ECG Blog #456 — Acute MI or Something Else?

Today's case was contributed by Dr. Magnus Nossen (from Fredrikstad, Norway). Dr. Nossen was at his computer — reviewing ECGs from patients recently admitted to his group's hospital service. He came across the ECG shown in Figure-1 — obtained from a woman in her 70s who was admitted to the hospital for new CP (Chest Pain).

QUESTION:

• How would YOU interpret the ECG in Figure-1?

Figure-1: The initial ECG in today's case — obtained from a woman with CP. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on ECG #1:

The rhythm is sinus bradycardia at a rate just under 60/minute. Intervals (PR, QRS, QTc) and the axis are normal. No chamber enlargement.

Regarding Q-R-S-T Changes:

• There may be tiny (normal septal) Q waves in a number of lateral leads.
• R wave progression — shows early transition, with the R wave abruptly becoming predominant already by lead V3. I wonder about precordial electrode lead placement — given the unexpectedly tiny V2 complex that is sandwiched between the deep S wave in V1 and the suddenly tall R wave in lead V3.

The most remarkable finding relates to ST-T Waves:

• Multiple leads in ECG #1 show ST segment straightening with ST depression that appears to be maximal in leads V3 and V4 (BLUE arrows in Figure-2).
• The tiny QRS complex in lead V2 is associated with a disproportionately large and peaked T wave — which is present, but to a lesser extent in neighboring chest leads.
• Prominent U waves are also seen (most marked in leads V2,V3 — but also seen in leads I, II).

My Impression of ECG #1: 

• I shared Dr. Nossen's concern that the ST segment flattening and depression in leads V2-thru-V6 — in association with the disproportionately large upright T wave in lead V2 in this older woman with new CP — strongly suggests posterior OMI (Occlusion-based acute MI), pssibly now with reperfusion T waves in leads V2-thru-V4. Could this be a posterior OMI that was missed by the original providers?
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• Additional Note: Assuming serum electrolytes (K+, Mg++) were normal — the upright U waves in leads II,V2,V3 are clearly larger than expected.

Figure-2: I've labeled the initial ECG. 

The ECG was Repeated:

As shown in Figure-3 — Dr. Nossen's chart review revealed that there was also a 2nd tracing on this patient ( = ECG #2 — which was recorded 21 hours after ECG #1). 

QUESTION:

• Does this repeat ECG (shown below in Figure-3) — change your impression regarding recent posterior OMI, now with reperfusion T waves?

 

Figure-3: The repeat ECG in today's case — recorded 21 hours after ECG #1. (Visualization improved using PMcardio).

MY Thoughts on ECG #2:

There has been dramatic change in the ECG picture since the initial tracing was done (See the comparison between these 2 tracings in Figure-4 below). At this point in time — ECG #2 no longer looked like a recent posterior OMI with reperfusion T waves but instead, like Takotsubo CM (CardioMyopathy). 

• T waves have dramatially filled out in ECG #2 — now with marked prolongation of the QT interval.
• Had I not first seen the prominent U waves in ECG #1 (BLUE arrows) — I would not have known that the extra "shoulder" (projection) seen near the bottom of the T wave descent in multiple leads in ECG #2 (best seen in those leads with the RED arrows) — was the result of a fusion between the upright T waves and U waves that have both significantly enlarged since ECG #1 was recorded. Technically then — rather than marked QT prolongation, we are seeing marked QT-U prolongation in ECG #2.
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• Note #1: Takotsubo on occasion may be associated with large U waves — so, the evolution to prominent T wave positivity with marked QT-U prolongation that we now see in ECG #2 is perfectly consistent with Takotsubo CM.
• Note #2: Retrospectively looking back at ECG #1 — the ECG changes of Takotsubo CM were already evolving 21 hours earlier at the time ECG #1 was recorded (ie, Virtually all leads with upright T waves in ECG #1 already had T waves that were subtly "fatter"-at-their-peak and wider-at-their base than might be expected — and the BLUE arrow U waves in ECG #1 were already larger than is usually seen when serum K+ is normal).
• Note #3: Given the overall better prognosis of Takotsubo CM compared to acute coronary occlusion MI — Dr. Nossen and I took comfort in knowing that acute OMI had not been overlooked (and that cardiac cath was not immediately needed).

Figure-4: Comparison between the initial and repeat ECGs in today's case (done 21 hours apart).

