The Hyperacute T Wave

David Didlake

Firefighter / Paramedic

Acute Care Nurse Practitioner

@DidlakeDW

UPDATE: Dr Stephen Smith has kindly shared with me the latest research into descriptive analysis of the Hyperacute T wave. His comments are provided at the end of the post.

CASE

A 46 y/o Female experiences sudden onset chest pressure while kickboxing. There is associated diaphoresis, nausea, and one episode of vomiting. Personal medical history is unremarkable, and she does not take any prescription medications. Family history is significant for MI (patient’s brother at age 49).

The symptoms mostly wax and wane, but she is compelled to seek medical attention and reports to a free-standing emergency room. All vitals stable. The first ECG is recorded at 0744 hours.

The computer interprets this as Non-specific ST abnormality while the attending provider documents Pericarditis. At 0905 the first labs return.

• Trop I 0.16 ng/mL (ref range <0.05)

• Myoglobin 259 ng/mL (ref range 0.0 - 107.0)

• CKMB 3.6 ng/dL (ref range 0.0 - 4.3)

• BNP-T 50.3 pg/mL (ref range 0 - 100)

• D-Dimer 765 ng/mL (ref range 0 - 500)

CTPA does not reveal PE. CXR shows no acute cardiopulmonary process. The provider arranges for transfer to a PCI center as the patient’s symptoms are not fully resolved and continue to wax / wane.

EMS makes contact and records the following ECG at 1109 hours.

Patient is delivered to the PCI center at the time of symptom recurrence, and the below ECG is captured at 1144 hours.

The first ED Trop I returns 2.38 ng/mL at 1200, and it is at this time that cardiology is consulted.

At the time of this case I was in my first semester of Nurse Practitioner clinical internship and was actually rounding at the respective hospital with one of the members of the cardiology team. He reviewed the ECG’s on his phone and dismissed the findings, advising no STEMI. I then asked to see the tracings and immediately identified Hyperacute T waves (HATW) and that the patient needed to be taken urgently to Cath. He told me that HATW’s are probably just folklore and only exist in the minds of cardiology authors from the 70’s and 80’s. I then replied that if this were my patient on the ambulance, as a paramedic, I would be activating Code STEMI (even though the more appropriate nomenclature is OMI).

Arterial access was made at 1226 and a 100% distal LCx occlusion was found. The cardiologist considered the vessel far too diminutive for intervention so medical management was agreed upon after consultation with a colleague. The cursor is placed at the occlusion with the adjacent OM1 extending beyond this terminal point.

Subsequent Trop I was 13.7 ng/mL at 1600 and peaking at 15.7 ng/mL the following morning at 0630 hours. Her remaining hospital stay was uneventful and she was discharged home on dual Metoprolol and Losartan therapy.

DISCUSSION

The concept of HATW’s is found in doses of relative paucity in conventional literature. For example, Chou’s 6th ed. provides only a cursory mention in Chapter 9 (Non-Q Wave Myocardial Infarction) by stating that T wave morphological changes in the setting of acute ischemia render them both wide and fat. The 13th ed. of Marriott’s Practical Electrocardiography (Chapter 8: Transmural Myocardial Ischemia from Insufficient Blood Supply) advises that ischemic T wave changes are, indeed, reliable indicators of insufficient coronary blood flow but limit the description of such to merely an increase in T wave amplitude.

Wide and fat. Changes in amplitude. This terminology falls dreadfully short of encapsulating what a HATW actually is, so it’s no wonder that many in the established medical community regard them as folklore. Moreover, there are many ECG entities that display “wide” and “fat” T wave characteristics, to include LVH and Normal Variant, for example.

Before extrapolating the idiosyncratic manifestation of HATW’s we must first revisit their clinical implications. The below image is from the previously discussed Marriott text (Chapter 6: Introduction to Myocardial Ischemic and Infarction) and it conveys the natural progression of QRS/ST/T changes in the setting of acute coronary occlusion with remaining viable myocardium.

