Saturday, May 6, 2017

Unusual ST Elevation in V1 and V2, and LVH, in a Patient with Chest Pain


This ECG was texted to me:
Computerized QRS is 114 ms
What do you think?












There is an rSR' in V1 and a qR in V2, suggesting incomplete RBBB.  There is some concordant ST elevation (concordant to the R'-wave) in both those leads and T-wave inversion in V5 and V6.  But V3 is normal without any evidence of STEMI, and with a low voltage T-wave.   And there is very large voltage in aVL that is diagnostic of LVH.  LVH can produce a wide variety of pseudoSTEMI patterns.

Here was my response: 


"Not a STEMI.  Unusual but does not look right for ischemia.  If you suspect MI, get an echo.  I’ll bet the anterior wall is fine."

He did suspect MI.  Here was the history: A middle-aged male with a family history of MI, history of hypertension, and who is a smoker, complained of substernal tightness that started several hours prior ("after eating pizza").  He was nauseated but there was no diaphoresis or radiation of the chest discomfort.
Not a STEMI.  Unusual but does not look right for ischemia.  If you suspect MI, get an echo.  I’ll bet the anterior wall is fine.

There was an ECG from 3 months ago available for comparison:
Very different
QRS is 107 ms.
So the incomplete RBBB is new.
There was LVH by voltage

Baseline ST elevation is even greater, due to LVH




Here are the ED cardiac ultrasounds:

 First, parasternal long axis:

LVH with good wall motion. Thick interventricular septum of LVH.

Here is the parasternal short axis:

Concentric LVH.  No anterior (or other) wall motion abnormality is visible



Here is parasternal short axis with strain speckle tracking:


This shows perfect wall motion.


A repeat ECG was recorded 37 minutes after the first:
This appears frightening, but I thought it was due to artifact, and requested another ECG.


Here is the next one, recorded 65 minutes after the first:
LVH with no evidence of STEMI.
There is no rSR's here either.



At this point, the troponin I returned at 2.4 ng/mL (quite elevated) and since the patient had active 3/10 chest pain uncontrolled with nitroglycerine, so the cath lab was activated.

Remember: no matter what the ECG shows, even if completely normal, if the patient has uncontrolled chest pain and an elevated troponin without another clear explanation (such as pulmonary embolism), emergent angiography is indicated.  Complete coronary occlusion can be invisible on the ECG.  These ECGs do NOT show ischemia, but that is not proof of absence of coronary occlusion.


Another ECG was recorded before the angiogram at 101 minutes:
Now there is qR in V2 again, with that same concordant STE.  QRS is 110 ms.  



The patient was taken for an angiogram, which was normal, with no evidence of ACS.  "No significant stenosis, thrombus or plaque rupture noted."

A formal echocardiogram showed LVH but was otherwise normal, with no wall motion abnormality.

Here is the troponin profile:



So what was the etiology?

The patient did not get a further diagnostic workup.  For example, he might have undergone MRI to evaluate for myocarditis.  But it was not necessary.  It could also have been a NonSTEMI with autolysis of thrombus and no residual culprit (no residual thrombus or ulcerated plaque visualized, which happens in 5-10% of NonSTEMI).

In such a case, the only way to know for certain if ECG findings are a result of ischemia is to see if subsequent ECGs evolve: any ischemic ST elevation, hyperacute T-wave, or ST depression will not remain static over time, especially after autolysis.  Unfortunately, no ECG was recorded later.  However, ischemia that is invisible on the ECG (as in this case) will not evolve over time.  Therefore, without MRI to distinguish 1) NonSTEMI with autolysis of thrombus vs. 2) myocarditis, we will never know for certain what happened.

As I suspected, these ECG findings are almost certainly manifestations of LVH.

Learning Points:

There are many PseudoSTEMI or PseudoMI patterns, including those due to LVH.  There is also Pseudo-Wellens' due to LVH.  They are recognizable.  They do not rule out coronary occlusion but they leave room for careful evaluation, especially with high quality echocardiography.

