Wednesday, January 9, 2019

A patient with chest pain and dynamic ST elevation

Written by Pendell Meyers

A female in her late 40s presented with chest pain, waxing and waning over the past 24 hours. Her history included end stage renal disease on dialysis, HTN, and DM. Here is her initial ECG around 4:30pm:

Sinus tachycardia.
The QRS is characterized by high voltage and nonspecific intraventricular conduction delay.
There is STE in V2-V4
However, this STE appears to be "secondary" STE in V2-V3 (repolarization abnormalities may be "secondary to an abnormal QRS", or "primary" in the context of a normal QRS), a result of the abnormal QRS complex.
The STE in V4 is concordant, and one must entertain the idea that such concordance is abnormal; however, this is not definite.
There is also STE in I and aVL, but it is difficult to tell if it is entirely secondary to the abnormal QRS complex. The T-waves are mostly discordant to the QRS complexes, as expected.

We would need a baseline ECG to comment on them further.

There is significant PR depression in leads I, II, aVF, V4-6, with obligatory reciprocal PR elevation in aVR. In fact, the PR depression in lead V4 accounts for some of the perceived STE in that lead.

Prior ECG on file from several months ago:

The QRS is mostly the same as before, however the T-waves in the limb leads above are opposite (essentially flipped) compared to this baseline ECG. This is difficult to interpret in the setting of tachycardia and abnormal QRS, and I would not take these changes to be definitively indicative of anything in clinical practice without further information. However, it would be appropriate to be worried about anterolateral and high lateral injury pattern based on the changes from prior to presentation.  I do not think the findings are conclusive of occlusion MI, and I would not activate the cath lab based on the ECG findings alone.

This ECG was read as nonspecific, and the first troponin T returned elevated at 0.20 ng/mL. At this point cardiology was emergently consulted, and it was discovered that the patient had a similar presentation roughly 1 year ago, in which she was emergently cathed and found to have no significant CAD. Here is her ECG during that presentation:

Diagnostic of inferolateral injury pattern, formally meeting STEMI criteria. Additionally there is widespread PR depression. This would have to be assumed to be STEMI until proven otherwise (takotsubo or myopericarditis) by cath.

Emergent cath showed no occlusions and no culprit lesion (the coronaries were completely normal). The EKGs reportedly returned to normal over the course of a few days. Troponin T was mildly elevated at 0.12 ng/mL and then downtrended. She had a trace inferolateral pericardial effusion at that time. She was diagnosed with myopericarditis.

Back to the present case:

Given her negative cath 1 year ago and her well appearance, cardiology elected not to cath emergently. She was admitted.

At 5am that night, the patient was noted to have persistent pain and a change on the cardiac monitor. A repeat ECG was done at 5:05am: 

Similar to the ECG from last year. Diagnostic of acute injury pattern to the inferior and lateral walls. PR depression is visible. There is also slight STD and dynamic negative T-wave in aVL.

Despite her history of a normal recent cath, it is hard to ignore such a dramatic, dynamic change which also meets formal STEMI criteria. Out of an abundance of caution, she was taken to the cath lab, where they again found no CAD (entirely normal coronary arteries). There was no vasospasm, no wall motion abnormalities consistent with takotsubo. Formal echo showed an inferior trace pericardial effusion.

Smith comment: If the prior cath from 1 year ago truly showed completely totally normal coronary arteries (in contrast to "no hemodynamically significant stenoses", which is sometimes also referred to as a "negative" cath), then I would prefer not to activate the cath lab without further data.  This is because new ACS in recently described totally normal coronaries is very unusual, and because the ECG strongly suggests pericarditis (especially with the profound PR depression).  Although I usually say that "you diagnose pericarditis at your peril," it is much safer to do so in a patient who was recently demonstrated to have normal coronaries. 

Rather, I might do an emergent high quality echo, because absence of wall motion abnormality would confirm absence of MI. The presence of WMA would still leave myocarditis as a possibility.

Repeat ECG after cath at 7:19am:

The next troponin decreased to 0.12 ng/mL. The following troponin was 0.15 ng/mL. The patients symptoms improved, and no further trops were measured.

The patient was diagnosed with myopericarditis and did well.

Learning Points:

Pericarditis produces dynamic ECG changes which may mimic Occlusion MI. This may be diffuse or localized. Sometimes pericarditis cannot be differentiated from ACS without an angiogram, and in these cases it is perfectly appropriate to activate the cath lab to differentiate these. The risk of missing occlusion MI is huge in comparison to the very small risk of a diagnostic cath (with no intervention) for a patient with pericarditis. However, a recent cath showing completely normal coronary arteries makes type 1 MI very unlikely.

