Sunday, July 1, 2018

Chest pressure during exertion, evolution of inverted T-waves and Troponins. Surprise Angiogram.

I was texted this ED ECG with the words: "40-something with chest pressure during exertion."  It is unclear whether the pain was gone at this time, but it was certainly better after receiving some sublingual nitro.

Presentation ECG 1

What do you think?









My response was: "Definitely ischemia. Probable high lateral MI.  If patient still has chest pain and you cannot relieve it with nitro, needs cath lab."

This is because there is ST depression in II, III, aVF, and also in V4-V6, with STE and T-wave inversion in aVL.  It looks as if there had been an occlusion resulting in STE in aVL (and reciprocal inferior STD), and that occlusion is now open so that the T-wave in aVL is now inverted (reperfusion T-wave), with reciprocally upright T-waves in inferior leads.

It turns out her BP was 165/112, so I added: "Nitro might do the trick.  Could try metoprolol too."


Here is an ECG from 2 months prior for comparison, without chest symptoms (ECG 2)
None of those findings were there previously



She had 2 negative troponins and was admitted for further serial troponins.

At 5.5 hours, she had this followup ECG when asymptomatic: (ECG 3)
Notice deeper T-wave inversion in aVL, and reciprocally increased T-wave size in II, III, aVF.  These inferior T-waves are NOT inferior hyperacute T-waves (which, in inferior MI, one might see early after onset of pain or early after offset of pain)
These appear to be reciprocal to the inverted (reperfusion) T-wave in aVL

Compare again to ECG 1:


Later, I was shown this prehospital ECG (ECG 4):
Even more pronounced STE in aVL, with more reciprocal STD in II, III, aVF.
This suggests that the ischemia had been more intense on first medical contact, and would seem to confirm the diagnosis if you were skeptical before.
But with T-wave inversion, it also suggests that the artery had reperfused prior to this ECG, but that it was so recent that the ST elevation had not yet resolved.


After the 5.5 hour ECG, the troponins rose above the 99% URL and peaked at 0.101 ng/mL (URL = 0.30 ng/mL).  So there is definite myocardial infarction.

There were ECGs from previous visits which were also worrisome:

During visit for seizure 4 months prior (ECG 5)
Some subtle T-wave inversion in aVL and V2.



During visit for chest pain 9 months prior (ECG 6), that had resolved.
Very worrisome T-wave inversion in V2, V3.  Looks like Wellens' syndrome and is changed from the ECG 9 days prior (below).

The patient was to be admitted for this, but left the ED without warning.


Baseline 10 days prior to ECG 6 (ECG 7)



I was sure that all these ECGs pointed to a reperfused high lateral MI, probably a first diagonal (since V2 was involved.)

Angiogram:

Normal coronary arteries!

Interpretation:

It is uncertain what the etiology was.  Spasm?  Thrombosis with complete lysis and no visible lesion?  Other?

It must be called a myocardial infarction as there was rise and fall of troponin in the context of chest pain and typical ECG findings.  And it must be called a type 1 myocardial infarction as there is nothing to suggest decrease oxygen supply (such as anemia or hypotension) or increased demand (such as tachycardia or severe hypertension).

But the exact etiology is unclear.

On the other hand, these are not false positive ECGs.  They are perfectly consistent with the elevated and rising troponins, and meet the definition of myocardial infarction, without any clinical features to suggest type 2 myocardial infarction.

Learning Point:

Not every type 1 Myocardial infarction has a lesion that can be stented.  But you still need to take a look.


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Comment by KEN GRAUER, MD (7/1/2018):
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Lead aVL is “the highest” of the high lateral leads. On occasion (as in this case) — it may be the only lead to show ST elevation. In such instances — it is through clinical context plus careful assessment of other leads that we can know that the slight ST elevation we see in lead aVL of ECG #1 is real and indicative of acute MI. So it is in this case — as each of the 3 inferior leads show a precise “mirror-image” opposite picture to the ST segment coving with slight elevation and T wave inversion that is present in lead aVL.
  • The “beauty” of this case is how Dr. Smith’s step-by-step “Sherlock Holmes-like” analysis proves his contention of a Type 1 Acute MI despite the normal cath. Nothing else could produce the serial ECG changes seen here in association with the patient’s evolving symptoms. Beyond-doubt confirmation was then forthcoming from finding the pre-hospital ECG that showed even more dramatic ST-T deviation.
  • Without this step-by-step clinical deductive process — the correct diagnosis of Type 1 Acute MI would never have been made.

2 comments:

  1. what would you say about EKG inferior ischemia inverted T waves but no following rise in troponin...

    ReplyDelete
    Replies
    1. One could say there is subendocardial ischemia (but why, with a negative angiogram?). But one could not say where that ischemia is (not necessarily inferior). The ST depression of subendocardial ischemia does not localize to the ischemic wall, unlike ST elevation. Proven by correlations of exercise testing and angiograms.

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