fact that some benign-looking features (that may be suggestive of BTWI) — may co-exist with subtle findings of acute OMI.

BOTTOM Line: The "good news" in today's case — is that this patient underwent immediate angiography, with identification of a mid-to-distal RCA "culprit" that was stented.