Electrocardiographically Silent High Lateral STEMI Equivalent

A 60s male woke up with chest pain and contacted 9-1-1 after self-administered nitro did not help.

Past medical history: hypertension, chronic back pain, stents “10 years ago”
Medications: hydrocodone, nitroglycerin

  • O: 15 minutes prior to 9-1-1 activation
  • P: Nothing makes the pain better or worse
  • Q: Dull and heavy “same as 10 years ago”
  • R: Left arm
  • S: 7/10
  • T: Constant

Patient ashen in color but not diaphoretic.
Breath sounds clear.

  • GCS: 15
  • RR: 16
  • HR: 64
  • NIBP: 162/69
  • SpO2: 99%
  • BGL: 231

12-lead ECG is obtained.

What do you see?

There is “down-up” ischemic ST-segment depression in lead III.

Because “ischemia does not localize” (as opposed to the ST-elevation of acute injury) this is more likely to be reciprocal to “electrocardiographically silent” high lateral MI than “inferior ischemia”.

If we scrutinize lead aVL there is a tiny bit of ST-elevation and a disproportionately large T-wave (considering the tiny size of the QRS complex).

Reciprocal behavior between leads III and aVL should make your spider sense tingle!

Please note, this does not meet our STEMI criteria! But it’s very suspicious. The ECG was transmitted for physician consult which is exactly how this case should have been handled.

By arrival in the Emergency Department the ECG had largely normalized.

Initial troponin was negative. The patient was admitted to the ICU. However, the patient continued to experience chest pain intermittently throughout the night.


“His EKG was unrevealing of acute myocardial injury current and initial troponin was negative. However, the patient had ongoing intermittent chest pain during the night despite intravenous nitroglycerin and blood pressure control and serial troponin levels have become elevated. Coronary angiography is recommended for further evaluation….”

“LCX — Left circumflex coronary artery is large in caliber, lateral wall obtuse marginal system, which is bifurcating along the lateral wall to the apex. A secondary stented branch is subtotally occluded with what appears to be left-to-left collaterals filling the distal PDA and tertiary marginal branches. The stented segment does not appear to have significant antegrade flow….”

In other words, the culprit vessel was consistent with the prehospital ECG! 

1 Comment

  • Hi Tom. This is a great case — so NICE that you posted it for others to learned from. But as I commented several times when you sent this case around to our group — the T waves in V2,V3 are disproportionately peaked and transition occurs early (between V1-to-V2) — so the chest leads are NOT normal. I understand that cath supported a LCx — but I feel: i) it important in your Discussion to indicate that the chest leads are NOT normal; ii) that this MAY change the potential “culprit” artery” if chest lead changes are new ….; and iii) that for this case to be complete — we really NEED to see the “baseline tracing” to KNOW if the abnormal findings we see in the chest leads are new or not (presumably they are not new — but you just can’t say that from this initial tracing alone). THANKS for your receptivity to my feedback — it is an EXCELLENT case! — 🙂

Leave a Reply

Your email address will not be published. Required fields are marked *