On Further Chart Review of Today's Patient:

Dr. Nossen discovered the following on further chart review:

• Troponin during this patient's hospital admission was modestly increased. This is consistent with Takotsubo CM — which is typically associated with Troponin peaks below that seen with larger MIs (although there is an "overlap range" regarding specific troponin levels — and some OMIs with limited occlusion duration before spontaneous reperfusion occurs, may manifest no more than minimal troponin elevation).
• Serum electrolytes were not abnormal. Neither hypokalemia nor hyperkalemia accounted for the ECG picture seen.
• Today's patient had a history of 3 previous "NSTEMIs". Each time, she underwent cardiac catheterization — and each time, she had patent coronary arteries! In retrospect — this patient never had acute MI (despite the fact that "NSTEMI" was the discharge diagnosis each time).
• For each of this patient's 3 previous hospital admissions that were diagnosed as "NSTEMI" — she had ECGs that showed evolution to the typical ECG picture of Takotsubo CM (See Figure-5 — which shows a representative tracing from one of those prior hospital admissions).

PEARL #1: Both the history and initial ECG from a patient with Takotsubo CM may be very similar to that seen with acute OMI. As a result — it may at first be difficult to distinguish between these 2 entities.

• At times — cardiac catheterization may be needed to rule out acute coronary occlusion.
• On the other hand, if the initial ECG looks similar to the tracing shown in Figure-5 (in which there is diffuse, deep symmetric T wave inversion with a markedly prolonged QT interval) — then, the diagnosis of Takotsubo CM becomes obvious. In such cases — noninvasive imaging (ie, with Echo; CT angiography) may provide sufficient support that the diagnosis truly is Takotsubo CM, such that cardiac catheterization is not needed (especially if the patient is not having ischemic CP).

PEARL #2: The term, "NSTEMI" (ie, a Non ST Elevation Myocardial Infarction) — is greatly overused. In my experience — the term, "NSTEMI" is probably inaccurate most of the time.

• In today's case — on each of this patient's 3 prior hospital admissions, she was diagnosed as having had "NSTEMI" — whereas retrospective review of her chart clearly showed she instead had Takotsubo CM each time.
• I've reviewed on many occasions in this ECG Blog — cases in which acute OMIs were overlooked and misdiagnosed as NSTEMI (See ECG Blog #400 — among many others).
• BOTTOM Line: In 2024 — We should always be suspicious of potential misdiagnosis whenever the label, "NSTEMI" is used. All-too-often this misdiagnosis is applied because providers fail to realize that a history of new CP which spontaneously resolves in association with "an unimpressive ECG" — may potentially reflect "pseudo-normalization" after the phase of ST elevation has begun to evolve into deep reperfusion T waves. And then, all-too-often the "tell-tale" sign of reperfusion T waves is simply overlooked (even when history and significant Troponin elevation say otherwise).

PEARL #3: The correct diagnosis for ECG #2 and ECG #3 is Takotsubo CM. But note how different the ECG pattern is for these 2 tracings!

• ECG #2 (in Figure-4) — is remarkable for large positive T waves with marked QT-U prolongation.
• ECG #3 (in Figure-5) — is remarkable for diffuse, deep and symmetric T wave inversion with a greatly prolonged QT interval.
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• BOTTOM Line: There is indeed variation in the ECG picture that may be seen with Takotsubo CM. Some of this is a function of when during the course of Takotsubo the ECG is taken. In addition — there are 2 distinct ECG patterns for Takotsubo — and depending on the anatomic region of the heart involved, the ECG picture may differ (See section below for review of Takotsubo ECG findings).

Figure-5: Representative ECG ~2 years earlier, from this patient's prior hospitalization. (Visualization imrpoved using PMcardio).

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ECG Findings with Takotsubo Cardiomyopathy:

By way of review in Figure-6 — I synthesize the findings most commonly seen for the 2 most common ECG patterns in patients with Takotsubo CM (which I've previously discussed in ECG Blog #277).

