Saturday, August 26, 2023

ECG Blog #392 — Repolarization T Waves?

 — See ECG Blog #408 — for a Video presentation of this case!

The ECG in Figure-1 was obtained from a man in his 60s — who described the sudden onset of "chest tightness" that began 20 minutes earlier, but who now (at the time this ECG was recorded) — was no longer having symptoms.
  • In view of this history — How would YOU interpret this ECG?
  • Should the cath lab be activated?  

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on ECG #1: 
We are not told details of this patient's previous medical history. No prior ECG is available at this time for comparison. This leaves us with having to make our initial impression without the benefit of additional information. That said, even without more history and without a prior ECG for comparison — the initial ECG in Figure-1 clearly is of concern! 

I see the following:
  • The rhythm is sinus bradycardia at ~55-60/minute.
  • The PR and QRS intervals are both normal. The QTc may be of borderline duration, but does not appear to be overtly prolonged. 
  • The frontal plane axis is leftward, consistent with LAHB (Left Anterior HemiBlock) — as the QRS complex in lead II is predominantly negative.
  • There is no chamber enlargement.

Q-R-S-T Changes:

  • There is a potentially significant Q wave in lead aVL — in that this Q wave seems wider-than-it-should-be considering small amplitude of the QRS in this lead.
  • R Wave Progression — overall is not necessarily abnormal (ie, since initial r waves are present in each of the first 3 anterior leads — with significant R wave amplitude occurring by lead V4, as it should). That said — the r wave in lead V3 is still relatively small at ~2 mm (NOTE: My concern about an acute anterior event is less if the r wave in anterior leads is taller, rather than as modest in size as we see in ECG #1).

Continuing with ST-T Wave Changes:
  • The most remarkable finding in ECG #1 — relates to the presence of tall, peaked T waves in multiple leads (ie, in leads II,III,aVF; and in leads V2-thru-V6)These T waves are disproportionately tall with respect to the R waves in these leads (ie, The T waves in leads V2,V3 tower over the 2mm r waves in those leads — and the tall T waves in leads II,III,aVF and in V4,V5,V6 are of comparable [if not greater] height than R waves in these leads). 
  • These tall T waves are associated with flattening (straightening) of the ST segment in the inferior leads — with slight ST elevation in leads V2-thru-V6 (albeit not enough to qualify as a "STEMI" — Akbar et al, StatPearls, 2023). That said, these are hyperacute T waves, in that they are "hypervoluminous" (ie, taller and "fatter"-at-their-peak than they should be — with a wider-than-it-should-be T wave base, especially in leads V2-thru-V5).
  • Lead aVL shows reciprocal changes to what is seen in the inferior leads (ie, ST segment coving with slight elevation is seen in lead aVL — followed by symmetric T wave inversion in this lead that manifests an inappropriately widened Q wave).

Putting IAll Together:
In view of the History in today's case (ie, of an man in his 60s — who presented with new "chest tightness" ) — We have to interpret ECG #1 as suggestive of an acute OMI ( = Occlusion-based MI)until you can prove otherwise.
  • Given markedly hyperacute T waves that begin as early as in lead V2, continuing through to lead V6 — with abnormal ST-T waves in leads II,III,aVF and aVL — ECG #1 most likely represents acute proximal LAD (Left Anterior Descending) occlusion.
  • As discussed in many posts in this ECG Blog — despite not satisfying the millimeter-based definition of a STEMI — in this patient with new chest pain, the ECG findings in Figure-1 merit prompt cath lab activation without any need to wait for serum troponin to return elevated (See ECG Blog #193 — regarding the new "OMI" paradigm).

PEARL #1: As I've emphasized often in this ECG Blog — the course of acute MI from acute coronary occlusion — is often staggered. By this, I mean that even without PCI or thrombolytic therapy — the "culprit" vessel may spontaneously reopen. Sometimes the "culprit" vessel stays open — but at other times, it may at any point in time reocclude. And, sometimes this process of spontaneous reopening and reclosing may occur multiple times in short succession.
  • The importance of correlating the presence (and relative severity) of CP with each serial ECG recorded on the patient — is that doing so may provide insight as to whether the "culprit" vessel at any time during the process is likely to be open or closed.
  • The "culprit" coronary artery is more likely to be occluded IF — the patient has ongoing severe CP (Chest Pain), especially if this occurs in association with ST elevation over the area of infarction.
  • Spontaneous reperfusion is likely IF — in association with reduction (or resolution) of CP, the ST elevation and reciprocal ST depression significantly improve.
  • Reperfusion of the "culprit" artery is even more likely IF — in association with CP resolution, one sees "reperfusion" T waves (ie, T wave inversion) in areas where there had been ST elevation.

  • KEY Point: Somewhere in between the phase of acute ST elevation and return of ST segments to baseline — may be a "transition" phase of pseudo-normalization, during which time the ECG may look relatively normal (or show no more than nonspecific ST-T wave flattening). IF attention is not paid to the presence and relative severity of CP in association with each serial ECG — it could be extremely EASY to overlook recent OMI if the initial ECG is being viewed during this phase of pseudo-normalization.

