A Patient with Vertigo

This patient presented with vertigo and had an ECG recorded

What do you think?

I saw this and was worried about inferior OMI due to some subtle STE in III with very worrisome reciprocal findings in aVL.  But the well-formed Q-wave and the presence of a normal T-wave in inferior leads led me to believe this was Old Inferior MI with persistent ST Elevation, otherwise known as inferior LV aneurysm.

Anterior LV aneurysm is much easier to recognize because the Q-wave is usually a QS-wave (no R-wave at all), in at least one lead.  Or at least only a very tiny r-wave (1 mm or so).

Thus, acute inferior OMI and inferior LV aneurysm is very hard to differentiate.

But the patient had previous ECGs on file from years ago, and records showed a h/o of inferior OMI with PCI:

10 years ago

This is a post PCI ECG of an inferior OMI

There are reperfusion T-waves (inverted, with well-formed pathologic Q-waves)

This previous ECG begs the question: do the upright T-waves on the presentation ECG, in contrast to the inverted T-waves on the old ECGs, represent "pseudonormalization" of T-waves, a sign of acute occlusion?

No!  Pseudonormalization can only be diagnosed in the early aftermath (days to weeks) of reperfusion.  Over time, T-waves normalize in the absence of new OMI.  So upright T-waves in the presentation ECG do NOT mean there is any re-occlusion.

5 years ago

Similar

Previous formal echocardiogram

Inferior posterior with dyskinesis

"Dyskinesis" is the technical echo term for LV aneurysm.

The combination of absence of chest pain and history of LV aneurysm made it easy to assess that this patient does not have acute OMI.

The patient ruled out by serial troponins.

I sent this ECG to the Queen of Hearts (PMcardio OMI), and here is the verdict:

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MY Comment, by KEN GRAUER, MD (7/26/2023):

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As regular followers of Dr. Smith’s ECG Blog have seen — some of the best cases that we post come from tracings that Dr. Smith or Meyers see while simply checking out “tracings on the system”. I find it especially interesting how important the History is for optimal interpretation of these cases.

• Today’s case provides perfect illustration of this observation. For clarity in Figure-1 — I’ve put the initial ECG in today’s case together with a prior tracing on the patient, done ~5 years earlier.

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NOTE: Today’s case is most insightful — IF you take another LOOK at the tracings in the sequence that Dr. Smith saw them!

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How would YOU Interpret ECG #1?

When I was given this case — I initially saw only ECG #1 — and I had not been given any clinical information.

• How would YOU interpret ECG #1 if this was the only tracing you saw — and — the only thing you knew about the patient, was that he/she was being seen in the ED?

Figure-1: Comparison of the initial ECG in today’s case — with a previous ECG recorded 5 years earlier. BUT — Please first imagine you were only given ECG #1 to look at, without the benefit of clinical information!

My Thoughts on the Initial ECG:

Systematic interpretation of ECG #1 shows:

• Sinus bradycardia at ~55-60/minute — normal intervals (PR-QRS-QTc) — normal frontal plane axis (about +20 degrees) — no chamber enlargement. 

Regarding Q-R-S-T Changes:

• Q waves — Large Q waves are seen in each of the inferior leads. A tiny q wave is seen in lead I — and narrow, but not overly deep q waves are seen in leads V5,V6.
• The QRS complex is tiny in lead V4. Given how small the QRS in this lead is — the Q wave that we see in lead V4 is disproportionately large (ie, as deep as the R wave in lead V4 is tall), wide and fragmented (ie, notched). This Q in V4 is more prominent than the narrow q waves in leads V5,V6 — which is not seen with "normal septal q waves".
• 
  
• R wave progression — Although an initial r wave is seen in lead V1 — and this r wave does become larger in lead V2 — there is loss of R wave as we move from lead V2-to-V3. We know this is not a normal finding because: i) The very next lead ( = lead V4) shows a disproportionately large and fragmented Q wave; and, ii) The initial r waves that we see in lead V1 and V2 are wider than is usually seen — and — if you look closely, the initial r waves in leads V2,V3 are also fragmented (notched).
• 
  
• ST-T waves — There appears to be subtle (minimal) ST elevation in lead III, and possibly also in lead aVF (but not in lead II). By itself — I would not know what to make of these inferior lead ST segments, as the amount of ST elevation is minimal and T waves are all upright and do not appear to be hyperacute.
• That said — there should be no doubt that the shape of the downsloping ST depression in lead aVL — and the subtly depressed flat ST segment in lead I are both abnormal. Whether this is a "new" or "old" finding is another matter.
• There are subtle-but-real ST-T wave abnormalities in the chest leads. These include: i) An upright T wave in lead V1 that is larger than the tiny upright T wave in lead V6; ii) Loss of the normal slight, upward sloping ST elevation in lead V2 (The ST segment is flat in this lead); and, iii) Disproportionately large T waves compared to the QRS in leads V3 and V4 — that may be hyperacute. 

