Thursday, July 21, 2022

A woman in her 40s with intractable nausea and vomiting, dyspnea, and lightheadedness

 Submitted and written by Oriane Longerstaey MD, peer reviewed by Meyers, Smith, and McLaren

A woman in her 40s with diabetes and HLD presented with nausea and vomiting x3 days. She was seen on day 1 of symptoms at an outside ED, no ECG performed, and sent home with return precautions and zofran, which she had been taking around the clock for persistent nausea and vomiting. She presented on day 3 of symptoms because of new onset dyspnea, tachycardia, lightheadedness, and heart palpitations. She had a "burning" sensation in her chest but no "pain".

A 12 lead EKG was obtained at triage:

 - Sinus rhythm at 96 bpm
 - Narrow, normal QRS
 - ST depressions in V3-V6, II, III, and aVF, with reciprocal STE in aVR, V1, (and potentially reciprocal in aVL)
 - Extremely long QT interval due to both prolonged ST segment and prolonged T wave, concerning for acquired long QT, drug induced long QT, hypokalemia, hypomagnesemia, or Takotsubo cardiomyopathy. Long QT can be subdivided by ECG into cases with long long QT due to long ST segment (hypocalcemia), long QT due to T wave (meds, takotsubo, etc.) and long QU (usually due to hypokalemia).

The computer QT/QTc was 486/540 msec (heart rate 96 bpm).

My quick QT interval measurement is at least 520 msec, with Bazett QTc 658 msec.

Given the long QT, she was given 2g magnesium.

Her initial high sensitivity troponin I was markedly elevated at 1950 ng/L.

Repeat ECG was performed about an hour after the first:

Mostly similar.

Several repeat troponins (ng/L) were:

Cardiology was consulted and felt that the overall clinical picture was not ACS, and advised against heparin for ischemia. She was admitted to medicine.

Inpatient Course:

QTC prolongation attributed to Zofran. QT prolonging agents held.

Echocardiogram and coronary CT ordered.

Repeat EKG the next morning with worsening QT prolongation and TWI in V1, V2.


Formal echocardiogram:

LV: cavity size is normal, moderate to severe concentric hypertrophy, EF 61%, severe hypokinesis of the basal anterior myocardium.

RV: systolic function is mildly reduced

No significant valve stenosis or regurgitation

Pericardium: small pericardial effusion anterior to the heart and at the apex, maximal 1cm.

Coronary CT results: mild to moderate nonobstructive coronary atherosclerosis.

CALCIUM SCORE: Not performed.
DOMINANCE: Right dominant coronary anatomy.

LEFT MAIN: Plaque - None. Stenosis - None.

Proximal- Plaque - Noncalcific. Stenosis <25%.
Mid- Plaque - Noncalcific. Stenosis <25%.
Distal- Plaque - None. Stenosis - None.
1st Diagonal- Plaque - Noncalcific. Stenosis <25%.
2nd Diagonal- Plaque - None. Stenosis - None.

Proximal- Plaque - None. Stenosis - None.
Distal- Plaque - Noncalcific. Stenosis <25%.
1st Obtuse Marginal- Plaque - None. Stenosis - None.
2nd Obtuse Marginal- Plaque - None. Stenosis - None.

Proximal- Plaque - Noncalcific. Stenosis 25-49%.
Mid- Plaque - None. Stenosis - None.
Distal- Plaque - Noncalcific. Stenosis 25-49%.
Right Posterior Descending- Plaque - None. Stenosis - None.
Right Posterolateral- Plaque - None. Stenosis - None.

Mild to moderate nonobstructive coronary atherosclerosis. Recommend aggressive risk factor management and medical therapy.

She next underwent EGD due to her intractable nausea and vomiting, which revealed some scattered musocal erosions but no other findings. CT abdomen was unremarkable.

After about 24 hours, her ECG began to normalize:

What happened to this patient? What is the diagnosis?

I think some unusual form of takotsubo cardiomyopathy fits best, though the echo is not at all typical of takotsubo (or of reverse takotsubo, for that matter). The CT coronary angiogram findings confirm the presence of CAD, and do not rule out ACS as the cause, but with all clinical information together it just does not seem like ACS to me. The bizzare T waves and extremely long QT remind me of many cases of takotsubo that I've seen and published on this blog. 

But there is still uncertainty in this case.

Learning points:

Current computer algorithms are suboptimal for measuring the QT interval. In this case the computer identified prolonged QT, though it still underestimated the QT interval.

We believe that bizarre long QT interval is sometimes a feature of takotsubo cardiomyopathy that may help to differentiate it from other etiologies of ECG abnormalities. It is unusual in my experience for OMI to have an extremely long QT interval.

Troponin should not be elevated in cases of simple drug-induced prolonged QT.

See these other relevant cases:

Spiked Helmet Sign


MY Comment, by KEN GRAUER, MD (7/21/2022):


Fascinating case presented today by Drs. Longerstaey and Meyers. Unfortunately — we do not have a definitive answer. That said — lack of a definitive diagnosis allows me the opportunity to offer another way of looking at this case.
  • I agree with Drs. Longerstaey and Meyers that this case most likely reflects "some unusual form of Takotusbo Cardiomyopathy".

  • Formal cardiac cath apparently was not done. Coronary CT scan revealed, "mild-to-moderate non obstructive coronary atherosclerosis". But as per Drs. Longerstaey and Meyers — synthesis of all clinical information (and especially assessment of serial ECGs) just does not appear consistent with an acute MI.

  • Assessment of LV function in today's case is limited to formal Echo results — which revealed an EF = 61%, but with severe hypokinesis of the basal anterior myocardium. Although this localized hypokinesis on Echo would seem more consistent with acute MI — as noted above, the rest of the clinical presentation in today's case is not suggestive of ACS.
  • These Echo results are clearly not consistent with typical Takotsubo — which generally presents with akinesia of the apical and mid-ventricular segments (often with apical "ballooning") — while the basal segments are hypercontractile. 

Regarding "Typical" Takotsubo:
We've reported numerous cases of Takotsubo Cardiomyopathy on Dr. Smith's ECG Blog. To name just 3 of many: 
  • In My Comment at the bottom of the page in the March 25, 2020 post in Dr. Smith's Blog — I reviewed KEY features for the ECG diagnosis of typical Takotsubo Cardiomyopathy. As a reminder — I've reproduced below in Figure-2 (from this March 25, 2020 post) — a summary for ECG diagnosis of this entity.
  • The January 22, 2018 post in Dr. Smith's ECG Blog showed the typical evolution of Takotsubo Cardiomyopathy.
  • The March 27, 2014 post reviewed tips on distinguishing between Takotsubo vs acute MI.

What About "Reverse" Takotsubo?
Areas other than the apex may be affected with disorders related to "typical" Takotsubo. Included among these is the variant known as Inverted (or "Reverse") Takotsubo Cardiomyopathy.
  • With "Reverse" Takotsubo — Echo shows sparing of the apex — with instead akinesis of the mid-ventricular and all basal LV (left ventricular) segments. That said — there can be variations and an evolution of the specific LV segments involved (Manzanal et al: Tex Heart Inst J 40(1):56-59, 2013) — Elikowski et al: Pol Merkur Lekarski 41(243):136-140, 2016).

  • The ECG pattern of "Reverse" Takotsubo is also variable — but in addition to QTc prolongation — "Reverse" Takotsubo tends to manifest diffuse ST depression rather than ST elevation or deep T wave inversion (Awad et al: Ann Translational Medicine 6(23), 2018 — