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? NOTE – Enlarge by clicking on Figures – Right-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 Wellens’ Syndrome – 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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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.
1) PDF of NEJM DeWinter article (DeWinter – NEJM 359:2071, 2008).
3) Wellens Syndrome.