What is the infarct artery? What does the post PCI ECG show? What does the convalescent ECG show?

What is the infarct artery? 

I usually don't ask this question, as it is rarely relevant to the decision to activate the cath lab.  

This is one case where it made a difference: Right Ventricular MI seen on ECG helps Angiographer to find Culprit Lesion

Nevertheless, it is sometimes a fun academic exercise to try to predict the infarct artery:

An elderly patient had onset of chest pain one hour prior.  He called 911.  Here is the prehospital ECG.

What do you think?

I think it looks like an inferior posterior OMI.  The medics thought so too and activated the cath lab from the prehospital.

The Queen also diagnoses OMI.

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Case continued:

The medics recorded another ECG 2 minutes later:

This was interpreted as an inferior posterior OMI, I think correctly.

Aside: there is artifact in V4

9 minutes later, this was recorded:

What do you think?

Smith: now there are precordial hyperacute T-waves with depressed ST takeoff (de Winter's).  The inferior STE is gone and there is actually STD, so it appears to be a proximal LAD occlusion now.

de Winter's T-waves have a depressed ST segment and an upright hyperacute T-wave.  They are usually quite distinct from posterior OMI, which also has a depressed ST segment and can have a T-wave that is either inverted, biphasic, or upright.  So they can sometimes be mistaken for each other.  This does not explain the apparent inferior OMI, and that ultimately remains unexplained.

Cath lab was activated.  Chest pain onset to balloon time was quite short (approximately 120-150 minutes)

Angiogram:

100% proximal LAD Occlusion

Post PCI ECG:

What do you think?

--There is RBBB (a very bad sign).  

--There is no initial r-wave, so this is a qR; thus there is loss of anterior forces of the QRS (another bad sign).  

--There is a QS-wave in V3 (another bad sign).  

--There is persistent ST elevation in leads V1-V4, with a lot of STE in V4 (another bad sign). 

All of this appears to be consistent with "No Reflow", or small vessel occlusion with persistent ischemia in spite of an open artery.  Small vessel occlusion is measured by "blush" on the angiogram, and codified by TIMI Myocardial Perfusion (TMP) Grading.  The best predictor of good blush and high TMP is the ECG, specifically resolution of ST Elevation on the ECG.  Thus, this ECG predicts poor myocardial perfusion and poor outcome.

For lots of information, read this post:

Poor Microvascular Reperfusion ("No Reflow"): Best Diagnosed by ECG

Next day Echo:

EF 20%

Regional wall motion abnormality-distal septum anterior and apex akinetic, large

Regional wall motion abnormality-distal inferior wall akinetic.

Regional wall motion abnormality-anterolateral akinetic.

Regional wall motion abnormality-anterior akinetic.

This poor echo can be seen even after very good reperfusion because myocardium that is still viable can be "stunned" and take weeks to recover.  But the ECG is telling us that the myocardium will probably not recover.

Such large infarcts have many complications.  His included cardiogenic shock, V Tach, AV block. He was hospitalized for 16 days.

ECG one month later:

What do you think?

This ECG is diagnostic of anterior LV aneurysm in the presence of RBBB.  There will be very little recovery.

See more such cases of RBBB with LV aneurysm here.  It is a particularly difficult LV aneurysm to diagnose on the ECG because the RBBB creates an R-wave that otherwise would not be there.

Echo 1 month later:

--Mildly enlarged left ventricular cavity size, normal wall thickness and severe LV systolic dysfunction.

--The estimated left ventricular ejection fraction is 20 %.

--Regional wall motion abnormality-mid and apical septum, mid and apical anterior and true apex, thinned out and dyskinetic. (Smith: this is the definition of LV aneurysm)

--Regional wall motion abnormality- apical anterolateral and apical inferior, akinetic.

Unfortunately, and predictably, he now has rather severe heart failure.

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MY Comment, by KEN GRAUER, MD (10/6/2023):

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We’ve reviewed multiple variations on the “theme” of deWinter T waves in Dr. Smith’s ECG Blog (See My Comment at the bottom of the page in the April 17, 2023 post — to name just one). 

• What has impressed me the most about this clinical entity (that predicts impending and/or ongoing LAD OMI) — is that depending on when during the process a given ECG is obtained — the ECG “picture” of deWinter T waves may vary in a number of ways from the 8 clinical ECG examples presented in the original NEJM manuscript by deWinter et al (Figure-1).
• 
  
• Today’s case presents yet another example of what clearly evolves to become deWinter T waves — after presenting as an acute infero-postero OMI on the initial ECG.

Figure-1: The deWinter T Wave Pattern, as first described by Robbert J. de Winter et al in N Engl J Med 359:2071-2073, 2008. ECGs for the 8 patients shown here were obtained between 26 and 141 minutes after the onset of symptoms. (See My Comment in the April 17, 2023 post for more on this pattern).

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Take Another Look at the initial ECG — and the repeat tracing done 9 minutes later (Figure-2):

• Was there any way to recognize acute LAD OMI from the initial ECG?
• HOW can you explain the atypical appearance of deWinter T waves in the repeat tracing? 
• What do you think another repeat ECG might have looked like — if one would have been recorded soon after ECG #3?

Figure-2: Take another LOOK at the initial ECG compared to the repeat tracing done ~9 minutes later (that for clarity, I have put together in this figure).

Posterior OMI vs deWinter T Waves? 