Comment by KEN GRAUER, MD (1/9/2019):
Fascinating case with superb commentary by Dr. Pendell Meyers. I found this case truly intriguing because of the dynamic ST-T wave changes that were beyond my expectations. For clarity (and ease of comparison) — I’ve put 4 of the 5 tracings in this case together in Figure-1.
Figure-1: The 1st, 2nd, 4th and 5th ECGs discussed in this case. Not shown is ECG #3 — which was from the patient’s admission a year earlier, and which showed similar ST elevation as is seen on ECG #4 (See text).
The initial ECG shown in this case ( = ECG #in Figure-1) — shows sinus tachycardia at ~105/minute. As per Dr. Meyers, the principal findings are high voltage — nonspecific IVCD (Intra-Ventricular Conduction Delay— and, potentially concerning ST-T wave changes.
  • I found ECG #1 especially challenging to interpret. Voltage criteria for LVH are clearly met (R in any inferior lead ≥20mm; deepest S in V1,V2 + tallest R in V5,V6 ≥35mm). That said, QRS duration is prolonged (between 0.11-0.12 second) — which given QRS morphology, qualifies as a nonspecific IVCD. Specificity of the ECG for LVH is reduced in the presence of a true conduction defect — though in this case, marked LVH (which is clinically expected, given longstanding HTN with end-stage renal disease) may widen the QRS due to the increased time needed to traverse the hypertrophied LV.
  • There are relatively small (considering large R wave amplitude) and narrow q waves in inferior and lateral chest leads. Given the inferior frontal plane axis — these are most probably normal “septal” q waves, and not indicative of infarction.
  • ST-T wave morphology in the inferior and lateral chest leads in part looks like LV “strain” (consistent with the ECG diagnosis of LVH) — but, as noted by Dr. Meyers, also shows slight-but-definite ST elevation in a number of leads. I share the feeling that this does not “look” like an acute cardiac event — thought without a baseline tracing, it is hard to be certain.
  • KEY Points  Tachycardia sometimes produces ST elevation that may raise concern about an acute event. This ST elevation often resolves when heart rate slows. In addition, both repolarization abnormalities and LVH on ECG can sometimes manifest dynamic ST elevation and T wave inversion that may mimic acute infarction — and which may evolve over a surprisingly short period of time (See Dr. Smith’s ECG Blog from May 25, 2017).

“baseline” ECG was found in this case ( = ECG #in Figure-1):

  • There are minor differences in QRS morphology between ECG #1 and ECG #2. That said, these are not enough to account for the fairly marked ST-T wave changes seen between these 2 tracings. How much of an effect the faster heart rate in ECG #1 might have had, vs the possibility of an acute event causing these ST-T wave changes — is difficult to say. That said, I completely agree with Dr. Meyers that I would not activate the cath lab on the basis of these 2 tracings.
ECG #was obtained at 5:05 am the next morning, in association with a recurrence and persistence of chest pain. I found this tracing especially interesting:
  • Even though a similar clinical picture of chest pain and ST elevation on ECG had been seen a year earlier (at which time cardiac cath showed “normal” coronary arteries) — I will quote Dr. Meyers comment above regarding ECG #4 = “It is hard to ignore such a dramatic, dynamic change that meets STEMI criteria”.
  • There is no appreciable difference in heart rate between ECG #1 (the initial ECG in this case) — and ECG #4 in Figure-1. The slight change in frontal plane axis and slight variation in chest lead QRS appearance can not explain the resolution of T wave inversion with development of increased ST elevation in multiple leads of ECG #4 in this patient who once again was found to have a normal cardiac cath.
Some 2 hours later (at 7:19am) — ECG #was obtained. Patient symptoms were now less — and the slight troponin elevation was decreasing.
  • The QRS complex to me now looks slightly less wide — with a morphology more consistent with LVH than IVCD.
  • Did you notice in ECG #5, that for the 1st time — the QRS complex in lead I is now predominantly negative? This QRS morphology (ie, a steep downsloping rS in lead I, and a qR in all inferior leads) is perfectly consistent with an isolated LPHB (Left Posterior HemiBlock— that was not seen previously. I’m uncertain of the clinical significance of this finding in this case (Perhaps it accounts for some of the inferior lead ST-T wave differences between ECGs #4 and 5?).
  • BOTTOM LINE  This case is remarkable for the dynamic ST-wave changes that are seen. It’s helpful to appreciate: ithat acute ischemia/infarction is not the only potential cause of such changes (cardiac cath on 2 occasions was normal in this case); iithat changes in heart rate, frontal plane axis, and/or patient positioning cannot always explain such changes; andiiithat entities such as repolarization variants, LVH, and/or acute myopericarditis may all contribute on occasion to produce an evolution of challenging dynamic ST-T wave changes on serial ECGs.


  1. Why does the diagnosis is not pericarditis but myopericarditis?

    1. the myocardium must be also involved as there is an elevated troponin. Elevated troponin with rise and/or fall diagnoses acute myocardial injury. in this case, the injury is due to inflammation.

  2. Thanks again Dr Smith Great case. I wonder if The absence of clear cut STD during ST elevation
    bears more weight on myopericarditis than STEMI Dx?

    1. Thanks!
      Probably not. Myocarditis is just as likely to have reciprocal ST depression as MI. Pericarditis is not. Myocarditis causes myocardial injury just like MI, whereas pericarditis does not.

  3. I'm little confused because you stated it might be pericarditis despite dynamic STD in aVL - and I thought STD excluded pericarditis (but not myopericarditis).

    1. Sorry, Misspoke: with STD in aVL, we should have stated myopericarditis, not pericarditis

  4. Myocarditis also gives recipricol changes, such as in aVL in both ECG #2 and #4. Pericarditis should not give recipricol changes. I always use your concept of diagnosing pericarditis at your own peril. And I teach this aswell. Good case!


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