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). 


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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).
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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).
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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 Wellens’ Syndrome (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.

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FINAL PEARLS:
     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.
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ACKNOWLEDGMENT: My appreciation goes to Andrew Bowman for allowing me to use this ECG and this clinical case.
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NOTE: ― Relevant PDFs on ECG diagnosis of acute MI:
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Posted by ECG Interpretation at 12:10 AM