Sunday, October 23, 2022

30 yo woman with trapezius pain. HEART Pathway = 0. Computer "Normal" ECG. Reality: ECG is Diagnostic of LAD Occlusion.

This is a repost of this amazing case: 

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 prehospital 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


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
These are hyperacute T-waves that are DIAGNOSTIC of LAD Occlusion.

Time = 24 min
S-wave depth is diminishing


These prehospital ECGs were lost and 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.
However, T-waves are still unusually hyperacute; the computer almost never sees this.
The T-wave in V2 is smaller.  QTc is 444 ms.
How about using the 4-variable formula?
STE 60 V3 = 1.5 mm, R-wave amplitude V4 = 15 mm, QRSV2 = 8.5
Formula value is 19.38, which indicates LAD occlusion 
(Most accurate cutpoint is 18.2 -- value > 18.2 has high probability of LAD Occlusion).


This patient has a non-diagnostic ECG by most rules.  

However, with attention to subtleties, especially when compared with the unseen prehospital ECGs, it is diagnostic of LAD occlusion with probable spontaneous reperfusion.

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:

hyperacute T-waves standard echo nstemi vid 3 from Stephen Smith on Vimeo.



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:

hyperacute T-waves speckle 1 x4 from Stephen Smith on Vimeo.

hyperacute T-waves speckle 2 x4 from Stephen Smith on Vimeo.


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 bubble 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. Risk scores + EKG and troponin should not be considered negative unless there are 2 troponins.
9. Risk scores should not be used at all in the setting of a diagnostic EKG.  These are DIAGNOSTIC of LAD OCCLUSION.



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MY Comment by KEN GRAUER, MD (10/23/2020):
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There are a number of important lessons worthy of repeating from today's repost of our case from March 28, 2017. As per Dr. Smith:
  • Always search for and find prehospital ECGs. These will often provide invaluable information.
  • Serial ECGs correlated to the presence (and severity) of chest pain — often reveal the status of the "culprit" artery (ie, occluded, reopened, reoccluded).
  • Hyperacute T waves may maintain their appearance for a period of time after reperfusion of the culprit artery.
  • Some patients are lucky — in that the culprit artery may spontaneously reperfuse — and then remain open until definitive diagnosis and treatment can be instituted. Other patients are not so lucky.
  • If spontaneous reperfusion occurs rapidly — serial troponins may be no more minimally elevated (if elevated at all). Echo may be normal (especially if the patient no longer has chest pain).

I found review of the 3 serial pre-hospital ECGs in this case to be especially insightful as to how lead-by-lead comparison often "tells the tale" — by confirmation of dynamic ST-T wave changes.
  • KEY Point: Subtle serial ECG changes may be EASY to overlook unless careful lead-by-lead comparison is performed.
  • Be sure to verify QRS morphology in both the limb leads and chest leads when performing lead-by-lead comparison. This allows you to ensure that neither frontal plane axis shifts nor variation in chest lead electrode placement are influencing ST-T wave appearance in the tracings you are comparing.

For clarity — I've taken the chest leads from the 3 pre-hospital tracings in this case, and placed them side-by-side in Figure-1. The reason I omitted the limb leads — is that I did not appreciate any significant ST-T wave change in the limb leads from these 3 tracings. In contrast — There are subtle-but-real changes in ST-T wave appearance in many of the chest leads.


CHALLENGE: 
Take Another LOOK at the serial chest leads in Figure-1What are the dynamic ST-T wave changes that you see?
  • HINT: When contemplating whether T wave size is increased from one tracing to the next — be SURE to compare relative size of the R wave in each lead you are looking at!

Figure-1: Comparison of the chest leads in the 3 serial ECGs performed by the EMS team prior to hospital arrival. What are the ST-T wave changes that you see?


MY Thoughts on the 3 Pre-Hospital ECGs:
T waves are tall and peaked in the chest leads from each of these 3 pre-hospital tracings shown in Figure-1.
  • Especially in lead V3 of ECG #1 — the T wave is already huge (>10 mm), and outsizes the R wave in this lead.

ECG #2 (Time = 13 minutes):
  • Beginning with lead V3 — the T wave is not quite as tall as it was in lead V3 of ECG #1. But this is most probably because the R wave in lead V3 of ECG #2 is relatively smaller. The R wave in lead V3 now only measures 7 mm — whereas the R wave was much taller in lead V3 of ECG #1. Relatively Speaking — the T wave is taller in ECG #2, because it is now almost twice the height of the R wave in this lead!
  • Even more important than this relative increase in T wave height — is the increase in "volume" of the T wave in lead V3 of ECG #2. Note how much "fatter-at-its-peak" and "wider-at-its-base" the T wave now is.
  • I thought all 6 chest leads in ECG #2 show a relative increase in both size and volume of their T waves, compared to T waves in the chest leads of ECG #1.

ECG #3 (Time = 24 minutes):
The difference in ST-T wave appearance between chest leads in ECG #2 and ECG #3 is more subtle — but still present!
  • Isn't the T wave in Lead V2 of ECG #3 more voluminous (ie, with a wider base— than it was in ECG #2?
  • Considering further decrease in R wave amplitude — Isn't the T wave in lead V3 of ECG #3 relatively taller and more voluminous than it was in ECG #2?
  • In lead V4 of ECG #3 — the T wave is taller than the R wave for each of the 3 QRS complexes that are shown. In contrast — the R wave is slightly taller than the T wave for each of the 3 complexes in lead V4 of ECG #2.

To Emphasize — The changes I describe above in ST-T wave appearance between ECG #2 and ECG #3 are extremely subtle. If I didn't have ECG #1 as my starting point — I would not have attributed clinical significance to the subtle changes between ECG #2 and ECG #3.

  • BUT — Given that we do have all 3 serial pre-hospital tracings as a basis for comparison — I think the trend that we see from one tracing to the next is real — and clearly suggests dynamic ST-T wave change (which in this patient with new cardiac symptoms — indicates an acute ongoing process until proven otherwise).
  • Take Home POINT: It would be EASY to overlook these dynamic ST-T wave changes if one was not meticulous in their lead-by-lead comparison.




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