This case was sent by Sam Ghali (@EM_RESUS)
A 65-year-old gentleman presented to the ED complaining of chest pain. He asked my thoughts on his presenting ECG:
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| Computerized QTc is 409 ms What do you think? |
Here is my response:
Strongly suspect normal variant or chest leads placed too high.
Possibly STEMI, but I strongly doubt.
In my life, I have seen one saddleback (such as this) that was a STEMI.
Outcome?
Here is Sam's analysis and outcome:
The obvious question at hand here: Is this acute LAD occlusion?
There is an rSR' in V1 and S-waves in the lateral leads, but QRS less than 120 ms, thus an incomplete RBBB. There is significant ST-elevation in V1-V3, which meets ACC/AHA STEMI Criteria in these leads (greater than or equal to 2.0 mm in an male greater than or equal 40 yo). Also concerning for coronary occlusion, the T-waves are upright, large, and broad in appearance (especially in proportion to the QRS). There is inferior ST-depression in II, III, and AVF which in LAD occlusion is reciprocal to anterior ST-elevation. What speaks against LAD occlusion is the very well-developed R-waves in V3-V4. (As the ECG evolves in LAD occlusion, there is a loss of R-wave height as R-waves transition to Q-waves; however you wouldn't necessarily see this early on). There is concave-up ST-elevation which makes occlusion less likely, but by no means rules it out. What is also unusual in this case is the “saddleback” morphology of the ST-segment elevation.
A prior ECG would be helpful here, but there was none. A bedside echo looking at LAD distribution wall motion might also be helpful but due to logistical reasons this too was not an option. The decision was made to activate the cath lab.
Outcome
The cath revealed chronic total occlusion of the RCA, with good collateral flow. There were multiple 40-50% lesions throughout the LAD and it’s Diagonals, as well as in the Circ. There was no acute occlusion. Serial troponins were negative. Echo did not show LVH.
Outcome
The cath revealed chronic total occlusion of the RCA, with good collateral flow. There were multiple 40-50% lesions throughout the LAD and it’s Diagonals, as well as in the Circ. There was no acute occlusion. Serial troponins were negative. Echo did not show LVH.
I shared the case with Steve Smith to gain his expert insight, but here are my comments:
1. STEMI Criteria are imperfect - not nearly sensitive nor specific enough for strict use
2. Even with other ECG features taken into account, diagnosing acute LAD occlusion can be very difficult. The Subtle Anterior STEMI formula which may provide diagnostic guidance here, technically should not be used in the presence of inferior ST-depression.
3. While “saddleback” ST-elevation is less likely to be coronary occlusion, it is still possible for STEMI to have this morphology.
4. Ultimately, if after all measures there is still concern for acute LAD occlusion, the diagnosis may be best excluded in the cath lab.
Smith comments:
This is saddleback ST elevation, such as one commonly sees in LVH or in type 2 Brugada. It can also happen if chest leads are placed too high. It is rarely due to STEMI. (I was a bit surprised to hear that the echocardiogram did not show any LVH).
The inferior ST depression is probably a false positive. If you look at the PR segment, it is downsloping. This is a frequently encountered atrial repolarization wave, and this wave is persistent after the end of the QRS, causing a mimic of ST depression.
Atrial Repolarization wave mimicking ST depression:
You can read about it at this post.
You can watch a K. Wang video about this at this post.
Thus, the formula can be used. The R-wave amplitude in V4 is the single most powerful predictor of early repol vs. LAD occlusion: a high amplitude, which here is very high at 25 mm, goes strongly against LAD occlusion. The formula value here, using STE60V3 of 2.5 mm, is very low at 18.97.
Even if the QTc were very long, at 460 ms, the formula value would still be very low at 21.98 (less than 22.0), which would all but rule out LAD occlusion.
The inferior ST depression is probably a false positive. If you look at the PR segment, it is downsloping. This is a frequently encountered atrial repolarization wave, and this wave is persistent after the end of the QRS, causing a mimic of ST depression.
Atrial Repolarization wave mimicking ST depression:
You can read about it at this post.
You can watch a K. Wang video about this at this post.
Thus, the formula can be used. The R-wave amplitude in V4 is the single most powerful predictor of early repol vs. LAD occlusion: a high amplitude, which here is very high at 25 mm, goes strongly against LAD occlusion. The formula value here, using STE60V3 of 2.5 mm, is very low at 18.97.
Even if the QTc were very long, at 460 ms, the formula value would still be very low at 21.98 (less than 22.0), which would all but rule out LAD occlusion.
