Tuesday, March 28, 2017

Echocardiography, even (or especially) with Speckle Tracking, can get you in trouble. The ECG told the story.

A completely healthy 30-something year old woman with no cardiac risk factors had sudden onset of bilateral trapezius pain that radiated around to her throat.  It resolved after about 5 minutes, but then recurred and was sustained for over an hour.  She called 911.

EMS recorded these ECGs:

Time 0:
In V2-V4, there is ST elevation that does not meet STEMI "criteria," of 1.5 mm at the J-point, relative to the PQ junction.  But there are also unusually Large T-waves

Called Normal by computer
This is the Zoll algorithm


I sent this to the Queen of Hearts:





Time = 13 min
T-wave in V2 is now taller and fatter, the ST segment is more straight.
T-wave in V3 is no taller, but it is fatter due to a straighter ST segment
This is highly suspicious for early LAD occlusion

Not identified as STEMI, but not normal either
This is the Zoll algorithm


Time = 24 min
No significant change
Zoll did not recognize acute MI, but did not call it normal

These prehospital ECGs were not seen.

The patient arrived in the ED.

The pain completely resolved after nitroglycerine 


Moments later, the this ECG was recorded in the ED when she had been pain free for moments only:
Computer read: Normal ECG.

This was by the Veritas algorithm

The ECG is diagnostic of LAD OMI

However, T-waves are still unusually large; the computer almost never sees this.
The T-wave in V2 is smaller. 
QTc is 444 ms.
STE 60 V3 = 1.5 mm, R-wave amplitude V4 = 15 mm, QRSV2 = 8.5
Formula value is 19.38, which indicates LAD occlusion 
(The most accurate cutpoint is 18.2 -- a value greater than 18.2 has high probability of LAD Occlusion).  

This patient has a nondiagnostic ECG by most rules.  

However, with attention to subtleties, especially when compared with the unseen prehospital ECGs, it is very worrisome.

And to my expert pattern recognition it is definitely LAD OMI


Since I taught the Queen of Hearts, she knows that it is OMI:


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For Americans, you need to wait for the FDA.  But in the meantime:

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The first troponin was below the level of detection (LoD).

If you use something like the HEART score:
1. H  History: She has atypical pain (trapezius) (score = 0)
2. E  EKG: a negative ECG (score = 0)
3. A  Age: = 0
4. R  Risk factors = 0
5. T:  Troponin = 0 [first troponin (contemporary, not high sensitivity) was less than the level of detection). 
Total HEART score = 0.  Risk of 30-day adverse events is less than 1.7%.   Some might send her home.

But maybe she has an acute LAD occlusion that will get even worse. 



The providers did a bedside echo and even used speckle tracking to look for strain:

I think maybe there is an anterior wall motion abnormality, but this is very difficult.  They read it as normal.

Here are a couple shots with strain, or "speckle tracking" on ED Echo:



To, me these look like anterior wall motion abnormality, but I showed them to one of our ultrasound fellows who is very interested in this.

She said:

This is a tough one. I see what you mean, initially when I looked at the image, I also thought there was an anterior wall motion abnormality.  But then on closer inspection, I suspect that maybe the anterior wall is just not being tracked well. In systole, you can see the anterior wall come down and outside of the area that is being tracked (more so than the other tracked walls). Even though the strain values are a little off in the graph (so is the posterior wall) it is still a value range (about -18) that would be considered non-ischemic by the cardiology literature, I believe.  I have been wrong before though! So it is possible that I am misinterpreting the clip. If it were me, I would get values at the level of the mitral valve, papillary muscles, and apex (all in PSS axis). Also, narrowing the area being tracked helps the walls get recognized much better.


As I wrote, the first troponin was below the Level of Detection.

She remained pain free, and was admitted without further serial ECGs.  

When in doubt, one should always get serial ECGs.  Bedside echo is not enough.


At time = 240 minutes (4 hours), the second troponin returned at 1.15 ng/mL.  That prompted recording of this ECG:
Back to normal for this patient.  This demonstrates that all ST elevation of the previous ECGs was ischemic, not normal.  She was having a transient STEMI, briefly.

It is very lucky that she spontaneously reperfused her LAD.  It did not progress to full STEMI with loss of the anterior wall, as in this case.

Also, persistence of a pain free state does not guarantee an open artery.  See this case.

A formal contrast echo was done at this point:
Normal estimated left ventricular ejection fraction, 65%.
Regional wall motion abnormality-distal septum and apex.

She was treated medically for NonSTEMI, pending next day cath, which showed  ulcerated plaque and a 60% thrombotic stenosis in the LAD distal to the first diagonal.  It was stented.


