Friday, September 18, 2015

ECG Diagnostic of STEMI. But Interventionalist cancels the cath lab.


A male in his 80s was crossing the street, felt weak, and sat down.  He denied LOC, chest discomfort or dyspnea.  He had no medical history.   

 Here is the prehospital ECG (sorry for the poor resolution):

There is profound ST elevation in anterior leads.  3.5 mm at the J-point in lead V3; 5 mm at 60 ms after the J-point.  There is convex ST elevation in aVL, with reciprocal concave ST depression in inferior leads.  This is diagnostic of STEMI due to proximal LAD occlusion, especially in an 80 year old.
Young men could conceivably have this much precordial ST elevation at baseline, but even in a young man, the limb lead abnormalities make this diagnostic.
There is also a large amount of PR depression in V3 and V4, which just goes to show that this finding is NOT specific for pericarditis.

ED course

He arrived by ambulance stating that he now feels fine. 

His exam was unremarkable, including no murmur.

The emergency physician was very concerned about the ST elevation and large T-waves, and activated the cath lab.  The interventionalist cancelled it, stating that it does not represent STEMI.  The K was 4.0 mEq/L.  

The emergency physician then used the early repol/LAD occlusion formula and obtained 24.7.  

With STE V3 60 of 5 mm and a computerized QTc  415 ms, and R-wave amplitude of 14, I calculate a formula value of 25.9.  

This is very high and just confirms the obvious.

Two more cardiologists came to look at the ECG.  Both said "No STEMI."

I don't know what they are thinking, but I am not inhibited about speculating: The patient had no chest pain.  He only had weakness.  Many physicians just cannot accept that a patient with minimal symptoms has anterior STEMI.

Furthermore, many still believe that if there is upward concavity in all of leads V2-V5, it cannot be LAD occlusion or STEMI.  There are at least 3 studies refuting this.
Kosuge 1999.
Smith 1 2016.
Smith 2 2012.

Here is a patient I had in which I made the same mistake:

Spontaneous Reperfusion and Re-occlusion - My Bad Thinking Contributes to a Death

In fact, the patient was feeling better and wanted to go home, but the emergency physician convinced him to stay.

The first troponin was below the level of detection.

Here are subsequent ECGs:

35 minutes after the first:

T-waves and ST Elevation are much less marked.  Limb leads have the same worrisome features.

78 minutes after the first:
There is the beginning of T-wave inversion

5 hours later:
More T-wave inversion (consistent with reperfusion).

A later troponin I was 3.6 ng/mL, but it was not checked after that.

Cath was done the next morning:
EF 45%-50%
Left Main: normal
LAD: 65-70% stenosis (culprit).  
severe aortic stenosis 

No intervention was done.  Patient was transferred for aortic valve replacement and CABG. 

Fortunately for this patient, his LAD spontaneously reperfused and remained open, unlike this case of mine which I have already placed a link to above.  

Learning Point:

1. Absence of Chest pain means little in the face of a diagnostic ECG.

33% of patients with both NonSTEMI and STEMI have no "chest discomfort".  This was not a study of "chest pain" but of "chest discomfort."  

After patients are diagnosed with MI, they may be browbeaten into saying they had chest pain, or may change their memory.  But when the history is taken before the diagnosis, 33% have no chest discomfort.

2. Not all cardiologists are proficient in diagnosing coronary occlusion on the ECG.  There are countless things cardiologists must learn, and diagnosing occlusion on the ECG is only one small part of their vast specialty.  They are very smart and hard working and knowledgeable, but they, like all people (and like me did in the case above), make mistakes and can suffer from group-think.  

Only you can advocate for your patient.


  1. 60-70%. Do u think it was 100% on presentation. Would the aortic stenosis had an effect on the ecg ?

    1. I would bet it was 100% at the time of the prehospital ECG, or nearly.

  2. Hi dr Smith!

    Isnt it possible that this patient in fact had a type 2 MI with ST elevation due to reduced coronary blood flow due to severe aortic stenosis + physical exertion (i e crossing the street, presumably fast?) in the presence of a fixed LAD stenosis? Is there any way to tell?


    1. Jacob,
      As I understand, there was a "culprit", which is different from "stenosis". Culprit implies there is angiographic evidence of ulceration or fissure of the plaque, or actual thrombus. This is seen on the vast majority of ACS. Otherwise, your hypothesis is certainly feasible!

  3. Hello Dr. Smith,

    An observation with respect to V3: In the prehospital ECG, the R/S ratio is significantly greater than 1, in the 2nd ECG is is approximately 1, in the 3rd it is significantly less than 1, and even more so in the 4th. If anterior occlusion attenuates the S wave, are we seeing a reversal in this attenuation with the concomitant reversal in STE and T waves? Is there significance to this, or am I over-reading?

    Thank you,

    1. Dave,
      You are seeing it just right.
      In fact, by making me look again, I see now that V3 in the prehospital ECG also has "terminal QRS distortion" which is a hard sign of anterior MI.
      This means that there is both no S-wave AND no J-wave in Either lead V2 or V3. Early repol virtually always has one of these in both leads.

  4. Hi Dr. Smith,
    Did the cardiologists comment on the hyperacute T-waves in pre-hospital EKG in leads V2-V4. I know we're not seeing the classic loss of R wave but in the absence of hyperkalemia I would be concerned about an anterior STEMI?

    1. Amina,
      It is unclear what the cardiologists were thinking. I can only guess that they saw a patient without chest pain and who had all upwardly concave ST segments, and jumped to a wrong conclusion.

  5. What was the outcome of the case?

    1. Patient was transferred for aortic valve replacement and CABG. No further info.

  6. Interesting case. Was the troponin high sensitivity? It seems very unusual to have zero chest pain plus negative hs-TnT and merit primary PCI - which would have come back to the the fixed stenosis theory and poor wording on the cath report. There's also the concern that had he been rushed to the lab he may have inadvertently ended up with the stent when he really needed an AVR+CABG.

    1. Alan,

      It does not matter what the troponin was. The ECG is diagnostic on its own, and especially with the dynamic changes. High sensitivity or not, there are false negative troponins. Studies of hs trop are almost always in combination with a negative ECG. So this does not apply. Furthermore, those studies even have 1-2% false negative rates (BOTH ECG and troponin negative). You must read them carefully and know them before thinking that hs troponin is the be all and end all.


  7. I think you misunderstand me, I'm not saying trop is the be all and end all, but similarly I don't rely on ECG alone - I look at that combined with clinical history and enzymes. I'm just trying to say that a rush to the lab isn't always in the best interest of every patient, especially those with a more complex story. In the UK at least the teaching is that the ECG is very important but it is one component. All good discussion though! :)

    1. But in some cases you only need one of those components if that component's positive predictive value for high risk ACS is very high. That is the case with the ECG in this case.


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