Tuesday, September 4, 2012

Male in his 40's with chest pressure: what is the diagnosis

This 40-some year old patient complained of chest pressure and had this ECG recorded:

See comments and diagnosis below








The providers were a bit worried about this ST elevation and I was in the department, so they showed it to me: my answer took 2 seconds and was unequivocal: LVH and early repolarization, no STEMI.

How did I know this?  Primarily because:

If inferior MI, there would be significant ST depression in aVL.
If anterior MI, there would not be such high voltage, especially in lead V4.

Though the early repol/anterior STEMI formula may give false positives in LVH (I'm actually not sure of this), the value obtained after plugging in STE60V3 = 5 mm, QTc = 400 ms, and R wave V4 = 33 mm = 18.2 (far less than 23.4, strongly arguing against anterior STEMI).  I did not use the formula, but one could do so and be reassured.

My colleagues appropriately did a bedside ultrasound and found completely normal function.  They did admit him for "rule out" and all troponins were negative.







Diagnosis: Anterior and "inferior" ST elevation due to LVH and early repolarization

12 comments:

  1. Replies
    1. By the ECG, one cannot rule out pericarditis. But the STE is easily explained otherwise. I could also say that it just doesn't look like pericarditis, but that would not be very helpful to a reader. Also, of course, pericarditis generally has sharper pain.

      But MOST IMPORTANT: it is not STEMI. What matters is whether it is STEMI vs. anything else. If it is pericarditis, then so what? Same therapy as chest wall pain, pleurisy, etc.

      Make sense?

      Steve

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  2. Isn't it so that the "blip" (as Amal Mattu would call it) at the end of each QRS-complex in V5 is also suggestive of early repol?

    ReplyDelete
    Replies
    1. In our study, although 14 % of STEMI (vs. 32% of early repolarization) had at least one lead with a 0.5 mm J-wave notch, only 5 of 143 had 2 such leads vs. 9 of 171 in early repolarization (unpublished data). So, in our formal analysis, we did not find that the "blips" were very helpful.

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  3. With that kind of voltage I would almost expect significant STe! However the flipped T-wave in aVL made me somewhat concerned, in my book (more like a pamphlet actually) that's indicative of badness. What's your input?

    As always, a very instructive ecg. Thanks a lot.

    Sam

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    Replies
    1. Sam, don't worry about the T-wave in aVL because the QRS is also down. The QRS axis is inferior and so is the T-wave axis. OK?

      Steve Smith

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  4. Dear Dr. Smith,

    I would have a question about LVH. How do we know it is LVH? What kind of criteria does this ECG meet?

    (It is interesting that the ECG shows P pulmonale, which is - as far as I know - in some cases due to left atrial abnormality, not right, so actually P mitrale. And if so, we have 6 points [R in lead II exceeds 2,0 mV + left atrial abnormality] by Romhilt-Estes criteria.)

    ReplyDelete
    Replies
    1. It meets a simplified criterion of S V1 + R V5 greater than 45 mm. however, more importantly, the ST elevation is proportional to the QRS voltage. I do not have any strict criteria for this, just subjective interpretation. It just looks right. Okay?

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  5. Yes, it's clear, thank you very much, Dr. Smith!
    After looking at SV1 and RV6 (seeing they are quite small), I simply did not check Sokolow-Lyon-index...That was a big mistake, no doubt, sorry for that.

    But two things came to my mind that I really wonder, let me ask you:

    1.
    Are there any rules about how big the ST-elevation should be in (not-so-)benign early repolarization?
    We look at an ECG, see (for example) concave ST elevation and the characteristic J waves in V5-6, no reciprocal ST depression, and so we calm down saying "No problem, it's just BER."

    I know you have a great formula differentiating high take-off and subtle anterior/anteroseptal STEMI, but what if the ST elevation is in V5-6 ("low lateral" STEMI) as in my example? Are there any rules about ST amplitude or ST/QRS ratio or something like that? BER is often a problem...

    2.
    Interesting that according to some authors high take-off of the ST segment in right +- mid-prechordial leads is neither BER, nor a normal variant, but a normal finding in men, and BER is a different entity. By other authors high take-off is the part of BER. (I think you belong to the latter group.)

    "Since the majority of men have ST elevation of 1 mm or more in precordial leads, it is a normal finding, not a normal variant, and is designated as a male pattern; ST elevation of less than 1 mm is designated as a female pattern. In these patterns, the ST segment is concave. The deeper the S wave, the greater the ST-segment elevation — a relation that is often observed in patients with left ventricular hypertrophy (Fig. 2, tracing 1)."

    (http://www.nejm.org/doi/full/10.1056/NEJMra022580)

    What is your opinion about this?

    (Sorry for the long questions, and thank you very much for your help!)

    ReplyDelete
    Replies
    1. Marton,

      1. the lateral ST elevation is certainly different. There is, in addition to anterior BER (or normal variant, or simply normal), there is inferior and lateral baseline ST elevation (see this: http://www.simeu.it/download/pubblicazioni/2529.pdf). I differentiate it from STEMI by: a) large voltage of QRS (not STEMI) b) presence of notching c) presence of anterior BER d) presence of inferior BER (inferior STE is NOT STEMI if there is no ST depression in aVL).

      2. I agree with this. terminology is the only difference.

      Steve Smith

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  6. Here's my question. Is there a simple formula to predict when ST elevation in the setting of LVH is predictive of acute ischemia (i.e. is there a Sgarbossa's criteria equivalent for LVH)? It seems the answer is no. Do you commonly apply your early repol/anterior STEMI formula to solve this problem? Thanks in advance for your input. I practice in an urban ED in Atlanta so LVH is very common and STE in the setting of LVH is sometimes reason for false activation of the STEMI

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    1. Dr. Upshaw,
      I've been meaning to address this, as there is a new paper on the topic.
      American Journal of Cardiology, Volume 110, Issue 7 , Pages 977-983, 1 October 2012
      I will do so in an upcoming post.
      Thanks,
      Steve Smith

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