Learning Points:
1. Always get serial ECGs when there is any doubt about what is going on.
2. Use the 4-variable formula!!

12 Example Cases of Use of 3- and 4-variable formulas, plus Simplified Formula, to differentiate normal STE from subtle LAD occlusion

3. Always find and look at prehospital ECGs.  They give extremely valuable information.
4. Hyperacute T-waves remain for some time after reperfusion of an artery.  I always say that "you get hyperacute T-waves both 'on the way up' (before ST segment elevation) and 'on the way down' (as ST elevation is resolving).
5. Wall motion abnormalities are very hard to see, even with advanced Speckle Tracking technology.  They require a great contrast exam and expert interpretation.
6.  This case does not demonstrate it, but a wall motion abnormality may disappear after spontaneous reperfusion (see this case).
7. Patients with transient occlusion may manifest only transient STEMI on ECG.  Subsequent troponins may be all negative and subsequent formal echo may be normal.  See this case








8 comments:

  1. This confirms that the typical Wellens-morphology do happen
    "only" in 15-20% of the anterior riperfusion-cases (de Zwaan 1981-1989): right ?
    merci dr Smith !

    Al

    ReplyDelete
    Replies
    1. Al,
      That would only be confirmed if I were showing a next day ECG, which I did not do here and I don't have (but maybe could find).
      It often takes longer for the Wellens' waves to appear, and they are also dependent on the amount of infarct. If very small, there may be no T-wave inversion, though usually when Troponin I is > 1.0 ng/mL, Wellens' waves appear.
      Thanks!
      Steve

      Delete
  2. Great as always.
    I would say that i see hypokinesis on the anterior septum and anterior wall. I'm agree that serial ECGs are more important and diagnostic. Only in circumflex stenosis and oclusion echo could be superior that ECG in some cases for obvious reasons.
    Thx Stivi :)

    ReplyDelete
  3. Hey, firstly I want to congratulate you on this blog. Ive been following it for years, the level of digestible and practical information, and you're ability to package it simply is actually outstanding. As a cardiologist, I can say you're ecg reading skills (particularly as it relates to ischemia) is superior to most cardiologists (especially us younger ones) and I do refer our trainees to this website (among a few resources) when they do their CCU rotations.

    I do want to comment that even tho it is my specialty, I would have trouble differentiating the first ECG, the "boxiness/fatness" of the ST/T on V2 in the second one is a bit suspicious. The echo in the short axis of the mid LV (ignoring the circumferential strain) however does show, to me, a very obvious wall motion abnormality in the anteroseptum and anterior wall which would have clinched the diagnosis. Selling this to an interventionist at 2am would have been hard at my institution. Although I imagine your ecg reading skills (just by negative feedback alone) cary a bit of weight with the interventional team at your institution.

    ReplyDelete
  4. Great case as always, and thanks a lot for putting such valuable information (and effort) for free on the web. I am a cardiologist in training and as a part of the cardiology program we work in the ER. I have at least catched a couple of STEMIs the last 6 months based solely on what I have learned on this blog.

    This case illustrates the importance of ECG in the diagnosis of ACS/STEMIs. In my opinion, echocardrdiography is overrated in acute settings and the findings in the exam might be to subtle to be noticed by a relative inexperienced examiner. It is however often hard to sell the "borderline" cases such as this to interventionalists without echo exam.

    Do you know of any numbers/litterature where someone has studied the sensitivity and/or specificity of an MI by echo in acute settings?

    Thanks

    ReplyDelete
    Replies
    1. Good to hear from you.

      Here is one article:
      Early Assessment of Strain Echocardiography Can Accurately Exclude Significant Coronary Artery Stenosis in Suspected Non–ST-Segment Elevation Acute Coronary Syndrome

      http://www.sciencedirect.com/science/article/pii/S0894731714000480


      Here is an article I wrote last year with co-authors. There is an excellent reference list.
      Diagnosis of acute coronary occlusion in patients with non–STEMI by point-of-care echocardiography with speckle tracking
      http://www.ajemjournal.com/article/S0735-6757(16)00096-6/fulltext?rss=yes

      Delete
  5. Thanks Steve for posting such an informative and useful post on echocardiography that too for free. I am a pediatric cardiologist by profession and have been reading on the web all about echocardiography. I enjoyed a lot reading your post and learnt many new things on this topic. I would like to again thank you for such a nice post. Keep writing for the benefit of readers like us.

    ReplyDelete

DEAR READER: I have loved receiving your comments, but I am no longer able to moderate them. Since the vast majority are SPAM, I need to moderate them all. Therefore, comments will rarely be published any more. So Sorry.

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