Monday, May 13, 2019

Acute chest pain in a patient with cardiomyopathy and a paced rhythm.

A 70-something with h/o cardiomyopathy, ICD, LVH was awoken with sharp chest pain, 8/10, non-radiating.   It worsened through the morning and she was eventually brought to the hospital.

An ECG was recorded:
What do you think?

Here is one from 3 years prior:

There is a paced rhythm in all 12 leads.  The new ECG has new ST Elevation that meets the Smith modified Sgarbossa criteria in leads I, aVL, and V2.  (ST elevation at the J-point is at least 25% of the depth of the preceding S-wave).  Meeting the criteria in just one lead is very specific for OMI in paced rhythm.

She was given aspirin, ticagrelor, and heparin, and the cath lab was activated.

The initial troponin was 0.138 ng/mL.  Previous values were approximately 0.030 ng/mL (chronic myocardial injury from cardiomyopathy).

Angiogram results:
"No evidence of plaque rupture, coronary occlusion or severe epicardial noted to explain chest pain, anterior ST segment changes in the setting of LBBB and troponin elevation."

"Patent mid-RCA stent and otherwise mild, diffuse CAD."

"Consider cardio-embolism, resolved thrombus with medical therapy or non-cardiac etiology for myocardial injury."

After angiogram:
The findings are still present.
This suggests that whatever caused this new ST elevation is still present, so it is hard to attribute this to transient thrombosis or lysed embolism.

Troponin profile:
baseline was about 0.030 ng/mL

Echo next day:

Enlarged left ventricular size with severe systolic dysfunction.
The estimated left ventricular ejection fraction is 18 %.
There is no left ventricular wall motion abnormality identified.
Asynchronous interventricular septal motion from right ventricular pacing .

The patient then developed supraventricular tachycardias and did not have another ECG with a paced rhythm for a about a week.

There was one in LBBB:
Sinus tachycardia with LBBB.
No evidence of ischemia.
No concordance or excessive discordance

Then a few days later, he had another ECG while being paced:
It is back to baseline.
What happened?  

It is a conundrum:
Why did she present with chest pain and a paced rhythm with excessively discordant ST elevation (OMI on ECG), and an elevated and dynamic troponin, both BEFORE and AFTER an angiogram showing good flow in the coronaries.  And no wall motion abnormality on echo?  

I have no good explanation.

However, I do know that if the same situation comes up in the future (chest pain and a positive modified Sgarbossa in paced rhythm), I will activate the cath lab.

