Sunday, March 28, 2021

Nonspecific symptoms with RBBB and New ST Elevation. Anterior STEMI, right? What does the echo show?

A 50-something male with a history of COPD and substance use disorder who presented with generalized weakness and exacerbation of chronic back pain that is now radiating to his neck, and headache. He also developed nausea, alternating "hot and cold flashes", and generalized weakness the previous evening. He became anxious about his symptoms and then used crack cocaine as well as drank alcohol last night. His symptoms have persisted since then. He states he has felt short of breath since last night. He denies any chest pain, though notes he has a "odd" sensation in his chest. 


Vital signs were normal and physical exam was unremarkable

He had an ECG recorded:

This is RBBB, which normally does not have ST Elevation anywhere.  In fact, it normally has ST depression in V1-V3 that is discordant to the previous R'-wave.  

In this case, there is no R'-wave in V1, which is unusual in RBBB.  
V2 and V3 do have rSR', and both of those also have ST elevation that is concordant to the R'-wave.  This usually is an indicator of LAD occlusion.
This is all but diagnostic of lead V1 - lead V3 lead reversal
Nevertheless, the T-waves appear hyperacute.

There was a previous ECG from 3 months prior
This ECG does have an R'-wave in V1, and (appropriately) without STE.  V2 and V3 are lacking an R'-wave; in fact, they have a wide S wave which is usually only seen in lateral leads of RBBB.  There is STE which is discordant to that wide S-wave; usually the ST segment in RBBB is isoelectric even AFTER the wide S-wave.

So this is an abnormal baseline ECG, but the acute ECG looks far more worrisome.

Let's look at V1-V3 side by side, presentation ECG on the left and old one on the right:

V1 T-wave sure looks hyperacute compared to the old one.
I have not applied the term "Terminal QRS distortion" to RBBB, but if one did so, then the acute ECG would definitely qualify in lead V3 (R'-wave does not return to baseline).


A Bedside echo (POCUS) was recorded:

Notice only the apex contracts; the base does not.  

Is it just an apical wall motion abnormality due to LAD occlusion?  

One might think so.


Angiogram:

--Large RCA without significant disease.  

--Left main is large with mild proximal plaque

--Circumflex is a small caliber vessel and supplies two small OM branches

--There is a medium caliber, multi-branching ramus intermediate without

significant disease.

--LAD is a large caliber vessel that extends to the apex.  No significant coronary artery disease is noted in the LAD, but the LAD is noted to dilate with IC nitroglycerin. LAD supplies four small caliber diagonal branches

--Left ventricular end diastolic pressure (LVEDP) 24-27 mm Hg (elevated) in the setting of SBP < 85

 

Impression and recommendation:

--No significant obstructive coronary artery disease to explain elevated troponin, dyspnea and ECG changes

--No evidence for plaque rupture or vessel occlusion

--Significant elevated left ventricular filling pressure in the setting of relative hypotension

--Consider non-ischemic cardiomyopathy; troponin elevation could be caused by decrease coronary perfusion pressure in the setting of elevated LVEDP.  Would not recommend further treatment of ACS

Contemporary troponin I peaked at 0.393 ng/mL, which is typical for a Non-OMI, but also for a variety of "acute myocardial injury" diagnoses.

An ECG was recorded the next AM:

Less hyperacute, but still has ST Elevation in V1-V3


Formal echo with contrast:

Possible atypical stress cardiomyopathy with sparing of the apex (It looked similar to the POCUS echo)

Assessment:

Intracoronary nitroglycerin suggests a component of coronary vasospasm, LVEDP was elevated to 24. Serial troponin testing was 0.227, 0.222, 0.343, 0.393 ng/mL. TTE revealed LVEF of 40-45% and possible atypical stress cardiomyopathy with sparing of the apex.  There may be some contribution of cocaine toxicity to epicardial and microvascular coronary spasm.

Apical takotsubo or "Reverse" Takotsubo.  (Of course it should not be called takotsubo because that name comes from the japanese octopus trap, which implies apical ballooning with good contraction of the base.)

Read about Reverse takotsubo here: 

Respiratory Failure and ST Depression: Is there Posterior STEMI?



12 comments:

  1. I know it’s only a technical point but don’t you think that the V1 and V3 connections were swapped in the first ECG?

    ReplyDelete
    Replies
    1. Dave, I noted that right from the start. There are about 7 comments on this when I made that observation! But thanks for sending comments.

      Delete
  2. Interesting case but would like to add that V1 to V3 are the wrong way around in the first ECG. Comparing the 3 ECGs confirms this. It doesn't change the findings but after seeing many ECGs with misplaced electrodes and leads connected to the wrong electrodes it is clear these leads are switched. Thanks Dr Smith for this case. Arron

    ReplyDelete
  3. Hello Dr Smith, once again a great post of reverse Takotsubho stress cardiomyopathy. Your ECG discussion was quite educative. I have a small point to ask. Cocaine can cause hyperkalemia by
    way of causing rhabdomyolysis and hyperkalemia is well known to cause pseudo-STEMI pattern especially in V1,V2 and V3. T waves are tall and too sharp in V1,V2 & V3, warranting urgent serum potassium measurement- also CPK level. With regards, Dr.R.Balasubramanian,PONDICHERRY-INDIA

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  4. Steve...

    Is it possible that lead wires for Leads V1 and V3 were interchanged on the ECG done in the ER? Leads I and V6 show classic RBBB morphologies, but there is no way you are going to have an S wave in V1 in any form of RBBB. I always make the point in my classes that the most RELIABLE lead for diagnosing RBBB is Lead I, because no matter how variant the morphology in V1, the QRS in Lead I will always look the same in RBBB (with very, very few exceptions).

    ReplyDelete
    Replies
    1. Jerry, thanks for the comment. I already pointed that out. --Steve

      Delete
  5. Just to add to your great case, V1 and V3 have been switched in the first ECG. It doesn't change the outcome but helps to explain why the first ECG looks so unusual.

    ReplyDelete
  6. In first ECG first 3 chest leads switched

    ReplyDelete

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