PEARL #2: Applying PEARL #1 to today's case — the fact that this patient's symptoms began before ECG #1 was obtained, and that his chest pain had resolved by the time ECG #1 was recorded — strongly suggests that the "culprit" artery may have spontaneously opened. It also puts us on the alert that an earlier ECG done during chest pain may have looked significantly "worse" than ECG #1.
  • This is the reason why despite not satisfying millimeter-based STEMI criteria — ECG #1 is diagnostic of an acute OMI until proven otherwise (and merits prompt cath with probable need for PCI).

PEARL #3: It is important to realize that during the course of acute OMI — the initial hs-sensitivity (high-sensitivity) troponin value will sometimes be normal!
  • Therefore — a single hs-troponin value within the "normal" range does not rule out OMI. (This point is discussed in detail in the March 24, 2023 post of Dr. Smith’s ECG Blog).

PEARL #4: Regarding today’s case — the  reasons I emphasized that we do not have to wait until an elevated troponin returns before activating the cath lab are: i) That in a patient who presents with a history of new chest pain (as today’s patient describes) — the ECG changes in Figure-1 (that are detailed above) — are already diagnostic of acute OMI (therefore already meriting prompt cath activation)and, ii) There is nothing that an initial hs-troponin value can tell us that will change this need for prompt cath activation. 
  • On the contrary — IF the initial hs-troponin value comes back normal (as it may — as emphasized in PEARL #3) — it is all-too-easy to be falsely reassured by an initially normal hs-troponin — which may cause further delay in performing the needed cath (which could turn out to be a lethal mistake — IF the “culprit” artery spontaneously reoccludes while providers are waiting “until” the hs-troponin finally becomes elevated).

PEARL #5: When discussing hs-troponin values — it is important to appreciate that not all “normal” values are “equally” normal.
  • For example, in the March 24, 2023 post that I refer to above — not only the 1st hs-troponin ( = 4 ng/L), but also the 2nd hs-troponin value obtained 2 hours later ( = 16 ng/L) were within the "normal" range (which for this particular hs-troponin assay was ≤16 ng/L for women; ≤26 ng/L for men).
  • As emphasized in the discussion of this March 24 case by Dr. Smith — the 2-to-3 hour "Delta" (ie, the difference between the 1st and 2nd hs-troponin values) — should be less than 3 ng/LTherefore, despite both of these first 2 hs-troponin assays falling within the “normal” range — the delta of 12 ng/L (ie, 16 ng/L — followed by 4 ng/L) is clearly abnormal, and indicative of acute OMI until you can prove otherwise.


The CASE Continues:
It turns out that an earlier ECG was done in today's case. For clarity — I have put both of these ECGs from today's case together in Figure-2.
  • NOTE: The reason I began today's case with ECG #1 — is to emphasize a number of important points.

Figure-2: Comparison between the 2 ECGs recorded in today's case. ECG #2 was actually done first, at the time the EMS unit arrived on the scene (at which time the patient was having severe chest pain). About 20 minutes later (on the way to the hospital) — the patient's CP resolved, and ECG #1 was recorded.

MY Thoughts on the ECGs in Figure-2:
The overall slow heart rate and the leftward frontal plane axis are essentially unchanged in the 2 tracings shown in Figure-2.
  • In the Limb Leads: Although QRS morphology looks similar in ECG #1 and ECG #2 — there clearly was more ST elevation in leads I and aVL and much more reciprocal ST depression in the inferior leads at the time ECG #2 was obtained.

  • In the Chest Leads: ST elevation is so dramatic in ECG #2, as to be evident from across the room (ie, with the amount of ST elevation exceeding 5 mm in leads V2,V3,V5 — and attaining 10 mm in lead V4).
  • It is of note that chest lead R wave amplitude was much greater in the initial ECG in today's case ( = in ECG #2).

  • KEY Point: When the EMS team first arrived on the scene — the patient had severe CP in association with the tall chest lead R waves seen in ECG #2, with marked ST elevation and marked reciprocal inferior lead ST depression.
  • Just 20 minutes later, ECG #1 was obtained — at which point the patient's chest pain had resolved, in association with significant loss of chest lead R wave amplitude and near resolution of ST segment elevation and reciprocal depression. Without the ST segment elevation and depression — only the hyperacute T waves remain in ECG #1.

PEARL #6: The above described correlation between ECG findings and the timing (and severity) of chest pain symptoms tells us the following:
  • That the proximal LAD was acutely occluded when the patient was having severe CP (on EMS arrival — when ECG #2 was obtained).
  • That the "culprit" artery spontaneously opened ~20 minutes later while the EMS unit was en route to the hospital (at which time the patient's CP had resolved — and ECG #1 was obtained).
  • That despite resolution of the patient's CP and of ST segment elevation and depression — that prompt cath with PCI remained essential in this patient who otherwise would be at risk that the "culprit" artery might at any moment spontaneously reocclude.

