Friday, August 16, 2024

60 yo with chest pain: why the abnormal QRS and abnormal repolarization?

 Written by Pendell Meyers


A man in his 60s presented with acute chest pain and normal vital signs. Here is his triage ECG:

What do you think?








The ECG shows massively hyperacute T waves of LAD OMI, plus WPW. V3-V5 also have the depressed HATW takeoff which qualifies them as the rare de Winter subtype of HATWs. Its hard to measure the STE in I exactly with the moving baseline, but there is almost certainly not enough STE to meet STEMI criteria. 

These HATWs are the epitome of what makes a T wave hyperacute: they have massively, symmetrically inflated area under the T wave compared to the QRS (either by size or area of the QRS). They are symmetric, fat, convex on both sides, etc. 

The ACC recognizes these findings as formal STEMI equivalents (though they do not define how to find them). 


Here is the Queen of Hearts (version 1) interpretation, of course:



Luckily for this NSTEMI patient, the ECG was recognized as LAD OMI despite lack of formal STEMI criteria. 


Immediate cath lab activation revealed acute total mid-LAD occlusion. 



Initial hs troponin T from arrival later returned at 9 ng/L (within normal limits). 

 
Here is the ECG soon after intervention:



Troponin T peaked at 2,923 ng/L. 

Here is the ECG hours later:
WPW, with anterolateral reperfusion T wave inversions.






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MY Comment, by KEN GRAUER, MD (8/16/2024):

===================================
As emphasized in the October 13, 2022 post in Dr. Smith's ECG Blog — the diagnosis of acute MI in a patient with WPW can be challenging. I noted some reasons why this is so in My Comment from that Oct. 13 post.
  • So, today's case offers a rare example of deWinter T waves in a patient with preexcitation — for whom acute OMI was promptly diagnosed — reperfused with PCI — and for which we are provided the luxury of serial ECG follow-up, culminating with reperfusion T waves

For clarity in Figure-1 — I've put together the 3 serial tracings in today's case.
  • ECG #1 — highlights the delta waves that are seen in most leads (RED arrows). As per Dr. Meyers — the extra "plump" precordial T waves, complete with J-point depression in leads V3,V4,V5 — are perfectly consistent with what I'd expect a classic deWinter T wave appearance to look like in a WPW patient with predominant positivity in lead V1. (See My Comments at the bottom of the page in the October 6, 2023 and April 17, 2023 posts for review of deWinter T wave patterns).

  • ECG #2 — shows the rare picture in each of the chest leads, of a complete deflation of the hyperacute deWinter T waves from ECG #1. That the effect of ongoing preexcitation has nothing to do with this complete precordial lead deflation — is apparent from complete preservation of the same short PR interval, with virtually identical delta wave and QRS morphology as was seen in ECG #1.

  • ECG #3 — proves that ECG #2 is a perfectly timed "snapshot", taken at the precise midway point (at least in the chest leads) between the super-"plump" deWinter T waves from ECG #1 — and the deep reperfusion T waves (most notable in leads V2,V3,V4) that we now see.

MY "Curiosity" Questions:
  • Curiosity #1: I found it interesting that without appreciable change in PR interval or delta wave appearance — QRS morphology in both ECG #1 and ECG #2 remains very similar to QRS morphology in ECG #3, with the exception of lead V1, that has lost its predominant positivity from the first 2 tracings. Is this a corollary for some sort of RBBB-like conduction defect resulting from LAD OMI in a patient with WPW — that then resolves immediately following reperfusion?

  • Curiosity #2: I'd love to see what this patient's pre-OMI ECG looked like? Perhaps that prior tracing would explain the extra-"fat" hyperacute T waves in ECG #1 — as well as the remarkably flat ST segments and T waves that we see in the chest leads of ECG #2. 
  • In My Experience — the effect of preexcitation on repolarization (ie, ST-T wave appearance) is not always predictable. It is for this reason that I have found ST-T wave changes of acute OMI much more difficult to assess in patients with WPW. I therefore found today's case especially insightful via the "timing" of today's 3 serial ECGs.

Figure-1: I've put together the 3 serial tracings from today's case.



 





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