Thursday, January 11, 2018

Incredible case of evolution of terminal QRS distortion, then resolution after thrombolytics

For more on Terminal QRS distortion, see these posts:


Best Explanation of Terminal QRS Distortion in Diagnosis of Electrocardiographically Subtle LAD Occlusion



The paramedic crew of Rick Morton and Kim Baker, of Ambulance Victoria in Australia, took care of this patient.  Their friend Shane Chapman sent the case to me.  He asked some questions which I put and answer at the bottom.

Case

A 60 something year old gentleman presented with chest pain radiating into left arm and a recent hx of SOB on exertion and fatigue for past 2 days.

Here are the ECGs and the times of their recording:
1529
This shows very high ST Elevation. 
There are well formed S-waves in V2 and V3.  The S-wave in V4 is beginning to disappear.

At 1544, the S-wave in V3 is much small, has almost disappeared.
The S-wave in V4 has completely disappeared.
A Q-wave is developing in V3

Prehospital Thrombolytics were appropriately given at 1600.
Good work, guys!!!
At 1620, the S-wave in V3 is almost completely gone.

More ECGs were recorded:

At 1655, there is even less S-wave in V3
Note: this never quite meets the criteria for terminal QRS distortion (TQRSD), which is zero S-wave or J-wave in either of V2 or V3.
These criteria have importance in our study of 171 cases of normal variant ST elevation (early repolarization), not one case had TQRSD by this definition.

Terminal QRS distortion is present in anterior myocardial infarction but absent in early repolarization

.


At 1656, there is now Left Bundle Branch Block
The heart rate has increased, so it is unclear if this change is due to rate dependent LBBB, or if it is due to ischemia of the left bundle branch.
There appear to be hyperacute T-waves in II, III, and aVF.  Is there also an inferior MI (wraparound LAD to inferior wall? --this was one question they asked.)

Notice we can't calculate the modified Sgarbossa ratio because the S-wave is cut off.

1659
Reperfusing!!
LBBB is resolved
Notice that the ST elevation is receding (but rate is a bit slower)
Notice that the S-waves are re-constituting

1716
Some persistent ST elevation, and persistent Q-wave in V3 and V4.
Successful reperfusion by thrombolytic therapy.





Now pain free, this ECG was recorded on arrival to the ED:
All ST Elevation is gone.  No Q-wave in V3 (these may indeed disappear with reperfusion)



Cath results:
Spontaneous coronary artery dissection (SCAD) of the mid LAD. 
No stent just managed medically and discharged home and doing well.


Could I please ask for your expert opinion?

Is this a wrap around STEMI?
        It has some features -- hyperacute T-waves appear to develop in II, III, aVF at 1656.
Can you explain the normal R-wave progression through the precordial leads? 
        This can be normal in anterior STEMI
Can you have normal R wave progression in the setting of STEMI?  

        Yes, you can.





7 comments:

  1. I'd almost say that the 16:56 ECG looks like AIVR from reperfusion (either that or a marked change in the PRi).

    Great case!

    ReplyDelete
  2. GREAT illustration of the importance of assessing the presence or absence of terminal QRS distortion — with the UNIQUE opportunity offered here by these serial tracings to see this important ECG sign come and go as a stemi evolves and after reperfusion. I’ll add 2 observations: i) In addition to terminal QRS distortion — the magnitude of J-point ST elevation in mid-chest leads in association with abnormal ST segment shape/overly wide base in an older adult with worrisome chest pain is clearly abnormal. T waves off the page on the 2nd ECG are diagnostic; and ii) At 16:56 — isn’t this picture more suggestive of AVIR rather than LBBB? (loss of P waves since the 16:35 tracing + very unusual QRS morphology in the limb leads for lbbb — with resolution of this pattern just 3 minutes later at 16:59 when P waves return again in association with slowing of the ventricular rate — all at about the time one might expect reperfusion to be occurring). Our thanks to Dr. Smith and the Australian team of Rick Morton & Kim Baker for sharing this insightful series of tracings.

    ReplyDelete
    Replies
    1. Could be AIVR, (as Ken above has suggested), and makes sense with reperfusion.

      Delete
  3. Steve — As I take another look at the cath results, I see there was “spontaneous coronary artery dissection of the mid-LAD that was managed medically” (ie, managed with thrombolytics). Was this a primary coronary artery dissection as a cause of this all? — or was the dissection secondary to the stemi and due to the cath itself? Just wondering about use of thrombolytics without stent as the management for this? Perhaps Rick Morton & Kim Baker might provide additional follow-up details on this case? THANKS!

    ReplyDelete
    Replies
    1. Ken,
      Details are missing and I just don't know them, so I can't judge whether treatment was appropriate or not. Angiography and PCI is very technical and I would not ever be in a position to judge whether an interventionalist did the right thing or not.
      Thanks!
      Steve

      Delete

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