Friday, November 1, 2024

Can you treat Non-STEMI with thrombolytics if it is OMI (Occlusion MI)? Of course!

This case was sent by an old residency friend, Kirk Lufkin.  He works in a small hospital in Northern Michigan.  

Case

A 61 year old female. hypertension no other past history presented with 30 minutes of fluctuating non-radiating heaviness in chest, with diaphoresis and nausea. VS normal. No cardiac past history. 

Here is her ECG:

What do you think?











There are inferior hyperacute T-waves (diagnostic of inferior OMI), with 1) reciprocal ST depression in aVL, 2) a reciprocally inverted hyperacute T-wave in aVL, 3) ST depression in V2 (diagnostic of posterior OMI) and 4) large lateral T-waves which are probably hyperacute.

So this is acute OMI.  But it does not meet the ridiculous "STEMI criteria" since there is not 1 mm of STE in any lead.

What does the Queen of Hearts say? (Dr. Lufkin did not need her)

OMI with High Confidence

Click here to sign up for Queen of Hearts Access.


Dr. Lufkin gave thrombolytics, with a "door-to-needle" time of 24 minutes.  The standard of care is < 30 minutes.

Minutes later, the pain resolved and this ECG was recorded:

Complete resolution of ST Elevation and of V2 ST depression, and of V4-6 hyperacute T-waves.


Later, the first troponin I returned at 0.057 ng/mL (4th generation, not high sensitivity). 


The patient was transferred to a hospital with PCI capability.


Here is the angiogram:


Very tight stenosis in circumflex, but with TIMI-3 flow, thanks to thrombolytics.


Here is the circumflex after stenting:


Wide open



The cardiologist called Dr. Lufkin back and said "Great call!!"


Learn to read the ECG for sublte OMI, and get the Queen of Hearts.




===================================

MY Comment, by KEN GRAUER, MD (11/1/2024):

===================================
The beauty of today's case is its simple efficiency. Working in a smaller emergency facility — Dr. Lufkin considered the history ( = new-onset, severe CP in a 61-year old woman— correctly interpreted the initial ECG (which I've reproduced and labeled in Figure-1) — and, given time constraints and distance from a PCI-capable center — he expediently initiated thrombolytic therapy ("door-to-needle" time = 24 minutes).
  • When promptly administered — thrombolytic therapy may be very effective (witness relief within minutes of this patient's CP — with marked improvement in ECG abnormalities).

As per Dr. Smith — the initial ECG is diagnostic of acute infero-postero-lateral OMI (consistent with acute LCx occlusion). I highlight KEY findings in Figure-1:
  • My "eye" was immediately drawn to the obviously hyperacute T wave in lead III (within the RED rectangle). Equally hyperacute are T waves in the other 2 inferior leads (RED arrows in leads II and aVF) — with each of these 3 leads featuring hypervoluminous T waves "fatter"-at-their-peak and wider-at-their-base than expected given QRS amplitude in each respective lead.
  • Confirmation in this 61yo woman with new CP that these inferior lead findings are "real" — is forthcoming from mirror-image opposite reciprocal ST-T wave depression in lead aVL (within the BLUE rectangle), and to a lesser extent in lead I.
  • Additional confirmation is seen in lead V2 (within the RED rectangle in the chest leads— with pathognomonic downsloping ST depression and biphasic T wave with terminal positivity (RED arrow in lead V2). Neighboring leads V1 and V3 are consistent with ongoing posterior OMI (T wave inversion in V1 — and ST straightening with depression in lead V3).
  • In view of the above findings — I thought the T waves in leads V5 and V6 were "bulkier" than expected (given modest size of the R wave in these leads).

  • BOTTOM Line: As emphasized by Dr. Smith — the above findings are absolutely diagnostic of acute infero-postero-lateral OMI. With practice — these diagnostic ECG findings can (and should) be recognized within seconds. Dr. Lufkin appreciated these findings, and given the worrisome history — he needed no more testing and no additional ECGs to justify immediate initiation of thrombolytic therapy.

Figure-1: I've labeled the initial ECG in today's case.


What about the Rhythm in Figure-1?
Did YOU notice the irregularity in today's rhythm? I'll preface my remarks by acknowledging that the rhythm in Figure-1 does not follow "the usual rules".
  • There appears to be some sort of group beating — initially with 4 sinus beats, and then 3 groups of 2 beats.
  • Upright P waves precede each of the 10 beats in the long lead II rhythm strip. That said — P wave morphology varies in no particular pattern, and to a greater extent than is usually seen in a normal sinus rhythm.
  • Given the acute infero-postero MI — I looked for AV Wenckebach, which is so commonly seen in this clinical setting. But I see no non-conducted on-time P wave after beats #4,6,8 and 10.
  • I also do not see any evidence of blocked PACs — as the T waves of beats #4,6,8 and 10 look identical to the T waves of other conducted beats.
  • The fact that there is variation in the R-R interval for the first 4 sinus-conducted beats suggests the possibility of a marked sinus arrhythmia — but I would not expect this degree of variable P wave morphology and such group beating.
  • The rhythm could represent Type I SA block with underlying sinus arrhythmia — but again, I would not expect this degree of variable P wave morphology (and in my experience — true SA block is rare).

  • By Default: I thought some form of unusual marked sinus arrhythmia, with uncharacteristically variable sinus P wave morphology to be the best I could come up with for the rhythm diagnosis.
  • The "Good News"  Normal sinus rhythm with consistent P wave morphology resumed following successful thrombolytic therapy. Perhaps the highly unusual initial rhythm in today's case was simply the result of SA nodal ischemia that resolved following coronary reperfusion.





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