Said differently, the Sclarovsky-Birnbaum grading system is the time sensitive prelude to Q-wave (irreversible transmural scar) formation. In the original publication Sclarovsky and Birnbaum discovered that with each grading escalation there is less salvageable myocardium and higher likelihood of heart failure at hospital discharge (an inversely proportional relationship). This is critical for the EMS provider, or ED clinician, as identification of Grade I ischemia (aka, HATW’s) addresses the culprit lesion at the earliest opportunity with excellent downstream prognosis for the patient. It’s the difference between leaving the hospital with normal heart function versus sojourning a new path in life with heart failure.

Attempts to objectively define the manifestation of HATW’s have been made. Below is an image of the Anderson-Wilkins Acuteness Score, which incorporates T wave morphology to a certain degree, but as you can see it is both complex and time consuming, and just not very practical in the setting of a busy ED or EMS system.

Dr. Stephen Smith has introduced the concept of proportionality to estimate raw T wave acuteness by juxtaposing the overall size / width / symmetry to its paired QRS. Much of this process, however, relies on the interpreter’s qualitative scrutinizing capacity. What helps, I think, is to first ask if the QRS is normal (that is, depolarization is not grossly imperiled by LVH, LBBB, WPW, etc.) because abnormal depolarization necessarily begets abnormal repolarization, and this can dramatically distort the ST/T morphology. Thus, if the QRS is normal then the T wave should, essentially, be an uninteresting afterthought in terms of size and voltage. But when there is demonstrable T wave “swelling / inflation” (as I like to think of it) and its voltage intimidates the size of the QRS one should pay close attention, especially in the right clinical context.

Let’s prime the optic nerve with examples of HATW’s before revisiting today’s case. Pay close attention to the width, height, and symmetry of the T waves and make sure to compare them with the respective QRS. Some have other ischemic signatures (e.g. reciprocal changes) while some do not. Remember what Sclarovsky and Birnbaum taught us – if we encounter Grade I ischemia then our patient has the best chance of discharging from the hospital with EF intact.

Back to the case. We will once again review the time-zero ECG (captured during pain) when the patient first entered the free-standing emergency room.

There is definitely artefactual beat-to-beat variability but many of the T waves just look a little too inflated / robust. As an aside, this ECG cannot be pericarditis, as previously dictated by the ED provider, because there is subtle ST depression in aVL. Additionally, there is subtle downsloping of the ST in V2.

Now, review the ECG after cessation of symptoms at the time of EMS transfer.

Scroll back and forth. Take your time making the juxtaposition, and pay close attention to how the previously enlarged T waves have now “deflated” and that the ST in aVL is not so depressed or with downsloping configuration. Moreover, there is an upright T wave in V2, suggesting the insipient phase of posterior wall reperfusion. There is plenty of data here to make the decision that emergent Cath is warranted.

Until there is a more quantitative descriptor of the HATW one must rely on qualitative proportionality assessment. This requires deliberate practice, and with time you will train the eye to catch pathology such as this in the earliest stages. Even if there is ambiguity at time-zero the mere suspicion of problematic Grade I ischemia will at least set the trajectory of surveillance for OMI with serial ECG’s. Our patients deserve a high level of scrutiny that affords them the opportunity to discharge from the hospital with intact, functional myocardium.

From Dr. Stephen Smith

"We believe, but have yet to prove, that the proportion of (area under the curve - AUC - of the T-wave) to (QRS amplitude) [or is it area under the curve of the QRS] is the best definition of HATW. AUC is dependent on T-wave height (amplitude) + width (which is partly measure by QT interval) + "bulk" which is increased by straightening of the ST segment. We have not published anything on this yet. The first thing to change after balloon occlusion of a coronary artery is QT, by lengthening."

And I should add that his eagle eyes spotted something that I completely missed. Am I shocked? Of course not, it's Dr. Smith weighing in! :)

"In fact, (and you don't mention this) the T-wave after reperfusion in lead III is larger than before!! How is that possible? Because the QRS is even larger so the PROPORTION shows resolution (absence) of hyperacute T-waves."

The attached literature shows that HATW's were found in 49% OMI patients that were not STEMI.

https://www.sciencedirect.com/science/article/pii/S2352906721000555