Thursday, November 9, 2023

Explain this ECG in the context of active chest pain, slightly elevated troponin without a delta, RCA culprit, and previous with LBBB

A 60-something yo female presented w/ exertional chest pain for 3 days. She had a recent positive stress test about one week ago. Pain was 8/10 and constant. 

She has been experiencing progressively worsening exertional dyspnea and chest tightness mostly when climbing up flights of stairs since early September.  She underwent exercise echocardiogram in mid October where she exercised for nearly 7 minutes on the standard Bruce protocol and had typical anginal pain and shortness of breath.  

Baseline echocardiogram showed moderate LV systolic dysfunction with no wall motion abnormalities. 

Over the last 1 week, her exertional chest pain became worse both in intensity and triggering threshold. 

She has been having waxing and waning pain even at rest over the last 24 horus.  Pain is described as dull and pressure-like over the retrosternal area radiating to her neck with associated tingling of the left hand.  It is rated 8/10 in severity.  She has associated shortness of breath.

Time zero, with pain

Sinus rhythm with normal narrow QRS

T-wave inversion that looks like Wellens' waves in V1-V3 (the distribution is a bit unusual).  

But the patient has active chest pain. 

 Is it Wellens' syndrome?

If so, one would expect that the chest pain is diminishing or gone & that the culprit would be the LAD.

Time 17 minutes

Not much different

One month earlier

This is Left Bundle Branch Block (LBBB) without any sign of ischemia.
It turns out that she spends much of her time in LBBB (see ECGs below)

What is going on???

The first hs troponin I returned elevated at 48 ng/L (URL for women is 16)

Because of active chest pain, abnormal ECG, and elevated troponin in a patient with a very strong history of ACS, it was agreed she should go to the cath lab relatively emergently

hs-troponin I at 2 hours was 51 ng/L (no real change)

Angiogram started approximately 3 hours after arrival:

RCA/RPAV: 90% stenosis distal RCA/RPAV.  Lesion on Dist RCA: 90% stenosis reduced to 0%. Pre procedure TIMI III flow was noted. Post Procedure TIMI III.

Ramus: There is a large caliber branching ramus intermediate

LAD is a medium caliber vessel that extends to the apex and is noted to have diffuse mild to moderate plaque in the midsegment.  D1 is a medium caliber vessel, distal diagonal branches are small in caliber


Normal LV cavity size and thickness. The estimated left ventricular ejection fraction is mildly reduced, to approximately 45%. There is inferoseptal hypokinesis
So this was NOT LAD and NOT Wellens' syndrome.

What explains the T-wave inversions in V1-V3?

Cardiac Memory:

After conversion from LBBB or Paced Rhythm back to normal conduction, T-wave inversion is common and is called "Cardiac Memory"

See this post and explanation: 

Chest pain and LBBB. LBBB resolves and there is V1-V3 T-wave inversion.

Previous ECGs in this patient

30 months prior:
Narrow QRS with T-wave inversion in V1-V3

30 months prior, the same week:
A Normal Appearing Left Bundle Branch Block

12 months prior:
Narrow Complex

11 months prior
Normal appearing left bundle branch block

Cardiac Memory
There is another more likely explanation of this T-wave inversion: "Cardiac Memory."  Cardiac Memory (CM) has been described for a couple decades.  It is most common after termination of pacing and other etiologies of abnormal depolarization such as Left Bundle Branch Block.  After resolution of the abnormal depolarization, there may be transiently inverted T-waves that last for hours to days (these T-waves are the heart's "memory" of the previous abnormal conduction).  This phenomenon is poorly understood, but involves "transient electrical remodeling."

Shvilkin et al. described the way to differentiate CM from ischemia:
In short, the combination of:
(1) positive TaVL (as in this case) and
(2) positive or isoelectric T-wave in lead I (as in this case) and
(3) maximal precordial T-wave inversion greater than the T-wave inversion in lead III (as here: maximal precordial T inversion is in lead V2, at 4.5 mm, and T-wave inversion in lead III is only 2.5 mm) was

92% sensitive and 100% specific for CM, discriminating it from ischemic precordial T-Wave Inversion.

