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

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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.

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

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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.