As per Dr. Smith — at times, the ST-T wave depression with terminal T wave positivity of posterior OMI can be mistaken for deWinter T waves (and vice versa). Such confusion may be more likely in cases in which there is a "wrap-around" LAD. That said — I had no idea when I initially looked at ECG #1 in today's case, that the patient was about to evolve into an extensive anterior infarction.

• ECG #1 in Figure-2 is completely typical for acute posterior OMI because: i) There is "shelf-like" ST depression in the chest leads that is maximal in leads V2-to-V4, with terminal T wave positivity (ie, positive "Mirror Test" — as discussed in My Comment in the September 21, 2022 post in Dr. Smith's ECG Blog); ii) There is early transition — with a predominant R wave already by lead V2; and, iii) There is evidence of associated inferior OMI (ie, Q waves in leads III,aVF — hyperacute T waves in all 3 inferior leads [in proportion to the tiny QRS in these leads] — and suggestion of reciprocal shallow-but-real reciprocal T wave inversion in lead aVL).

The ECG picture dramatically changes 9 minutes later — with the repeat tracing shown in Figure-2:

• A relatively late-cycle PVC is seen in ECG #3.
• The shelf-like ST depression that had been maximal in leads V2-to-V4 in ECG #1 — has now resolved. This has been replaced by now virtually all positive (hyperacute) T waves, that are most prominent in leads V2-to-V4.
• NOTE #1: T wave positivity now begins in lead V1!

Additional Observations I Found Interesting:

• The QRS complex in lead V1 of ECG #3 — is now predominantly positive. That this change is real — is supported by finding that the QRS is now virtually all positive in neighboring leads V2 and V3.
• 
  
• NOTE #2: I was initially tempted to attribute this new predominant QRS positivity in leads V1,V2,V3 to evolution of the posterior OMI that I thought the patient was having — but further review suggested instead the unexpected evolving pattern of deWinter T waves!
• 
  
• NOTE #3: The ST segments in leads V2 and V3 of this repeat ECG are actually elevated! That this is real — is apparent from the difference compared to ECG #1, in which ST segments in these leads were depressed.
• 
  
• NOTE #4: Considering that definite S waves were previously seen in ECG #1 — I interpret the subtle notching at the end of the QRS in leads V2,V3 of ECG #3 as consistent with T-QRS-D (Terminal-QRS-Distortion) — thereby providing further evidence of acute evolving LAD OMI.
• 
  
• NOTE #5: The ST segment, that had been "shelf-like" and relatively long in ECG #1 — has now noticeably shortened in ECG #3. As suggested in the clinical ECG examples from the original deWinter manuscript (shown above in Figure-1) — typical deWinter T wave patterns manifest J-point ST depression that is immediately followed by rapid T wave upsloping into the overly large T waves characteristic of this entity. 
• I suspect that IF another repeat ECG would have been done a few minutes after ECG #3 — that this rapid T wave upsloping would have been further accentuated (as it is beginning to be in lead V4 of ECG #3).
• 
  
• NOTE #6: As shown above in Dr. Smith's discussion — subsequent ECGs manifested complete RBBB. I suspect that the now predominant R wave positivity seen in leads V1,V2,V3 of ECG #3 represent ongoing evolution toward this RBBB pattern. After all — this patient is evolving a huge anterior infarction (which very soon will manifest with complete loss of anterior R waves) — such that the only logical explanation for the now predominant R waves in V1,V2,V3 of ECG #3 is from beginning development of RBBB. (RBBB has of course not yet evolved — as the QRS is not yet wide in ECG #3 — and there are not yet terminal S waves in lateral leads).
• 
  
• NOTE #7: I was initially tempted to attribute the new T wave inversion in lead III of ECG #3 (as well as the beginning T wave inversion in lead aVF) to inferior reperfusion — BUT — given all of the above changes suggesting deWinter T waves (including now T wave positivity beginning as early as in lead V1) — it makes much more sense to attribute limb lead ST-T wave appearance to reciprocal changes from the proximal LAD occlusion seen on cath.
• 
  
• NOTE #8: As I emphasized at the beginning of my Comment today — the ECG picture of deWinter T waves tends to vary depending on when during the process a given ECG is obtained. The fact that ECG #3 is already showing ST elevation (along with T-QRS-D in leads V2,V3) — together with the RBBB/LAHB pattern with marked ST elevation on the post-PCI ECG — suggests that we either missed more classic deWinter T wave findings (such as those shown above in Figure-1) — or more likely, typical deWinter T wave findings were masked by the initial ECG appearance in today's case that was much more suggestive of infero-postero OMI.
• 
  
• NOTE #9: I think it worthwhile to contemplate WHY the initial ECG did not at all suggest today's patient was about to evolve an extensive anterior infarction. We know today's patient was "elderly" — but we don't know the patient's prior history, nor do we know other cath findings beyond that there was acute 100% proximal LAD occlusion. Answers might be forthcoming — IF we had a prior (baseline) ECG — and/or if we knew whether the patient had prior coronary disease (perhaps with some unusual collateralization pattern).

BOTTOM Line in Today's CASE:

• Although I was completely fooled as to the "culprit" artery in today's case from the initial ECG — this does not matter clinically. This is because in a patient with worrisome new chest pain — regardless of what the "culprit" artery turns out to be — the ECG picture in today's initial tracing provides clear indication for prompt cath!
• 
  
• The above said — I found it highly insightful to learn that despite the initial ECG picture — the "culprit" artery was a completely occluded LAD!