  • Final "Take-Home" Point: Imagine if ECG #2 had not been obtained — and instead, the first (and only) EMS tracing was ECG #1. This is why correlation of the timing of the presence (and severity) of symptoms in association with each ECG obtained is essential — and why in a case such as this one, the hyperacute T waves in ECG #1 despite not satisfying millimeter-based STEMI criteria are more than enough to justify prompt cath without the need to wait for a positive troponin value.

CASE Conclusion:
Timely cardiac cath was performed on today's patient — with successful reperfusion and stenting of his proximal LAD occlusion.

Acknowledgment: My appreciation to Roy van Melfoort (from Venhorst, Noord-Brabant, Netherlands) for the case and this tracing.

Related ECG Blog Posts to Today’s Case:

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
  • ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Rhythm Interpretation.
  • mmm
  • 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 "culpritartery.

  • ECG Blog #194 — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused using clinical and ECG data.
  • ECG Blog #294 — How to tell IF the "culprit" artery has reperfused.

  • ECG Blog #183 — Reviews the concept of deWinter T-Waves (with reproduction of the illustrative Figure from the original deWinter NEM manuscript).
  • ECG Blog #318ECG Blog #340 — and ECG Blog #341 — More on deWinter and deWinter-like T waves.

  • ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute?
  • ECG Blog #260 — ECG Blog #222 — and ECG Blog #292 — Reviews when a T wave is hyperacute — and the concept of "dynamicST-T wave changes.
  • ECG Blog #387 — Dynamic change in 2 minutes.

  • ECG Blog #230 — How to compare serial ECGs.

  • ECG Blog #337 — an OMI misdiagnosed as an NSTEMI ...

  • ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post)
  • ECG Blog #167 — another case of the "magical" mirror-image opposite relationship between lead III and lead aVL that confirmed acute OMI.

  • ECG Blog #271 — Reviews determination of the ST segment baseline (with discussion of the entity of diffuse Subendocardial Ischemia).

  • ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.

  • The importance of the new OMI (vs the old STEMI) Paradigm — See My Comment in the July 31, 2020 post in Dr. Smith's ECG Blog.
  • For review on when despite acute OMI — the initial hs-troponin may come back normal — See the March 24, 2023 post in Dr. Smith’s ECG Blog.


ADDENDUM (8/26/2023)
  • I've added several Audio Pearls below with material relevant to today's case.

Today’s ECG Media PEARL #1 (3:00 minutes Audio) — Reviews the concept of deWinter T waves (and the common occurrence of variations on this "theme" ).


ECG Media PEARL #35a (4:50 minutes Audio) — WHEN is a T Wave Hyperacute vs a Repolarization variant?

ECG Media PEARL #39a (4:50 minutes Audio) — Reviews the concept of Dynamic ST-T Wave Changes (and how this ECG finding can assist in determining if acute cardiac cath is indicated).



ECG Media PEARL #46a (6:35 minutes Audio) — Reviews HOW to compare Serial ECGs (ie, Are you comparing "Apples with Apples" — or — with Oranges?).

ECG Media PEARL #10 (10 minutes Audio) — reviews the concept of why the term “OMI” ( = Occlusion-based MIshould replace the more familiar term STEMI — and — reviews the basics on how to predict the "culprit" artery.

ECG Media PEARL #11 (6 minutes Audio) — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused, using clinical and ECG criteria


  1. Dear dr.Ken, I'd like to know how can we tell the T wave is "fatter" than normal just from its appearance? Because ECG experts seem to know by heart (pun intended) that some T waves are "fat" or a ST segment is not normal, too straight etc.. If you have covered this topic on your audio pearl I'd love to listen to it. So far I've only been listening to the arrythmias audio but the basic turns out to be out of my knowledge. Thank you.

    1. Hi. If you scroll down the page in Blog 392 to the References — You’ll see that Blogs #260 — #222 — and #292 ( — — ) all review the concept about recognizing when ST-T wave changes are “hyperacute” — as well as some of the Audio Pearls in the Addendum to Blog 392. That said — it DOES take time and experience to gain comfort in recognizing when a T wave is “too-fat-at-its-peak” or “bulky” ( = hypervoluminous). A KEY point is that T wave size will vary depending on QRS amplitude in the lead you are looking at (ie, if the R wave is very small — then for a T wave to be “tall” will be less than in leads in which the R wave is much bigger).

      This DOES take experience — so KEEP LOOKING at tracings. You’ll find that I describe T wave appearance in all of my ECG Blogs in which I say that there are “hyperacute” ST-T waves.

I will finish by saying that when you check with clinicians who are knowledgeable in recognizing “hyperacute” ST-T waves — there IS excellent reproducibility! However, many clinicians (including all-too-many-cardiologists) do not yet accept this important concept. I hope the above provide you with insight! — :)

    2. Thanks a lot doctor. Will keep on practising.

    3. "Practice makes for constant improvement!" — :)

    4. VERY true — the more ECGs you see — the better you become at recognizing what they show! — :)