Monday, October 12, 2015

A Missed STEMI. How could the Diagnosis have been certain?

A middle aged patient presented to the ED with "ischemic-sounding chest pain" of unknown duration. An ECG was recorded: 
The ST Elevation in V1-V4 by itself is not diagnostic.  The computerized QTc was 410 ms.
What feature(s) makes this ECG diagnostic of LAD Occlusion?

The emergency physician at the small referral hospital made the diagnosis of STEMI and activated the cath lab pathway, which includes faxing a copy of the ECG to the referral center.  This was done.

The referral center instructed the emergency physician to hold onto the patient and repeat the ECG in one hour.

This was done:
There is still more ST elevation.  Now it should be super obvious that this is a STEMI, and even meets STEMI "criteria" of at least 2 mm in 2 consecutive leads.

This prompted another discussion with cath lab staff (including another faxed ECG) who stated that as the ECG was improving (???? -- my italics and question marks), the patient should be kept locally in the cardiac ICU and treated as a non-ST-elevation-MI. The patient at this point had been given dual anti-platelet therapy, opiate analgesia which relieved his chest pain, and a Xa inhibitor. Initial highly-sensitive troponin T (hsTnT) returned at 150 ng/L (normal is less than 14 ng/L).  

Comment: now can there be any doubt about the diagnosis?

In the cardiac ICU, the patient had further chest pain overnight (comment: the opiates wore off) and was re-discussed with the PCI center. Advice given at that time was to start a nitro drip.

Patient went for PCI the following day (greater than 12 hours after onset of pain). This showed LAD occlusion.  Peak hsTnT > 10,000 ng/L.

Comment: This is a massive MI.  Most STEMI have a TnT greater than 1000 ng/L.  A TnT of 10,000 is a very large MI, especially if it is not after reperfusion (release at the time of reperfusion results in a high troponin spike).  In this case, there was no reperfusion and such a peak is therefore especially high and indicative of very large MI.

Transthoracic echo showed "good LV function" (this is hard to believe) with Anterior and Apical WMA. 

Post-PCI ECG is here:
This shows the typical QS-waves of completed transmural anterior MI.  The T-wave inversion is shallow compared to the T-wave inversion of reperfused MI, as T-wave amplitude correlates with amount of viable ischemic myocardium.  There is so much nonviable myocardium here that the T-wave inversion will not be deep.This ECG shows that the patient lost the entire anterior wall.  Irreversibly.

What made the first ECG diagnostic?

There is about 1.5 mm of ST elevation in V2 and V3.  This alone could be normal or due to ischemia.  Therefore, one must explain the ST elevation.  If it is normal, then the rest of the ECG should conform to normal, and that includes normal QRS, R-waves, and R-wave progression.  The presence of a Q-wave in lead V2 makes normal variant impossible.  Furthermore, there is Reverse R-wave progression.   The R-waves get smaller from V2-V4.  This never happens in normal variant ST elevation.  

Reverse R-wave progression is analogous to presence of Q-waves.   When there are Q-wave present, one should mark the ST elevation in V2-V4 as either acute occlusion or as old MI with persistent ST elevation.  This ECG is clearly not due to the latter, therefore must be acute LAD Occlusion.

Since it should be "obvious" LAD occlusion, one should not use the LAD-early repol formula.  However, if one did use the formula, and one used 2 mm for STE at 60 ms after the J-point (an underestimate), 410 ms for the QTc, and 2 mm for the R-wave amplitude in V4, one would get 25.93, which is far higher than 23.4 and indicates LAD occlusion.

Further comment:

1. Opiate analgesia.  This should never be given in ACS unless you are committed to the cath lab!  It only hides the symptoms and obscures the diagnosis.  If a patient has refractory pain from ACS, that patient needs emergent angiogram and PCI!

2. A nitro drip is fine, but only precludes emergent angiogram if it resolves the pain and the ischemic ECG findings.  By the time of the second ECG, this patient has STEMI, and so even if it resolves with medical therapy, emergent cath must be done.

3. Serial ECGs.  These should not wait one hour!  If you are doing serial ECGs, they should be every 15 minutes.  In one hour, a lot of damage can be done.

4.  Your referral center may be wrong.  If you are worried about the patient, tell them you are not comfortable keeping that patient and insist on transfer.

5.  In this case, thrombolytics are indicated.  In this patient, thrombolytics were indicated if PCI could not be done within 90-120 minutes of arrival at the outlying institution.


  1. first 2 ECGs could ~ correspond to LAD occlusion distal to the 1. diagonal branch but prox to the 1. septal branch ? (... Wellens/Conover's Book 2006, pag 14, figure 1-14): ... wich results in STE in V1, aVR (... V1 > aVR) and ~ III, with (little) STD in I + aVL

    merci, Al

    1. I don't have full angio results, but I suspect that this LAD is a wraparound to the inferior wall and is causing just a bit of inferior MI with minimal ST elevation in III, and minimal reciprocal depression in I and aVL. As you say, it may be proximal to the septal perforator but must be distal to the first diagonal, as there is no apparent lateral involvement.

  2. This is a fantastic post. Excellent teaching as always, but I found this one particularly well done from a learning perspective. Thanks Dr. Smith!


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