• As noted below in Figure-6 — the 2 most common ECG Patterns for Takotsubo CM consist of: i) ST elevation on initial ECG; and/or, — ii) Deep, diffuse T wave inversion (especially in the chest leads) with marked QTc prolongation. That said — neither of these patterns is seen in ECG #2 (ie, Rather than either ST elevation or deep, diffuse T wave inversion — there are overly tall, positive T waves present in multiple leads).
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• To Emphasize: I completely agree with Dr. Nossen that the serial ECG evolution that occurs between ECG #1 and ECG #2 in today's case strongly suggests Takotsubo CM (and not acute OMI). That said — the KEY to appreciate is that a variety of ECG patterns are associated with Takotsubo CM.
• Typical Takotsubo CM manifests apical ballooning with hypercontractility of the base. But instead of LV dysfunction localized to the apex — the dysfunction may be of the base = "Reverse" Takotsubo, in which case there will not be apical ballooning. Or, there could be mid-ventricular Takotsubo, in which there is poor function (and ballooning) of the mid-LV, with good function at both the base and the apex (See the June 24, 2014 post — and My Comment in the July 21, 2022 post of Dr. Smith's ECG Blog regarding Takotsubo variant patterns).
• Therefore — I thought the marked increase in QTc with huge, "bulky" upright T waves that we see in ECG #2 (especially given evolution to this ECG picture over the 21 hours since the initial tracing was done) — was perfectly consistent with some form of Takotsubo CM other than the 2 more common patterns described in Figure-6.
• As per Dr. Nossen — Takotsubo on occasion may be associated with large U waves, which accounts for the extra "shoulder" seen deforming the descent of the large T waves in ECG #2 (most prominent in those leads with the RED arrows in Figure-4). Technically then — the terminal part of what was thought to be T wave is actually U wave (ie, producing marked QT-U prolongation).

Figure-6: ECG Findings in Takotsubo Cardiomyopathy — adapted from Namgung in Clin Med Insights Cardiol (See text).

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By way of historical perspective on Takotsubo CM — I've added these 2 pages that I've excerpted from my 2014 ECG-Pocket Brain ePub.

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Figure-7: Brief review of clinical features of Takotsubo Cardiomyopathy (Excerpted from Grauer K — ECG-2014-ePub).

Figure-8: Clinical features of Takotsubo CM — continued (Excerpted from Grauer K — ECG-2014-ePub).

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Acknowledgment: My appreciation to Magnus Nossen (from Fredrikstad, Norway) for the case and these tracings.

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ADDENDUM:  — ECG Evolution in another Patient with Takotsubo:

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As emphasized above — the evolution of ECG changes with Takotsubo Cardiomyopathy is highly variable (and depends on many impossible-to-predict factors). 

• That said — I thought it would be interesting to review the sequential ECG changes as they occurred over time in another patient (different than the patient presented in today’s case) — in he hope that this helps to convey a general idea of the ECG changes to expect.
• My THANKS to Dr. Magnus Nossen for contributing the 8 sequential tracings in this case.

Figure-9: The initial ECG in this 2nd case (contributed by Dr. Nossen). There is sinus tachycardia at ~100/minute — with diffuse ST-T wave depression. The QTc appears to be at least borderline prolonged (being more difficult to assess true QTc duration given tachycardia and terminal T wave positivity vs U wave deflection in many leads).

Figure-10: The 7 sequential tracings that appear in Figures-10-thru-16 are compared with each prior ECG, in order to facilitate recognizing the changes. The rate in ECG #2 is slightly slower than in ECG #1. The differences in ST-T wave morphology in ECG #2 compared to the initial ECG (done 40 minutes earlier) are subtle. There is less J-point ST depression; less ST segment downsloping — and more rounding (coving) of many ST segments in the chest leads.

Figure-11: The rate is slightly faster. ST segment coving continues to increase — and is associated with relative lengthening of the QTc, and deepening of symmetric T wave inversion.

Figure-12: The rate is now significantly slower (~65-70/minute). The presence of this slower heart rate makes it easier to “step back” and better appreciate the overall picture = deep, diffuse symmetric T wave inversion (in all leads except right-sided leads III, aVR, V1 and vertical lead aVF) — with a clearly prolonged QTc. This ECG picture is typical for Takotsubo Cardiomyopathy.

Figure-13: The sinus rhythm rate remains slower than it was for the first 3 tracings. While the amplitude of ST-T wave changes is less in the limb leads of ECG #5 compared to ECG #4 — the symmetric T wave inversion in the chest leads is now clearly deeper.

Figure-14: The amplitude of chest lead T wave inversion has decreased in ECG #6 (ie, the ECG picture of Takotsubo is resolving).

Figure-15: One month has passed — and there is further improvement in ST-T wave appearance, with decidedly more flattening in ST-T waves in the chest leads of ECG #7.

Figure-16: 3 months have now passed — and the ECG has essentially returned to its previous "baseline" appearance.