Comment by KEN GRAUER, MD (5/13/2019):
This is a highly interesting case of a 70-ish year-old woman with a history of cardiomyopathy + an ICD, who presented to the ED for severe new-onset chest pain of several hours duration.
  • I limit my Comments to 2 of the 5 ECGs presented in this case. For clarity — I’ve reproduced in Figure-1 the initial ECG obtained in the ED — and the 4th ECG obtained some time after cardiac cath (ie, a few days later?).
  • The tracings in this case are complex. The patient has a biventricular pacer — and at least in the 2nd and 5th tracings presented (neither of which appear in Figure-1) — there was evidence of atrial pacing.
  • COMMENT: Not knowing the specific parameters that the ICD was set at — I fully acknowledge not understanding aspects of the rhythm in the long lead V1 rhythm strip shown at the bottom of the 5th tracing. Pacemakers are amazing devices — and, most of the time they perform as programmed. Awareness of this programming usually provides reasons for virtually all events that are seen. Input from readers of this blog who have pacemaker expertise is welcome!
Figure-1: The 1st and 4th ECGs shown in this case (See text).
MThoughts on ECG #1:
  • Interpretation of paced tracings for potential acute ischemic changes is challenging! Use of Smith-modified-Sgarbossa criteria helps by providing a user-friendly calculation with predictive value. As per Dr. Smith — these criteria are clearly positive for ECG #1 (TOP tracing in Figure-1).
  • COMMENT — There is great variation in QRS morphology for paced tracings — especially when there is biventricular pacing. This may make comparison of ST-T wave changes between serial tracings (as well as with prior ECGs on a given patient) difficult. This challenge is clearly evident in this case — since scrutiny of QRS morphology in each of the 12 leads for each of the 4 paced tracings ( = ECGs #1, 2, 3 and 5) reveals that QRS morphology of paced complexes in certain leads is not the same in all tracings! That said — I completely agree with the general conclusions described in detail by Dr. Smith for these 4 paced tracings. BOTTOM Line: Judgment is needed when comparing ST-T wave changes in serial tracings (and when comparing to prior ECGs on the patient) when QRS morphology differs in some of the leads.
  • In addition to consideration of Smith-modified-Sgarbossa criteria — I also routinely use a qualitative approach. Realizing that conduction defects (LBBB, RBBB, IVCD) and ventricular pacing may each alter expected ST-T wave appearance — I look for those leads that clearly show ST-wave findings that should not bthere. Thus, ECG #1 shows marked J-point ST elevation with sharp angulation (highlighted by GREEN arrowsin leads I, aVL and V2. Of the remaining leads — the PURPLE arrow in lead III shows equally sharp angulation of the J-point ST-depression in this lead. Thus, the “magic” reciprocal relationship between leads III and aVL is present (ie, the sharp-angled ST elevation in aVL is the mirror image of the sharp-angled ST depression in lead III) — and this reciprocal relationship when present in leads III and aVL, suggests an acute STEMI until proven otherwise. This shape for the ST-T waves in these 4 leads should not be there ...
  • Finally, despite a minimal amount of ST depression in lead V1 — the PURPLE arrow in V1 highlights a flat shelf for this ST depression that just shouldn’t be there
  • Regardless of the fact that numeric criteria for Smith-modified-Sgarbossa are met in ECG #1 — it is the shape of the above abnormal ST-T waves in these 5 leads that tells me this patient with new-onset chest pain merits prompt cardiac cath.
MThoughts on ECG #4:  As per Dr. Smith — Following cardiac cath, this patient developed a series of SVT (supraventricular tachycardia) rhythms — one of which is shown in the 4th ECG of this case (BOTTOM tracing in Figure-1).
  • I suspect that the regular WCT (= Wide-ComplexTachycardiathat is shown in ECG#4 is not sinus tachycardia. Assessment for atrial activity in all 12 leads suggests there are regularly-occurring P waves at a rate of ~210/minute in a number of leads (RED arrows).
  • Atrial activity is BEST seen in lead V1. Reasons that I believe this is real 2:1 atrial activity are: iRED arrows march out perfectly with precise caliper measurement — and the spike of the P wave in V1 produces an identical-slope spike at the end of the QRS in this lead V1; iiI can see similar 2:1 precise atrial activity in lead V2; iiiRegular atrial activity continues in simultaneously-obtained leads I, II and III despite the “break” (PVC) in the rhythm (RED arrows in these 3 leads); ivP wave amplitude is very small in lead II (much smaller than the atrial activity seen in lead I) — and that is unusual with sinus rhythm; andvWhenever what is initially thought of as a sinus P wave in a tachycardia rhythm manifests a “longish” PR interval — there is an excellent chance that rather than “sinus tachycardia”, there is really 2:1 atrial activity (ie, if anything, the PR interval usually shortens a bit with sinus tachycardia).
  • I suspect the rhythm in ECG #4 was Atrial Tachycardia with 2:1 Block.
Final Thought: Our THANKS to Dr. Smith for presenting this case! I completely agree with his ending comments = I have no explanation for the negative cath findings given the initial ECG in this case. That said, given recurrence of the same scenario — I would also once again activate the cath lab for the ECG findings we see in ECG #1. Isn't this a fascinating case study ...


  1. Ive seen myocarditis present as STEMI-mimic. Could this explain the patients presentation?

    1. It could, but one would expect higher troponins with this degree of STE, and also expect a wall motion abnormality. But that might be the correct diagnosis.


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