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To EMPHASIZE: Although the amount of "words" in my above descriptive analysis is large — in practice, it literally takes me NO MORE than seconds to recognize all of these findings. The reason I continue to use this systematic checklist more than 50 years after I first began to interpret ECGs — is that this does not slow me down, while it prevents me from missing any findings.

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Putting It All Together:

How I would clinically interpret ECG #1 will depend on the History. As I stated above — I initially had no information about the patient or the clinical setting. Not knowing any clinical information about the case at the time I first saw ECG #1 — my thoughts were the following:

• Given how deep Q waves are in lead II, and especially in leads III and aVF — there has been an inferior MI at some point in time. I suspected the inferior MI was old — since the amount of ST deviation (elevation and depression) was minimal.
• There also appears to have been anterior infarction at some point in time — given "loss of R wave" (from lead V2-to-V3) + subtle-but-real fragmentation (in leads V2,V3,V4) + the disproportionately large and fragmented Q in lead V4, with tiny R wave in this lead.
• Overall — I did not get a "sense" that ECG #1 represented an acute cardiac event. That said — the T waves in lead V3 and V4 are definitely abnormal (ie, "fatter"-at-their-peak and wider-at-their-base than I would expect given modest QRS amplitude in these leads) — such that IF the history was of a patient with new-onset, worrisome chest pain — I could definitely not discount the possibility that these were hyperacute T waves.
• I thought that finding a prior ECG on this patient could prove invaluable for distinguishing between what might be "new" vs "old". Without availability of a prior tracing — I would defer my final interpretation until I had a chance to find out the clinical situation.

MORE Information is Provided!

At this point — I learned a bit more about today's patient:

• The patient is a man who had an inferior STEMI in 2010.
• He presented to the ED for today's visit because of vertigo. He did not complain of any new symptoms that might suggest an acute cardiac event.
• 2 prior ECGs were found in his medical record — the latest of which was done circa 2018 (which would be ~8 years after his inferior MI — and ~5 years before ECG #1).

To facilitate comparison in Figure-1 — I put this 2018 prior tracing ( = ECG #3) — together with ECG #1.

• The large inferior lead Q waves were present in ECG #3 — but instead of upward sloping and minimally elevated ST segments with upright T waves — ST segments were coved with T wave inversion in the inferior leads of the 2018 tracing.
• The opposite is seen for ST-T waves in high-lateral leads I and aVL, which are upright in the 2018 tracing — which is also a complete change compared to ECG #1.
• In the chest leads — QRS amplitude was much greater without Q waves, loss of R wave, or fragmentation in leads V1-thru-V4 of the prior 2018 tracing.
• The narrow q waves in leads V5,V6 are unchanged — but there is some T wave inversion in the prior tracing that is not seen in ECG #1.
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• Impression: There definitely have been changes in this patient's current ECG ( = ECG #1) — compared to his prior tracing from 2018. Evidence of the 2010 inferior infarction (in the form of large inferior Q waves) is present in both ECG #1 and ECG #3. I thought the deep S waves in leads V1,V2 with associated ST-T wave changes may have represented LVH on the 2018 tracing. In between the time from 2018 until the current tracing was recorded — the current ECG suggests there has been anterior infarction.
• In view of the History with the current admission (ie, presenting to the ED for vertigo — with no new chest pain) — I interpreted ECG #1 as no OMI.
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• Follow-Up: Cardiac troponins were negative — ruling out an acute event.

FINAL Thoughts:

• Optimal clinical ECG interpretation is impossible in the absence of a brief, relevant history.
• We know today's patient had a documented inferior STEMI in 2010. Comparison of present and prior ECGs suggest that the patient has also had an anterior infarction since 2018.
• It will be important for optimal longterm clinical management of this patient to figure out what happened when — but this is not yet possible from the limited information we have available. Close follow-up will be essential — but there was no acute OMI today ...