Sunday, November 11, 2012

ECG Interpretation Review #53 (Peaked T - Hyperacute - DeWinter - Wellens - aVR)

The ECG in Figure 1 was obtained from a patient who walked into the ED (Emergency Department) with new-onset chest pain.
  • Should the cath lab be activated for acute STEMI?
  • If so – what do you suspect the “culprit artery” is likely to be?
  • How many ECG signs support your impression?
Figure 1: ECG from a patient with chest pain. What are the findings of concern? (Reproduced from ECG-2014-ePub)NOTEEnlarge by clicking on FiguresRight-Click to open in a separate window.
INTERPRETATION:  The ECG in Figure 1 is shows normal sinus rhythm. All intervals and the axis are normal. There is no chamber enlargement. There are however, a series of alarming findings that were recognized by the emergency team. Emergency cardiac catheterization was performed within 15 minutes after the patient walked into the ED  with successful reperfusion of a 100% proximal LAD (Left Anterior Descending) coronary artery occlusion.
     Clues to the need for immediate catheterization and clues indicating localization of the “culprit artery” to the proximal LAD include the following:
  • Hyperacute T waves in multiple leads. These are best seen in leads aVL, V2,V3,V4.
  • DeWinter T wave complexes ― in which there is 1- to 3-mm of upsloping J-point ST depression in one or more precordial leads that continue into tall, positive symmetrical T waves (DeWinter – NEJM 359:2071, 2008). Although seen in Figure 1 to some extent in all precordial leads except for V1 ― the DeWinter T wave is best manifested in leads V3,V4.
  • Loss of anterior R waves (with reduction in R wave amplitude between leads V1-to-V2).
  • Marked inferior reciprocal ST depression.
  • ST elevation in leads aVR and V1.
  • Incomplete RBBB (rSr’ in lead V1; narrow terminal S waves in leads I and V6).
DeWinter T Waves: A Sign of Proximal LAD Occlusion:
     Awareness of the relatively uncommon but highly characteristic DeWinter T wave sign is essential for not overlooking the approximate 2% of acute anterior infarction patients who present with this ECG manifestation (Ref 1). Rather than frank ST elevation that usually accompanies acute LAD occlusion  there is instead the unique DeWinter complex with upsloping J-point ST depression blending into tall upright hyperacute T waves in a number of precordial leads (esp. leads V3,V4 in Figure 1). We emphasize the following key points about this syndrome.
  • In patients presenting with new-onset chest pain ― there is extremely high specificity for the DeWinter T wave pattern and acute proximal LAD occlusion.
  • Rather than evolution of tall, peaked (hyperacute) T waves into frank ST segment elevation ― the DeWinter T wave pattern was surprisingly static over the next few hours in the DeWinter series of patients.
  • None of the patients in the DeWinter series who manifested this ST-T wave pattern had acute left main occlusion on catheterization.
  • Despite prompt recognition and intervention ― a significant percentage of patients developed positive cardiac markers for acute infarction. One ECG sign that infarction may have already occurred is loss of anterior r wave amplitude (as is seen in Figure 1).
TAKE-HOME POINT: Prompt recognition of the DeWinter T wave sign in patients with new-onset chest pain with immediate mobilization of the interventional cardiology team On-Call is essential for minimizing the extent of acute anterior infarction. 
  • As is the case for WellensSyndrome (See Section 10.54 of the pdf in the References below) ― precordial DeWinter T waves is another unique ECG sign with high correlation to acute anatomic coronary occlusion with mandate for immediate intervention.
     In addition to precordial DeWinter T waves and loss of anterior R wave amplitude between V1-to-V2  there are several additional ECG signs in Figure 1 suggestive/consistent with acute proximal LAD occlusion. These include:
  • Significant ST segment elevation in leads aVR and V1.
  • Incomplete RBBB (that is presumably new).
  • Marked reciprocal inferior ST depression.
  • Hyperacute T wave in lead aVL.
ACKNOWLEDGMENT: My appreciation goes to Andrew Bowman for allowing me to use this ECG and this clinical case.

NOTE:  Relevant PDF on ECG diagnosis of acute MI:


  1. hello doctor
    is the ST depression in inferior leads due to reciprocal changes in anterior leads or is it reciprocal of the slight st elevation in AVL ? even if in AVL the STE is not egregious its existance may also give another proof of involvement of the proximal LAD .
    the other clue is the amount of qrs amplitude in V3 wich is very "tiny" if we compare it to the Tall T wave, isn't that highly suggestive that some ischemia is going on ?
    merci beaucoup

    votre plus grand fan d'Algérie.

  2. Salut Lot Ben! Good question you ask. Leads III and aVL are almost directly opposite each other - so they often show a mirror-image picture of ST elevation in one lead and ST depression in the other. If you FLIP OVER (in your mind's eye) the picture of ST elevation we see in lead III - the "mirror-image" of this would be the same shape for the ST segment in lead aVL - so I do think there IS inferior reciprocal ST depression. That said - given the cylindrical shape of the LV - any lead area can in theory be opposite any other lead area. Thus you can see "reciprocal changes" in any other lead area away from the acute of acute ongoing infarction.

    ST elevation in Lead aVL is often seen with anterior MI. The picture here I think is very typical for DeWinter T waves given the dramatically tall T wave (esp in lead V3 given small height of the QRS) with J-point ST depression in V4-V6 before forming the tall T waves - so to me, highly suggestive of a proximal LAD lesion. You may want to review the 3 links I give above under References for more on these entities. THANKS again for your comment!

  3. Is there any reliable ECG criteria for accurate identification of hyperacute T wave ?

  4. The best "tool" for accurate identification of "hyperacute" ST-T wave changes is YOUR EYES! This comes with experience of becoming totally comfortable with what is "normal" vs abnormal. Rather than focus on any one lead to see if the ST-T wave looks to be "hyperacute" — all 12 leads should be looked at (ie, support that what looks to be a hyperacute T wave may be forthcoming from the finding of reciprocal ST depression elsewhere on the tracing). The best way I can describe "hyperacute" T wave changes is that the T wave just does not look proportionate/normal given the QRS complex in that lead — that is, the T wave is taller or fatter-than-expected, or that it looks like it is "trying" to elevate, but hasn't yet done so, or has only minimally elevated ... (look at leads II,V5,V6 in my ECG Blog #80 — ).

  5. Dr. Grauer, it seems that the usually benign upsloping STJ depression becomes malignant in the context of hyperacute T (=DeWinter pattern). If it happens to happen in other lead groups (does it?), would it be localizing like STE (is it a localizing sign?)?

    Thank you!


    1. Thanks for your comment. Although in V2, the shape of the ST segment per se might seem consistent with a repolarization variant — there are MANY clues in this case that tell us this is not a benign pattern. These include — the history (chest pain) — dysproportionately tall ST-T waves in V2,V3 (compared to the tiny r wave in these leads) — frank ST elevation elsewhere (ie, aVL) — frank reciprocal ST depression elsewhere. The diagnosis of early repolarization should always be one of exclusion. And yes, given that the ST-T wave pattern we see here in the chest leads reflects DeWinter T waves — this DOES localize the lesion to the proximal LAD.