Often, even if you suspect PseudoSTEMI, angiogram may be the only way to be certain there is no acute coronary occlusion.

However, if you are unaware of all the pseudoSTEMI patterns, you will pull the trigger on the cath lab too soon too often.

In the context of an angiogram showing no obstructive coronary disease and elevated troponins, only evolution of the ECG, or its absence, can establish the etiology of ECG findings that are questionable for ischemia.

Other LVH PseusoSTEMI cases:

This very important case posted a few days ago:

Is it important to recognize LVH Pseudo-infarction patterns?


posted just last week:

A 60-something with Syncope, LVH, and convex ST Elevation

Severe LVH and PseudoSTEMI




Here is an extensive discussion of the LVH pseudoSTEMI phenomenon:  

LVH with anterior ST Elevation. When is it anterior STEMI?



PseudoWellens' due to LVH

Pseudo-Wellens' Syndrome due to Left Ventricular Hypertrophy (LVH)


Wellens' waves are NOT equivalent to Wellens' syndrome: Pseudo-Wellens' due to LVH and HTN



10 comments:

  1. I would have thought about stemi because of the changing ECG. Is it normal that lvh shows this kind of variability in one person in such short time span?

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    Replies
    1. No. I suspect there were changes in lead position to account for the variability

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  2. Fascinating case for which I wish we knew the answer. The 1st ECG looks highly unusual as you have stated. There does appear to be a prominent negative component to the P wave in leads V1,V2 in ECG #1 that is not seen in ECG #2 (the “baseline” ECG from 3 months earlier) — with negative P waves in V1 and/or V2 sometimes indicating too-high placement of these leads on the chest. Both tracings show clear voltage for LVH (R in aVL >12mm, and in ECG #2, very deep S wave in V2). The unusual qR in V2 with ST elevation and prominent T wave is seen again in ECG #5 (at 101 minutes just before the angiogram), albeit with too much artifact in V1 to comment on the P wave at this time, and perhaps a negative P in V2 … That said, I find it difficult ( = my opinion) to explain away this bizarre intermittent qR complex in V1,V2 on the basis of just LVH, especially given persistent troponin elevation. I’m glad the angiogram was done, and fortunately it was normal. I do not have an alternative explanation for the ECG changes we see — but rather than “manifestations of LVH”, I submit ( = my opinion) that we just do not know the answer in this case. This will not be the 1st time that an answer is not known, and it won’t be the last. THANKS for presenting!

    ReplyDelete
    Replies
    1. Ken, thanks as always for the great comments. As you can see from my answer to the comment above, I agree that there may be some lead placement issues here. But that doesn't explain it all. But I did not and do not think the ST elevation is ischemic.

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    2. Steve — I do agree with you that ST elevation in V1,V2 is probably not indicative of acute coronary syndrome. It IS an interesting case, and I wish we knew the answer (which I suspect lies within my P.S. comment below). THANKS again for presenting this fascinating case!

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  3. P.S. ECG #5 (at 101 minutes, just before the angiogram) — just does NOT make sense (ie, deep S in artifact-laden lead V1; qR in V2 — then rS in V3 …. ). Since that ECG was done IN the hospital — perhaps someone can “back track” to find out who did the ECG? Perhaps someone noted whether there was some kind of chest deformity that this man had which may have predisposed to anterior chest lead misplacement to the extent needed to produce these bizarrely different ECG appearances on serial tracings in this patient who has underlying LVH … I suspect therein may lie the answer …

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  4. I don't agree about absence of wall motion abnormality.
    If you carefully look at the first clip (parasternal long axis ) you can see a reduced systolic thickening (perhaps postsystolic thick.) of mid segment of posterior wall.
    Wath about?
    Thanks for very interesting case.

    ReplyDelete
    Replies
    1. Sergio,
      I defer to your expertise. However, a formal contrast ultrasound was done immediately after the angiogram and read by an expert. It showed no wall motion abnormality.
      Steve

      Delete
  5. This comment has been removed by the author.

    ReplyDelete
    Replies
    1. I have no idea what "thoracic angiotac" is.

      Delete

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