ECG Blog #218 (ECG MP-35) — What is a Hyperacute T Wave?

The ECG in Figure-1 was obtained from a man in his 40s — who presented with new-onset chest pain that began 1 hour earlier.

• HOW would you interpret this tracing?
• Should you immediately activate the cath lab?
• OR — Could the anterior T waves represent a repolarization variant?

 

 

Figure-1: Initial ECG obtained from a man in his 40s — who presented with new-onset chest pain (See text).

 

 

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NOTE #1: Some readers may prefer at this point to listen to the 5:20 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-35).

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Today’s ECG Media PEARL #35a (4:50 minutes Audio) — WHEN is a T Wave Hyperacute? (ie, How to distinguish from the T wave of repolarization variants?).

 

 

MY Approach to this Tracing:

As always — I favor a Systematic Approach for every ECG I encounter (This Systematic Approach reviewed in ECG Blog 205). My descriptive analysis of the ECG shown in Figure-1 is as follows:

• The rhythm is fairly regular at ~55-60/minute. Upright P waves with a constant PR interval are seen in lead II — so the rhythm is sinus bradycardia. Intervals (PR, QRS, QTc) and the axis (which is about +45 degrees) are normal. There is no chamber enlargement.

 

Regarding Q-R-S-T Changes:

• There may be the tiniest of Q waves in the inferior and lateral chest leads.
• R wave progression is normal — with “transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V2-to-V3. If anything — there is already a prominent R wave (of ~11 mm) by lead V3 — suggesting preservation of anterior forces.

 

Assessment of ST-T waves:

• Especially in this patient, who presents to the ED with new-onset chest pain that began just 1 hour earlier — there are a number of abnormal findings on this ECG that I have labeled in Figure-2.

Figure-2: I’ve labeled KEY findings from the ECG in Figure-1 (See text).

 

 

  

Assessment of ST-T waves:

• The most remarkable finding in Figure-2 is the disproportionately tall T waves in leads V2 and V3. As discussed in the above Audio PEARL ( = ECG MP-35) — T waves are considered “hyperacute” when they are taller-at-their-peak and/or wider-at-their-base than expected (considering relative R wave and/or S wave amplitude in the particular lead you are looking at). Therefore — the 10 mm tall T wave in lead V2 especially (given the tiny r wave in this lead) — as well as the disproportionately tall T wave in lead V3 — are both clearly beyond the expected height for T waves in these leads. 
• Note also how wide the T wave base is in both leads V2 and V3 (compared to a more normal width for the base of the T wave in leads V5 and V6).
• The RED dotted lines show 2-to-2.5 mm of ST elevation in leads V2 and V3. Whereas some ST elevation may normally be seen in these leads — the amount seen here seems excessive considering the worrisome history and the hyperacute T wave appearance (given relatively modest QRS amplitude in these leads).
• In the context of what we have just described regarding the ST-T wave appearance in leads V2 and V3 — the ST-T wave in lead V4 also appears to be abnormal (ie, showing ST elevation and a wider-than-expected T wave base).
• Normally — you do not see ST elevation in lead V1, and certainly not the coved ST segment shape (“frowny”-configuration) with subtle-but-real ST elevation as seen here in lead V1 of Figure-2.

PEARL #1: I find the concept of “patterns of neighboring leads” extremely helpful when assessing for potential acute ST-T wave changes. There should be no doubt that the ST-T waves in leads V2 and V3 are abnormal in this patient with new-onset chest pain. 

• The ST-T wave changes I describe in neighboring leads V1 and V4 are less pronounced — but in the context of obvious marked abnormality for leads V2 and V3 — it is virtually certain that the ST-T waves in these neighboring leads represent an extension of the changes we see in lead V2 and V3.

PEARL #2: The last clear abnormality in ST-T wave appearance in the anterior leads of Figure-2 — is the terminal T wave inversion that we see in leads V1, V2 and V3 (BLUE arrows). 

