Monday, March 7, 2016

A 30 year old with Chest Pain, Anterior ST Elevation, Terminal QRS distortion, and a High Troponin

This was contributed by Brooks Walsh, who has contributed many interesting cases and articles to this blog.   I edited and added comments, of course.

The Case

A 30 year-old man presented to the ED with chest pain.  It had started 2 days ago, was constant, and radiated down his left arm. It was only mild, but he also endorsed mild dyspnea. He had no medical problems. He denied cocaine or other stimulants. Vital signs were normal, and the exam was notable only for a thin body habitus.

Here is his ED ECG:
There is significant anterior ST segment elevation (STE). However, the tall R waves and T waves suggest early repolarization, as do the upward-convex ST segments, and the lack of reciprocal depression.
So is this just Early Repol?
A calculation of the “subtle anterior STEMI score” returns a value of 23.4 (using QTc = 399 ms, R in V4 = 15 mm, and STE V3 = 4 mm). This borderline score suggests this is an ACO. 

However, this score should not be used, however, since lead V3 shows clear terminal QRS distortion (TQRSD), was is an exclusion for using the score.

The S wave does not descend below the baseline, and the J-point is neither slurred nor has a “fishhook”, i.e. no “J wave” (although one of two complexes comes very close to having a J-wave, this is clearly artifact, as the other two do not.)

Terminal QRS distortion
When TQRSD is found with an obvious acute coronary occlusion (ACO), aka STEMI, it portends a worse response to reperfusion, and higher mortality. It is defined as:
  • In an inferior ACO, a J-point that is > 60% of the R wave height.
  • In an anterior ACO, loss of the S wave in V2 or V3.

It can also be used to identify an ACO when a subtle anterior occlusion is suspected. In this case, however, extensive clinical experience suggests that such a TQRSD will NOT show a slurred J-point (aka J wave). TQRSD was an exclusion when the score was developed and validated.

Of 355 Consecutive cases of LAD Occlusion studied, 212 were excluded as "Obvious" and 40 of these 220 had as the primary reason for exclusion "terminal QRS distortion," defined at absence of BOTH an S-wave and a J-wave in EITHER of leads V2 or V3.  Of 171 cases of proven early repol (patients who presented to the ED, had all negative troponins, had at least 1 mm of ST elevation in V2 and V3, and whose ECGs were coded as "early repolarization" by the reading cardiologist), zero had QRS distortion.

The cath lab was activated and the patient was taken for angiography

Angiography showed no significant coronary disease. The troponins, however,
initially returned at almost 7 ng/ml [normal, less than 0.034 ng/mL (99% reference)], and peaked at 13 ng/ml. Cardiac MRI showed, however, “patchy mid myocardial enhancement … consistent with myocarditis.”

An ECG the next day:
The STE in leads V2 and V3 has decreased, as have the dramatic T waves in those leads. There are also new T wave inversions in many leads. This could be attributable to myocarditis.

Note that V3 now DOES have a J wave, with an elevated J-point with a “fishhook” QRS/ST morphology:

False-positive TQRSD?
This is NOT a false positive, as TQRSD is used to differentiate early repolarization from pathologic ST elevation.  In this case, it certainly detected pathologic ST elevation and correctly ruled out early repolarization as the cause of ST elevation.  

Learning Points

1. Although TQRSD is not seen in early repol, it does NOT differentiate between myocarditis and STEMI.  

2. Other cases of myocarditis show how it is often impossible to differentiate from myocardial infarction without an angiogram and MRI.  Both have positive troponins, wall motion abnormalities, and even reciprocal ST depression




10 comments:

  1. As I’ve previously discussed with Steve Smith and Brooks Walsh — I LOVE this case, because it illustrates so many important concepts. This case helped me understand the concept of TQRSD ( = Terminal QRS Distortion) — with insightful blow-up illustration above.

    I’ll add a few points: i) Acute anterior STEMI is not always accompanied by reciprocal ST depression in inferior leads, especially if one is not dealing with a proximal occlusion. So lack of inferior ST depression in the initial ECG here does not rule out acute stemi.

    ii) Acute pericarditis should be in the initial differential diagnosis. That said, the amount of J-point ST elevation in leads V3 and especially V2 is much more than is usually seen with simple pericarditis. In addition, T wave peaking in these leads is not the typical picture of acute pericarditis.

    iii) The shape and relative amount of ST elevation in lead aVL instantly told me this was not simple early repolarization.

    iv) In the follow-up tracing — Note that there is at least beginning T wave inversion in a number of leads that still show ST elevation. This feature tells us we are not dealing with acute pericarditis — because with typical pericarditis, ST segments return to the baseline BEFORE the T wave inverts. So once cath ruled out acute STEMI — this left us with acute Myocarditis (or MyoPericarditis) as the obvious diagnosis in this young symptomatic adult with positive troponins.

    v) Being aware of the phenomenon of terminal QRS distortion (as described by Dr. Smith) adds a very useful new tool to your armamentarium for sorting out when J-point anterior ST elevation is unlikely to be benign.

    THANKS for presenting this case!

    ReplyDelete
  2. Hello.

    Thank you so much for this post. There's ST elevation in anterior and lateral leads along with PR elevation and ST depression in aVR, can we conclude to myopericarditis ? Did the physician caring for the patient perform an echo to check the pericardium ?

    ReplyDelete
  3. Thank you Smith
    Every time I visit your page I learn something new.

    ReplyDelete
  4. Another very insightful case, as usual. I (we) are indebted, Dr. Smith.

    I learned now, besides many other things, that QRS distortion is not only due to MI but also due to myocarditis. Does a current injury (analogous to that seen in MI) occur in myocarditis which can explain the terminal QRS distortion?

    I was 'favourably' surprised that the interventionalist did angiogram. How did the emergency physicians persuade the interventionalist to perform angiography? In other words, was the inteventionalist persuaded just by QRS distortion (besides of course all other clinical features)? I can still hear a voice saying 'I told you that was no a STEMI!'...
    Many thanks
    Mario Parrinello

    ReplyDelete
    Replies
    1. Mario,
      I'm sure the very elevated troponin had a great influence. In many cases, it really is impossible to diagnose myocarditis without an angiogram: same EKG, same troponin, same echo.
      Steve

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  5. Very interesting and informative, many thanks, again. When I look at this ECG, I see a right downright descending TP-PR, so a Spodick sign. How do you see the impact of this ECG sign of pericarditis on actual probability of both MI and pericarditis? Is it enough to influence our conduct or do you look at it merely as the non-specific PR depression?

    ReplyDelete
    Replies
    1. Alain,
      Many talk about Spodick's sign, but I have never seen hard data that shows it accurately differentiates MI from pericarditis. Have you? Amal Mattu tells me he has a manuscript pending that shows that it does NOT help.
      Steve

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    2. Not really. We did wrote to the author and wait for his answer.

      Delete

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