Thus, the very well informed physician could differentiate these ECGs from those of an LBBB patient with MI:
1) no concordance
2) no excessive discordance
3) LBBB with tachycardia, probably rate related
4) subsequent T wave inversion that, according to Shvilkin et al., is diagnostic of cardiac memory.  It is NOT Wellens' syndrome.

This case fits this definition of cardiac memory.

MY Comment, by KEN GRAUER, MD (11/9/2023):
I found Dr. Smith's presentation of today's case highly insightful for the changes in ST-T wave appearance that may sometimes be seen, depending on whether or not LBBB (Left Bundle Branch Block) is present.

Intermittent Bundle Branch Block:
We are used to seeing conduction defects (ie, RBBB, LBBB, IVCD, hemiblocks) occur with every beat. That said — conduction defects may sometimes be "rate-related". This usually occurs in association with an increase in rate — in which the QRS widens when the rate accelerates to a certain amount — and then narrows again after the rate slows down (For more on the phenomenon of rate-related BBB — See My Comment in the April 22, 2020 post in Dr. Smith's ECG Blog).
  • Conduction defects can also be intermittent. Usually this occurs with a "fixed" interval of time between beats that conduct normally, and wider beats that manifest the conduction defect (ie, most often showing the intermittent conduction defect every 2nd, every 3rd, or every 4th beat).
  • On occasion — the intermittent conduction defect may show random alternation between normal and impaired conduction, with no "fixed" interval between narrow and wider beats (See My Comment in the June 25, 2020 post in Dr. Smith's ECG Blog).

The Effect of "Memory":
Today's case is especially interesting — because of the potential role of "Memory"  in producing ST-T wave changes that only become manifest after BBB resolves. As per Dr. Smith — We know that today's patient "spends much of her time in LBBB". However, we don't quite know how much of her time is spent in persistent LBBB (although she potentially spends enough time to produce a memory effect — with resultant ST-T wave abnormalities that persist long after resumption of normal conduction with a narrow QRS). We also do not know if the anterior T wave inversion seen in today's initial tracing ever resolves during persistent periods of normal (narrow QRS) conduction. 
  • As per Dr. Smith — despite the Wellens'-like ST-T wave appearance in leads V1-thru-V3 of today's initial tracing — today's initial ECG does not qualify as "Wellens' Syndrome" because: i) The patient had ongoing, active CP (whereas with Wellens' Syndrome — CP has resolved at the time the ECG is done)andii) The distribution of ST-T wave changes seen in today's initial ECG differs from the usually later precordial lead distribution more typical of Wellens.

  • To Emphasize: Regardless of the anterior T wave inversion in the initial ECG — cardiac cath was clearly indicated in today's case, because of the patient's persistent chest pain with elevated troponin, and potentially ischemic-induced LBBB.

What Can Sometimes Be Learned from Intermittent BBB Conduction!
By contrast with today's case — I offer this tracing from a 60-year old woman with dyspnea and the ECG in Figure-1 showing LBBB conduction every-other-beat.
  • To facilitate comparison between normally-conducted beats vs beats conducted with LBBB — I have shaded out much of the tracing (The complete case seen HERE).
  • Beats #3 and 11 are conducted with a narrow QRS complex — and clearly show diffuse ST depression with ST elevation in lead aVR, consistent with DSI (Diffuse Subendocardial Ischemia).
  • Beats #4 and 12 show LBBB conduction — that with the exception of excessive ST depression in lead V6 (for beat #12) — do not appreciably show abnormal ST-T wave findings on alternate beats when there is LBBB conduction.

  • BOTTOM Line: Because conduction defects alter the sequence of ventricular depolarization — the sequence of ventricular repolarization will also be changed! As a result — it will always be more challenging to evaluate ST-T wave changes in association with a conduction defect (especially with LBBB — which alters the initial vector of ventricular depolarization). Rather than a "memory" effect — I thought the markedly abnormal diffuse ST depression seen every-other-beat during normal conduction in Figure-1 was more likely to represent indication of DSI that was not evident during LBBB conduction.  

Figure-1: Direct comparison between normally-conducted beats vs beats conducted with LBBB.

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