Tuesday, June 18, 2013

A Tough ECG, But Learn From It!

I have to tell this story from my point of view because I don't want anyone to think that the recognition of LAD occlusion was made in retrospect.  I want all to know that, with the right mind preparation, and the use of the early repol/LAD occlusion formula, extremely subtle coronary occlusion can be detected prospectively, with no other information than the ECG.

The Case:

I was reading dozens of leftover ECGs from over a weekend and saw this one:
There are symmetric T-waves and poor R-wave progression.  There is 1 mm of ST elevation at the J-point in leads V2 and V3.  This formerly met "criteria" for thrombolytics in the ACC/AHA guidelines of 2004, though of course this amount of ST elevation is very nonspecific.  It is nonspecific because normal variant ST elevation can be even much greater.  However, normal variant ST elevation always has better R-wave progression and asymmetric T-waves which have a slow upstroke and a rapid downstroke.  See image below:

Slow upstroke, fast downstroke.  Asymmetric.

This was my thought: if this patient presented to the ED with chest pain, then this is an LAD occlusion.  So I went to look at the chart and here is the history:

This patient with no h/o CAD had a couple of episodes of chest pain during the day, then presented with one hour of substernal chest pain that had some reproducibility but also improved from 10/10 to 5/10 with nitroglycerine.

This is such a subtle ECG that I was worried that it had gone unnoticed, and, in fact, it did go unnoticed:  

His pain continued and his ECG was read as normal.  His first troponin was normal.  He was admitted to the hospital for a "rule out."  His second troponin I returned at t = 5 hours and was + at 3.8 ng/ml.  His ECG was repeated at this point:

This shows a well developed anterior STEMI.

The cath lab was activated and an LAD occlusion was opened.  The peak troponin I was over 100.  On echocardiogram, there was a 40% ejection fraction with anterior wall motion abnormality.

I applied the LAD occlusion/early repol formula and, with a QTc of 402ms, STE60V3 of 1.5, and R-wave amplitude in V4 of 3 mm, the result was = 24.5, which is in the range of LAD occlusion (even if you read the STE as 1.0, the result is 23.9, greater than 23.4).  The formula results in such a high number because of the very low R-wave amplitude, which (in comparing subtle LAD occlusion to early repol) is the single best predictor of LAD occlusion, better than ST elevation.

To not see these findings is very common, and this patient would be given the diagnosis of NonSTEMI, with subsequent development of STEMI.  

It is not a missed STEMI, but it is a missed coronary occlusionAs you can see, the subtle findings are apparent and, with a prepared mind, can be detected.  Studies show that 30% of NonSTEMI have an occluded infarct artery at the time of angiography done 24 hours after presentation.  This is because of subtle ECG findings.  These patients have worse outcomes: higher mortality, more CHF, higher biomarkers, and worse ejection fractions than the NonSTEMI patients with open arteries.

This patient had continued and ongoing pain.  If there had been serial ECGs, then the evolution of ST elevation would have been detected much earlier and there would be less myocardial injury.  

Fesmire et al. showed that, with continuous ST segment monitoring, the sensitivity of the ECG for STEMI rises from 48% to 62% of all MI as diagnosed by CK-MB.  In other words, NonSTEMIs are frequently diagnosed as STEMIs if you give them time to evolve. 


Continuous ST Segment Monitoring

Fesmire FM, Percy RF, Bardoner JB, Wharton DR, Calhoun FB. Usefulness of automated serial 12-lead ECG monitoring during the initial emergency department evaluation of patients with chest pain. Ann Emerg Med 1998;31(1):3-11.

