Wednesday, April 9, 2014

Chest pain in a patient with previous inferior STEMI. Scrutinize both the ECG and the history!

I was looking through a stack of ECGs (I can't help myself) and saw this one, which caught my eye:
What do you think?  Computerized QRS duration is 120 ms.

My thought was that it looked like there was likely very subtle anterior injury.  In spite of the slightly prolonged conduction, I applied the anterior STEMI calculator (see sidebar excel applet, or "subtleSTEMI" iphone app), using:

1. ST elevation at 60 ms after the J-point in lead V3: 2 mm (it is probably really 2.5 mm, but I wanted to be conservative)
2. computerized QTc = 413 ms
3. R-wave amplitude in V4 = 9 mm

Result = 23.83 (greater than 23.4 and thus indicating likely LAD occlusion)

One reader thought this was LBBB and that the modified Sgarbossa rule should apply instead.
My answer: It is not a true LBBB.  The intrinsicoid inflection in V5 and V6 is only about 30 ms and must be 50 ms to be LBBB.  That is to say, it must take a long time for the left ventricle to depolarize.  Furthermore, it just doesn't "look" like LBBB.  It is simply a slightly wide QRS.

He did come in by EMS and the prehospital ECG was identical.

Here is his previous ECG:
Note the inferior ST elevation that was present even after opening the infarct artery causing the inferior STMEI.  But also look at V1 and V2.  The ST segments and T-waves are different from the ED ECG.  Thus there is new ST elevation, suggesting anteroseptal STEMI and greatly increasing the suspicion for LAD occlusion.

So I went to look at the chart:

He was a male in his 60s who complained of chest pain.  He had h/o inferior STEMI which was stented.

As I suspected, these ST and T-wave changes were not seen.  Most physicians do not see such abnormalities, even if they are changes, as in this case.  They are extremely subtle.  That is why I recommend scrutinizing them, comparing carefully with the previous ECG, and using the formula to see if your suspicions are worth pursuing.

A positive result with such scrutiny does NOT mandate cath lab activation, but does require further intense scrutiny.

One area of further scrutiny is to look at the previous cath findings:  was there LAD or left main disease?  Is LAD ischemia a real possibility?  If they had looked, they would have found that the left main had a 50% lesion and the LAD had a 90% distal stenosis.  The distal stenosis does not fit with this ECG which looks like septal STEMI, but the left main does.

This patient was treated for unstable angina medically.  His initial troponin was negative.

However, he did not get evaluated for possible acute LAD occlusion.


Later, his next troponin 3 hours later was 1.3 ng/mL.  At this time, he underwent another ECG, five hours after the first:
The ST elevation is resolved.  This again strongly supports that the first one had acute ischemia causing ST elevation

The next day he went for an angiogram and was found to have severe 3 vessel disease involving the left main and the LAD.  The LAD had a new, open, 80% ostial lesion.  The left main had a new 60-70% stenosis.  I am not sure which (or both?) was the culprit, but either could have resulted in death.

It is all but certain that one of them was occluded, or nearly so, when the patient was having chest pain and ST elevation.

Fortunately for all involved, this LAD (or left main) reperfused spontaneously, with the aid of aspirin, plavix, and heparin.  Had it not done so, it could have been disastrous for the patient.

He went for CABG.


Scrutinize the ECG
Scrutinize the History

These findings are discoverable: I found them by just glancing at the ECG in a random stack, without any other information.  They are there on the ECG.  You just have to get good at looking for them, use the formula, compare with the previous, and look at the previous angiogram results.  If suspicion persists, pursue even further scrutiny.


  1. Great case. What do you think of the new upright T-wave in V1 seen in the first EKG? This finding would raise my suspicion as well.

    1. Anand,

      The T-wave was also upright on the old ECG, though not by much. In our study of 355 consecutive anterior STEMI, comparing to 240 consecutive patients who came to the ED with chest pain, ruled out, and were diagnosed with early repolarization, (, this finding had no utility.

      by far the best measure is the formula value greater than vs. less than 23.4, with + LR of 9 and - LR of 0.1. Far better than ST elevation. Neither T-wave upright in V1 nor T-wave in V1 greater than T-wave in V6 had any utility.


  2. What is the significance, in general, of the "Terminal QRS slurring" like it is seen in leads I, II, III, and aVF? Thanks.

    1. It is part of the intraventricular conduction delay. I don't think it is related to the ischemia. Good observation.

    2. Thank you. I had read that terminal QRS slurring in the inferior leads, even in the absence of significant Q waves in those leads, can potentially indicate a previous inferior MI. In this particular case there was a previous inferior MI so I thought that the terminal QRS slurring in the inferior leads, as seen in the first ECG, could be the evidence of the previous inferior MI, especially since there are no significant Q waves appearing in the inferior leads in the first ECG. What are your thoughts on this specifically? Thank you sir.

    3. Jeff,
      I have not heard that, but it may well be true. Do you have any good references?
      Steve Smith

    4. I will have to try to locate those sources again and post them when I find them. Thank you for your comments and consideration sir.

  3. I am from Pakistan and we donot have Cath Lab Facility in our Cardiology ward Just Streptokinase how can we manage these patients with subtle ECG changes?

    1. Very good question and difficult to know in many cases. This case is definitely an LAD occlusion, and it is lucky that it opened on its own, and I would give lytics to this patient on the first ECG. After it reperfuses spontaneously, and the artery is open, then the benefit of lytics is less certain, but you definitely want antiplatelet and antithrombotic therapy.

      The risk of lytics is indeed much higher than the risk of PCI. In many cases of subtle occlusion, the MI is usually smaller than it is in overt STEMI, and usually of less risk, but that is on average only. I think you have to risk stratify. Do you have bedside ultrasound? Is there poor LV fct, in which case any MI has higher mortality and morbidity. Is there any instability, pulmonary edema, etc.?
      Steve Smith

  4. Thanks for another awesome case again.

    Your dedication in scrutinising these changes have taught us invaluable insights, but I afraid that it may, at least for me, cause some loss in specificity while increasing sensitivity.

    Why I am saying this as follows: If I were you, happening to this ECG from a random stack, I'd rather think this was a acute inferior MI, since there is ST subtle elevation in II, III, aVF and reciprocal depression in aVL. Adding this to minimal STE in V5-6 I would conclude that this was an inferolateral MI. But after finding a previous ECG, it became clear that inferior STE was an old change, actually there was some new added inferior ST depression, which is also another proof that you were right at the first place.

    So could you comment on the inferior ST changes in the first ECG ? How did you know these were not important ? How did you choose to ignore it and focus on anterior derivations?

    I am really looking forward to hearing your comments.

    Thanks in advance

    1. Emre,
      T-wave is size is critical to acute coronary occlusion, and the inferior leads have almost zero T-wave. So acute MI is very unlikely.

    2. Oh my ! I can't believe I have missed such a simple clue. Simple, but elegant and critical answer. Thanks for that.