Are there hyperacute T-waves? And how can we know?

A 50-something man presented with worsening severe exertional chest pain which was just resolving as he had an ECG recorded in triage.

Time zero.

Are the T-waves in leads I and II hyperacute?  

Hard to tell. 

How can we know?

By the evolution of the ECG! 

Watch what happens as the heart recovers from its episode of ischemia. The T-waves deflate, demonstrating that the first one was indeed hyperacute.

2 hours

T-waves in lead II are significant smaller

In lead I not much difference

Troponins returned elevated, so the patient was scheduled for urgent angiography.

3 hours

Now they are smaller in both leads I and II.

But also in lead aVL

Post Angiogram

Next day

T-waves are smaller in many leads now, including V4-6.

Lead II, all in sequence

Troponins over 26 hours, from right to left:

Echocardiogram:

Mild concentric left ventricular wall thickening, normal cavity size, and

normal systolic function.

The estimated left ventricular ejection fraction is 64%.

There is no left ventricular wall motion abnormality identified.

Angiogram:

Severe two-vessel coronary artery disease of a left dominant system including 70 to 80% stenosis involving the distal left main/bifurcation.  This is the culprit for the patient's non-ST elevation myocardial infarction

AV groove circumflex, proximal LPDA, and mid LAD stenoses may also be

hemodynamically significant

Occlusion of the proximal nondominant RCA is not likely clinically relevant.  

Smith: not sure why that is.  The ECG shows inferior ischemia.

Heart Team evaluation with preference for urgent coronary artery bypass grafting in the setting of elevated syntax score (30), young patient age, and stenosis involving the left main bifurcation and a left dominant system

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MY Comment, by KEN GRAUER, MD (12/6/2024):

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To paraphrase a famous saying: The ischemic process "is often just a matter of time". Today's discussion by Dr. Smith is highly insightful in showing how dramatically the timing of the ECG (or hopefully ECGs) that we obtain may be with respect to the ECG picture that we receive.

Today's patient is a 50-something year old man who presented with increasingly severe exertional angina, for which his CP (Chest Pain) was just resolving at the time his initial (triage) ECG was recorded (TOP tracing in Figure-1).

• BUT — How often do patients present for evaluation in this timely a manner?
•   How many of the patients that YOU see wait 2 hours? — or 3 hours? — or longer?
•     How many patients do not present to the ED until the next day?

QUESTION:

• What is the usual treatment that all-too-many of these patients receive, if they are among those who delay their visit to the ED for 2 or 3 hours (or longer)?
• 
  
• KEY Point: Dr. Smith skillfully illustrates how the ECG picture we see is so often "a matter of timing" — depending greatly on when each ECG is obtained with respect to the relative degree of CP the patient is experiencing at the time each particular ECG is recorded.
• Implicit in Dr. Smith's discussion, is how important it is to compare serial ECGs in the context of this relative CP severity.

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ANSWER: If the timing is "wrong" (ie, If enough time has passed after CP resolution) — then the ECG may look fairly normal, and the patient's ischemic episode may be overlooked (ie, "pseudonormalization" ).

I limit my comments to comparison of just 2 of the 5 ECGs in today's case. I've labeled KEY findings in the initial ECG (TOP tracing in Figure-1). No labeling of the bottom ECG is needed for comparison between the 2 tracings. 

• Given the history of resolving CP in a patient with recently increasing anginal severity — My "eye" was immediately drawn to the T wave in lead II of ECG #1 that simply stated, looked "too big" for its QRS (within the RED rectangle in lead II).
• In the context of this hyperacute T wave in lead II — the T waves in lead I and lead aVL also looked disproportionate to the QRS complex in these respective leads (the T wave in lead I being more than half the height of the QRS in this lead — and the T wave peak in lead aVL being "fatter"-than-expected, with a T wave base that is wider-than-expected, considering the R wave in this lead).
• My "eye" was next drawn to the deep, symmetric T wave inversion in lead V1, that is perhaps as deep of an isolated T wave inversion in lead V1 that I have seen (within the RED rectangle in V1).

In the context of a recent anginal CP episode — I knew that the T waves in leads II and V1 clearly represent an acute process until proven otherwise. The appearance of all other leads in this initial ECG need to be interpreted with the knowledge that ECG #1 is definitely abnormal!

• In marked contrast to the exceedingly deep T wave inversion in lead V1 — is the subtle-but-real J-point depression in leads V2 and V3. Considering that these 2 leads normally manifest slight gently upsloping ST elevation — this J-point depression (especially with the T wave flattening in lead V2) suggest posterior involvement until proven otherwise (these slightly depressed J points highlighted between opposing BLUE arrows in these leads).
• Whereas in isolation, it might be difficult to distinguish between a repolarization variant vs hyperacute T waves in the 4 leads with blue question marks — in the context of knowing that all the leads so far mentioned are clearly abnormal — I interpreted the T waves in leads aVF; V4,V5,V6 as also hyperacute.

Which leads me to the ST-T wave appearance in leads III and aVR (the PURPLE question marks). 

• Normally, with DSI (Diffuse Subendocardial Ischemia) — there is ST depression in multiple leads with ST elevation in leads aVR>V1 (with occasional ST elevation also in lead III). But in today's initial ECG — we essentially see the opposite ECG picture in this patient who had been having a severe anginal episode that has just now resolved at the time ECG #1 is recorded!
• I interpreted these ECG findings as, if not indicative of a recent event — then consistent with DSI in a patient with multivessel disease (albeit difficult to localize a "culprit" given how generalized these ST-T wave findings are).

Dr. Smith's discussion above follows serial ECG evolution over the course of 5 tracings.

• That said — I thought straight comparison between the 1st and last ECGs in this serial evolution (as I show in Figure-1) — to be humbling in making us better appreciate the matter of "timing" in our assessment of patients whose CP may have decreased by the time we get to see them.
• We need to remember to include notation of the presence and relative severity of CP at the time that each ECG in a CP patient is recorded.

P.S.: Did YOU notice the S1Q3T3 pattern in the 2 ECGs shown in Figure-1?

• Although the T wave in ECG #1 is only shallowly inverted — this still qualifies as an S1Q3T3. The S1Q3T3 is more distinct in ECG #5.
• PEARL: Keep in mind that an S1Q3T3 pattern in the absence of a suggestive history and other ECG findings of acute PE is a purely nonspecific sign. By itself — seeing this ECG pattern does not necessarily mean that the patient has a pulmonary embolism. 

Figure-1: I've reproduced and labeled today's initial ECG — with comparison to the repeat ECG done the next day.