Occlusion in NonSTEMI

1.  Wang T, Zhang M, Fu Y, et al. Incidence, distribution, and prognostic impact of occluded culprit arteries among patients with non–ST-elevation acute coronary syndromes undergoing diagnostic angiography Am Heart J 2009;157(4):716-23.
2.   From AM, Best PJM, Lennon RJ, Rihal CS, Prasad A. Acute Myocardial Infarction Due to Left Circumflex Artery Occlusion and Significance of ST-Segment Elevation. Amercan Journal of Cardiology 2010;106(8):1081-5.
3.   Sorajja P, Gersh BJ, Cox DA, et al. Impact of delay to angioplasty in patients with acute coronary syndromes undergoing invasive management: analysis from the ACUITY (Acute Catheterization and Urgent Intervention Triage strategY) trial. J Am Coll Cardiol 2010;55(14):1416-24.
4.     Pride YB, Tung P, Mohanavelu S, et al. Angiographic and Clinical Outcomes Among Patients With Acute Coronary Syndromes Presenting With Isolated Anterior ST-Segment Depression: A TRITON–TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel–Thrombolysis In Myocardial Infarction 38) Substudy Journal of the American College of Cardiology: Cardiovascular Interventions 2010;3(8):806-11.
5. Marti D et al.  Incidence Incidence, angiographic features and outcomes of patients presenting with subtle ST-elevation myocardial infarction.  Am Heart J December 2014; 168:884-90.


  1. Yet another great case! Thank you very much

  2. Fantastic teaching points.

    One question: what do you think about the ST segments in leads II and III in the presenting ECG? Though there is no ST depression at the J point, they have downsloping, straight contour with terminal T wave inversion (upright in this case) that strikes me as reciprocal changes.

    Other than the poor R wave progression and symmetric T waves in the LAD distribution, this was the most worrying feature to my eyes since I was looking for reciprocal changes in these leads to help figure out whether this was LAD occlusion or not.

    What do you think?

    1. Pendell,
      Did you mean III and aVF? Yes, there are "down-up" biphasic T-waves and these are very suspicious for ischemia.
      Steve Smith

  3. Yes, III and aVF is what I meant to say. Thanks!

  4. Dr Smith,
    What would be your thoughts on this ECG if the pt had presented with no symptoms suggestive of myocardial ischaemia?

    1. Good Question. I would be much less worried. I would have to evaluate on a case by case basis, and take a thorough history.

      Steve Smith

  5. Steve,
    Any explanation for the terminal T-waves inversion (Wellen's-like waves) in the precordial leads on the 2nd ECG where the vessel was apparently closed?


    1. Sam, with prolonged occlusion and transmural myocardial infarction, T wave inversion eventually evolves. It happens more slowly than with reperfusion and does not become as deep.

      Look at the schematic on the upper right corner of page 50 of my book:


  6. Excellent Diagram, Steve! But it seems this terminal inversion only seems to generally represent evolution in the direction of reperfusion (as opposed to persistent occlusion)? I suppose there must be great variation.

    1. No, even with persistent occlusion, eventually shallow (as opposed to deep) T-wave inversion evolves.

  7. Seems to be a lot of potential overlap!

    For ex:
    The terminal T-wave inversions in this case (persistent occlusion) look very very similar to the terminal T-wave inversions from this case:

    http://hqmeded-ecg.blogspot.com/2013/11/why-we-need-12-lead-st-segment.html (artery open)

    1. Sam,
      Not similar at all.
      In the case you refer to, there are no other signs of prolonged persistent occlusion, particularly QS-waves. In the case you mention, there are no Q-waves at all, so it doesn't even approach minimally prolonged occlusion. Again, in the case you mention: it is the first ECG after chest pain resolves, it was short duration chest pain, there are no Q-waves, so this is NOT the shallow inversion of prolonged occlusion.


  8. ECG 1.... Lead 2 has a comparatively tall T wave(low voltage of QRS) any comments on that??? many times this is seen in patients with non cardiac symptoms... Links to any posts which addresses these issues???? Thank you

    1. I agree the T-wave in lead II is a bit proportionally large. Not sure if it is related to this LAD occlusion. This case would easily be identified using the LAD-normal variant formula.

    2. I have a question regarding the seemingly proportionally large T wave in lead II, my interpretation is that the QRS axis is somewhere along -30 which would lead to a diminutive or biphasic complex in lead II where as the T wave axis is somewhere around +30 degrees which would lead to normal morphology and sized T waves in II.

      Secondly it appears to me that there is some suggestion that the patient had a previous inferior MI, with QS waves and QRS fragmentation in leads III and aVF. Would you agree with that assessment?

    3. Myles,
      Yes. Good observations!
      You are an astute reader of ECGs.
      Steve Smith


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