• This terminal T wave inversion in Figure-2 resembles the shape of the terminal T wave inversion seen with Wellens’ Syndrome (fully discussed in ECG Blog #209). In a patient with new-onset chest pain, this terminal T wave inversion that follows after disproportionately tall and hyperacute anterior T waves is definitely not a normal finding. Whether it represents some component of spontaneous coronary reperfusion is uncertain from viewing this single ECG — but what is certain — is that these ST-T waves in leads V1-thru-V3 do not represent a simple repolarization variant.

 

MY Impression of Figure-2 at this Point:

• In this patient with new-onset chest pain — we see a combination of abnormal ST-T wave findings in the anterior chest leads. These include: i) Hyperacute T waves in leads V2, V3, V4; ii) Abnormal ST elevation in leads V1-thru-V4; and, iii) Terminal T wave inversion in leads V1-thru-V3.
• These ST-T wave findings alone clearly justify immediate cath lab activation — with a presumptive diagnosis of acute proximal LAD (Left Anterior Descending) Occlusion until proven otherwise. Onset of abnormal ST elevation as early as in lead V1 (in association with terminal T wave inversion in this lead) — is the reason for suspecting a proximal LAD occlusion.

PEARL #3: The more leads you see that show abnormal ST-T wave changes — the greater the likelihood that an acute cardiac event is ongoing.

• After identifying the definite ST-T wave abnormalities (that we see in leads V1-thru-V4) — I always take another much closer look at the remaining leads. Although there is no ST depression in the inferior leads in Figure-2 — the ST segments in leads III and aVF are clearly straighter than normal (short, horizontal BLUE lines in these leads). 
• Although admittedly subtle (!) — Can’t YOU see a difference between these straightened ST segments, compared to the more normal, gentle upsloping of the ST segment in lead I?
• Lead aVL is a KEY lead to focus on in association with anterior infarction. Although there is no ST elevation in this lead — I thought the ST segment takeoff looked a bit straighter-than-expected (horizontal BLUE line in lead aVL).
• NOTE: These changes in leads III, aVL and aVF are exceedingly subtle! The only reason I mention them — is that in the context of this patient with new-onset chest pain and clearly abnormal ST-T waves in leads V1-thru-V4 — identifying other subtle abnormal findings adds support that an acute cardiac process is ongoing.

 

FOLLOW-UP on Today’s Case:

• Unfortunately, I do not have follow-up ECGs on today’s case. IF I did — I would have satisfied my personal curiosity by looking for: i) Evolution of the anterior hyperacute T waves into more profound ST elevation; ii) Loss of anterior R wave forces (which would be expected if reperfusion was delayed); iii) Deepening of the shallow, terminal T wave inversion (if chest pain resolved and reperfusion was successful); and, iv) Looking to see IF those very subtle ST-T wave changes I noted in leads III, aVL and aVF evolved over time.
• What Happened: On seeing the initial ECG in today’s case — the cath lab was immediately activated. As shown in Figure-3 — there was 100% occlusion of the proximal LAD — with achievement of excellent reperfusion following successful PCI.

Figure-3: Cath films on this patient before and after PCI. LEFT: WHITE arrows in the before-PCI picture highlight complete absence of the LAD, due to 100% occlusion of this vessel at the ostium. RIGHT: RED arrows show successful reperfusion of the LAD following PCI (See text).

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23-LINK in Blog #205). 
• ECG Blog #183 — Reviews recognition of deWinter-like T waves vs repolarization variants. 
• ECG Blog #193 — Reviews the concept of why the term “OMI” ( = Occlusion-based MI) should replace the more familiar term STEMI — and — reviews the basics on how to predict the "culprit" artery.
• ECG Blog #194 — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused using clinical and ECG data. 
• ECG Blog #209 — Reviews the ECG diagnosis of Wellens’ Syndrome.