On its way from occlusion to reperfusion (or vice versa), the ECG can be normal or near normal

Written by Pendell Meyers

I was reading ECGs in a database (without any clinical information) when I came to this one:

What do you think?

Seeing only this ECG with no context, I thought this ECG was within normal limits. The upright and large T wave in V1 is unusual, but if it were hyperacute, I did not see reciprocal findings in V6 which would be concerning for LAD OMI pattern (we call that "precordial swirl").

So, if I had to interpret this ECG with no other context, I would say I see no clear evidence of OMI.

But I was able to see ECGs just before and after the ECG above.

So I went back to the first ECG in this sequence, at time zero:

EKG#1 (time zero)

This is clearly done with right sided precordial leads. There is obvious evidence of inferior, posterior, and right ventricular OMI, including hyperacute T waves and STE.

The next ECG recorded was at time = 3 hours:

EKG#2 (time = 3 hours) (this is the same ECG at the top of the post)

What do you think of this same ECG now?

The ECG now shows resolution of inferior and posterior hyperacute T waves and STE, likely now with posterior reperfusion T waves seen in V1-V2/3. 

This ECG, which was almost within normal limits by itself, shows how close to normal an OMI ECG can pass through normal, on its way from OMI to reperfusion. 

Here is the OMI progression of ECG findings for review:

You can see that OMI ECG findings must "deflate" and pass through normal or near-normal in order to get to reperfusion findings. In other words, to get from hyperacute T waves and STE to terminal T wave inversion, the ST and T wave must pass transiently through a state of near-normal. This is termed "pseudo-normalization."

An ECG taken during this transition period can be normal or near-normal, even with both ECGs before and after show clear occlusion and reperfusion. 

The next ECG was recorded at tome = 16 hours:

EKG#3 (time = 16 hours)

Unfortunately, there is still STE in inferior leads, with developing Q waves. But also T wave inversion of inferior reperfusion (V1 also possibly showing posterior reperfusion T waves). 

Next ECG available was two months later:

EKG#4 (two months later)

Still showing T wave findings of inferior and posterior reperfusion.

One year later:

EKG#5 (one year later)

Inferior Q waves persist, as do inferior T wave inversions. 

Learning Points:

The ECG can pass through normal or near-normal on its way from occlusion to reperfusion, or vice versa. You must understand this and the dynamic nature of ACS to provide excellent care for such patients.

Serial ECGs are important to perform and incredibly helpful at all stages of expertise.

To understand the ECG in OMI, you must know the OMI progression and how it manifests at each stage on each major area of the myocardium. Posterior reperfusion T waves, for example, would be T wave inversions on posterior leads, and manifest reciprocally in V1-V3 as abnormally tall anterior T waves.

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Comment by KEN GRAUER, MD (12/12/2022):

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I will summarize in 4 words the important message conveyed by Dr. Meyers in today's post = "Be Aware of Pseudo-Normalization!"

• The truism, "What goes up must come down" — applies not only to life phenomena — but also to the course of ST segment deviations during the evolution of an acute OMI (as per the above Figure in which Dr. Meyers reviews the ECG findings of OMI progression).

For clarity in Figure-1 — I've reproduced the initial ECG that was shown above in today's case, which Dr. Meyers ventured to read without the benefit of any clinical information.

• As experienced ECG interpreters charged with overseeing the interpretation of others — overreading tracings without the benefit of clinical information is the unenviable task we face all the time. This can be challenging — and today's case emphasizes how difficult this can be when the tracing placed before us was obtained during the period of "pseudo-normalization".

I'll expand my comment by 2 short Questions relevant to today's case:

• What is the History?
• What is "Normal"?

POINT #1: With full awareness that we may not always be privilege to the history — I'll emphasize that optimal ECG interpretation is impossible without a brief relevant history. The challenge for those of us charged with overseeing (and overreading) the ECGs interpreted by others — is to know WHEN we need to go to the patient's chart and/or to contact the interpreting provider to find out essentials of the clinical history.

• KEY: If the ECG in question was obtained from an acute care center or from an EMS directory — then the chances increase greatly that the history may entail, "new-onset chest pain" — in which case awareness of the "pseudo-normalization" stage of acute OMI progression should prompt us to lower our threshold for pulling the patient chart and/or immediately contacting the interpreting clinician. Failure to do so may result in overlooking subtle ST-T wave changes in a patient "in passage" from a frank STEMI toward reperfusion changes.

POINT #2: The initial tracing in today's case does not show acute changes. That said — ECG #2 is not a "normal" tracing, in the sense that subtle (albeit nonspecific) ST-T wave abnormalities are present in multiple leads.

• There is significant baseline artifact in ECG #2, especially in the limb leads. While this does not prevent interpretation of this tracing — it does make assessment of limb lead ST-T wave findings more difficult. Hopefully, effort will be made in follow-up tracings to minimize (as much as possible) this artifact.
• There appears to be subtle-but-real ST elevation in leads III and aVF (ie, with respect to the dotted RED baseline I drew in these leads). While this is clearly not diagnostic (especially given the absence of reciprocal ST depression in lead aVL) — it could be important.
• Despite the artifact in leads I and aVL — the ST segments in these leads appear to be flat (as suggested by the parallel BLUE lines). Again — while nondiagnostic and clearly nonspecific — this is not a "normal" finding.
• Similar nonspecific (and nondiagnostic) ST segment straightening is present in leads V3-thru-V6. This subtle-but-real finding could be relevant, depending on the history. For example — the ST segment in leads V2,V3 should normally manifest a gentle upsloping until it joins the upright T wave in these leads. Instead — the parallel BLUE line in lead V3 of ECG #2 shows abnormal (albeit subtle) ST straightening.

POINT #3: When T waves in each of the chest leads are upright (as they are in ECG #2) — the T wave in lead V1 is usually not taller than the T wave in lead V6. This "imbalance of precordial T waves" is not seen very often — and in the “right” clinical setting, has been associated with recent OMI from a LCx culprit artery (See Manno et al: JACC 1:1213, 1983 — and the July 17, 2013 post by Salim Rezaie in ALiEM).

• NOTE: This is not to say that tall, upright T waves in lead V1 might not sometimes be the result of a repolarization variant or a mirror-image reflection of LV “stain” that can sometimes be seen in anterior leads. Instead — it is simply to say that on occasion — I have found recognition of a tall, upright T wave in lead V1 that is clearly taller than the T wave in lead V6 to be a tip-off to an acute coronary syndrome that I might not otherwise have recognized (For 3 more examples of this finding — See My Comments at the bottom of the page in the October 23, 2020 post — the March 26, 2022 post — and in the June 1, 2022 post of Dr. Smith's Blog).
• 
  
• To Emphasize: As an isolated finding — I might not think much of the surprisingly tall T wave in lead V1 of ECG #2 (which by itself in an asymptomatic patient, could be a normal variant). But given that this T wave in lead V1 is so much taller than the T wave in lead V6 (as per the BLUE arrows in Figure-1) — and given the subtle ST-T wave findings I described above in no less than 8/12 leads — I would want to know the History (and see additional tracings done on this patient) before I would render my interpretation.

In Today's Case: 

Dr. Meyers of course recognized the subtle abnormalities that I detail above. This is why he inquired about the case. The moment he saw the dramatic acute ST elevation in the 1st ECG recorded on today's patient — in context with the follow-up ECG done at 16 hours — he knew that ECG #2 represented the "pseudo-normalization" stage in this patient evolving an acute OMI. 

Figure-1: I've reproduced and labeled the initial ECG that was shown in today's post (See text).