Doctor, should we activate the hospital's "STEMI alert"?

Written by Pendell Meyers

I received this prehospital ECG (we receive prehospital ECGs by telemetry from EMS in a large area around our hospital) and was told that there was a patient in her 50s with chest pain who was headed to an outside hospital (which happens to be a catheterization center). They wanted to know if I would like them to activate the outside hospital's "STEMI alert."

Here is the ECG:

What do you think?

There is sinus rhythm with perhaps 1mm STE in aVL, and also in V2 with hyperacute T-wave. There is STD in V3-V5, as well as II, III, and aVF, with hyperacute T-waves in all these leads as well, thus de Winter's pattern in the anterior and inferior leads. This is essentially pathognomonic for Occlusion MI of the anterior and apical walls (de Winter pattern more likely represents ~99% thrombotic stenosis with just a trickle of flow, but essentially the same overall event, with progression to full occlusion extremely likely). The OMI is therefore occurring in the LAD, and the LAD is likely a type III "wraparound" which supplies the apical and distal inferior wall in addition to the anterior wall.

Aside: This case proves that de Winter's waves are not limited to anterior leads, but may be seen in any location.  This is similar to Wellens' waves, which were first described in the LAD distribution, but may occur in inferior and/or lateral leads as well.

But of course, this is not a STEMI by definition as it does not meet STEMI criteria. The STEMI guidelines do state that hyperacute T-waves "may indicate early acute myocardial infarction" but do not discuss it as a "STEMI equivalent."

I told them to activate their "STEMI alert" anyway, because this patient needs emergent reperfusion and I will not be able to advocate for the patient at another hospital. Whether or not a "STEMI" is recorded, she is at very high risk of VF arrest or decompensation, or at the very least a large anterior full thickness MI if her OMI is not understood. I also told them to get one more 12-lead before they get to the ED.


They shot this ECG right before going into the ED:

Clearly meets STEMI criteria with large STE in V2-V5. Hyperacute T-waves in V2-V5, I, and II, III, and aVF. Because lead aVR = the aVerage Reciprocal to all other leads (and almost all other leads have hyperacute T-waves), aVR is of course obligated to show a negative hyperacute T-wave.

The patient had a 100% proximal thrombotic occlusion of the LAD. I was unable to confirm whether the LAD was indeed type III (wraparound), however the ECG implies that it was functionally equivalent.

Learning Points:

In this era where we must endure a suboptimal paradigm of MI, we must sometimes break the "rules" in order to benefit patients. Some NSTEMI patients like this one receive huge benefit from emergent angiography, yet are denied this benefit under the current paradigm until their ECG later manifests STEMI (if it ever does!).

Serial ECGs are extremely helpful.

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Comment by KEN GRAUER, MD (5/4/2019):

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In 2008 — de Winter et al described “A New ECG Sign of Proximal LAD Occlusion” (NEJM 359:2071-73, 2008), that they found to be present in ~2% of 1,532 patients admitted with acute anterior MI. I’ve excerpted Figure-1 from their original manuscript — in which de Winter et al illustrate ECG changes in 8 of their patients. The original description by de Winter et al of this ECG pattern was as follows:

• “Instead of signature ST segment elevation — the ST segment showed a 1-3 mm upsloping ST depression at the J-point in leads V1 to V6, that continued into tall, positive symmetrical T waves”.

Other Features that de Winter et al found in association with this pattern included:

• Usually 1-2 mm of ST elevation in lead aVR.
• Normal QRS duration (or no more than minimal QRS widening).
• A loss of R wave progression in some patients.
• Of interest — this de Winter pattern was noted an average of 1.5 hours after symptom onset — and a wraparound LAD was found at cath in 50% of patients.
• Many of these patients did not manifest ECG evolution from this de Winter T wave pattern to frank ST elevation — but instead they maintained these de Winter T waves as a “static” pattern until cath was performed.

Figure-1: Illustration of 8 of the patients studied by de Winter et al, showing characteristic ECG features of de Winter T waves (Excerpted from NEJM 359:2072, 2008).

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MY Experience: Since I began active participation on ECG internet blogs in 2010 — I’ve seen numerous cases posted on the internet of patients with new-onset chest pain, in which there are hyperacute anterior T waves that do not yet fulfil criteria for ST-Elevation MI. My anecdotal impressions on this pattern are the following:

• PEARL: There are many variations on “the theme” of de Winter T waves. Many of the cases I’ve seen posted that go on to evolve to anterior STEMI do not show J-point ST depression as De Winter et al described (or at most, show minimal J-point depression in only 1-2 leads). The degree of T wave peaking is not always as predominant — and the pattern is often not “static”, but rather evolves (as occurred in this case) to frank ST elevation in serial tracings. 
• 
  
• My Opinion: For many patients who do not manifest the “static pattern” described by de Winter et al — What you see on ECG depends on when during the process the ECG is obtained ... And, the pattern may evolve!

The ECG in This Case: Keeping the original description by de Winter et al in mind — the 1st ECG in this case manifests a series of important diagnostic findings (Figure-2):

Figure-2: The initial ECG in this case (See text).

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• As per Dr. Meyers — typical de Winter T waves are seen in a number of chest leads. These findings are most marked in leads V3 and V4. Note j-point depression in leads V3, V4 and V5 — which leads up to a giant T wave in V3, and a slightly smaller T wave in V4.
• The J-point is not depressed in lead V2. Instead, there is already slight ST elevation in lead V2 (RED arrow in this lead).
• There is also some ST elevation in lead V1 (RED arrow in this lead).
• More than just de Winter T waves in the inferior leads — I believe there is ST depression that lasts longer than the momentary J-point depression we see in chest leads V3 and V4 (compare the slope of the RED ST segments — with the more rapid upsloping PINK ST segments that much sooner rise above the baseline). I interpreted this difference in upslope as suggesting both inferior lead de Winter T waves — and also inferior lead reciprocal ST depression.
• Together with subtle-but-real ST elevation in lead aVL (RED arrow in aVL) — the finding of reciprocal inferior lead ST depression predicts a more proximal location for the LAD occlusion.
• The finding of de Winter T waves in both inferior and anterior lead locations is consistent with likely LAD “wraparound” anatomy.

Other Findings in Figure-2 include:

• Slight ST elevation in lead aVR (as noted by de Winter et al).
• Loss of R Wave Progression (as noted by de Winter al al) — with enhanced predictive power of acute infarction-in-progress conveyed by: i) subtle notching at the onset of the QRS in lead V2 (BLUE arrow); and, ii) marked fragmentation of the QRS in leads V4 and V5 (and to a lesser extent in V3 and V6).
• Finally — there is an acute conduction defect = LAHB (predominant negativity of the QRS in each of the inferior leads).

CONCLUSION: In this patient with new-onset chest pain — there should be more-than-enough indication for emergency cardiac catheterization from the ECG findings on the initial prehospital tracing alone (Figure-2). The 2nd ECG performed in this case confirmed the need for immediate cath — but it should not have been needed … Our THANKS to Dr. Meyers for highlighting this case!