That said, one cannot entirely rule out STEMI with the formula and such a case should always of course be approached carefully.
If available, I would do a stat formal echo rather than activate the cath lab.
Steve - What about the concordant ST segments? Does that tell you anything?
ReplyDeleteOne only thinks of concordance in the context of BBB, and there is no BBB here. There is an rsR' but the QRS duration is less than 120 ms, so it is not BBB. Most BBB is at least 130 ms.
DeleteVery interesting case discussion by Sam Ghali & Steve Smith. I would have liked to know a little more history on this case — since the ECG picture is clearly not typical. Was the “chest pain” of new-onset and worrisome for acute MI (which of itself might justify diagnostic cath)? — or was the chest pain so-so in terms of generating concern, such that with a less typical picture one might gather more data before rushing to conclusion.
ReplyDeleteMy initial impression on looking at this tracing was that in the absence of evidence to the contrary — this patient was going to go to cath. True, that the significantly negative component to the P in V1,V2 with rSR’ complexes in these leads suggests lead malposition — though I don’t expect 2-3 mm of ST elevation in V1,V2 as is seen here from such lead malposition. The ß-angle doesn’t quite look wide enough to satisfy Brugada-2 criteria — so this is more of an incomplete RBBB appearance — and you should not normally get 2-3mm of ST elevation in V1 from typical incomplete or complete rbbb. And, there remains significant J-point ST elevation in V3 …. As per Dr. Smith, R wave amplitude is clearly greater than one would expect with anterior stemi — but early on, that is possible (and there are those rSR’ complexes in V1,V2 … ). There really isn’t appreciable ST “depression” in the inferior leads — but to me, all 3 inferior leads show abnormal ST flattening that extends beyond what I’d expect for any P wave repolarization effect — and this abnormal shape may qualify at the least as a possible “reciprocal equivalent”. And, even though the shape of the ST segment in aVL is peculiar — the ST segment in aVL IS elevated, which always catches my attention whenever I contemplate early anterior stemi. BOTTOM LINE — If the history was at all concerning (sounds like it was) — I don’t know how you can avoid timely cath for diagnostic purposes. If we call this a “false positive” because there was no acute stemi — it is not a “false positive” that bothers me in the least, since there IS need for certainty in diagnosis. Review of prior tracings, Echo at the bedside — and perhaps additional information on the history may all have avoided immediately need for cath — but if any of the above ECG findings are new, I am skeptical this patient would have escaped cath at some time during this admission to the hospital. GREAT case — THANKS for presenting!
Thanks for the great comments, Ken.
DeleteSo that ST elevation is due to RCA marginal occlusion that runs anteriorly?
ReplyDeleteNo. There was no occlusion at all. It is a false positive.
DeleteDear Dr Smith,
ReplyDeleteCould have the slight T-wave inversion in avL (Reciprocal change?) added to the patient's initial clinical presentation been a sign that something acute was happening then? If I remember correctly, you demonstrably stated several times that any repolarisation abnormality in avL should be considered wary of an underlying event.
Besides in this case, could the peak T-wave/saddleback morphology in V2, V3 represent a deep T-wave inversion in posterior wall?
Thank you again for this interesting case.
Olivier.
Olivier,
DeleteLook at the downsloping PR segment. I believe what seems to be ST depression is really an atrial repolarization wave.
See here: https://hqmeded-ecg.blogspot.com/search/label/atrial%20repolarization%20wave
Steve
So, after following this blog for a while, this is how I'd read this ECG:
ReplyDeleteThere is sinus rhythm with an incomplete right bundle branch block; the PR interval is normal. P-wave morphology raises suspicion of left atrial dilatation. Obvious ST-elevation, most apparent in the right precordial leads but also subtly present in aVL, with reciprocal changes in the inferior leads.
Now, the saddleback morphology would suggest a non-ischaemic type of ST-elevation, like pericarditis (but the ECG does not fit this diagnosis) or benign early repolarisation. There appears to be a miniscule J-wave in V3.
One thing bothering me though, is the morphology of the QRS complex in V3. There is a monophasic R-wave, while V3 should normally have Rs morphology. Could you expand on why you're not worried this might represent terminal QRS distortion in acute MI? If I had been alone in making such a call, I'd probably have requested cath lab activation.
Thanks in advance,
Maarten Van Hemelen
Internal Medicine Resident
Maarten,
DeleteGood question.
Most important is that there is an S-wave that dips below the isoelectric line. So there is no terminal QRS distortion by my definition.
Combine that with the other findings typical of early repol, and I am not worried about this one.
Steve Smith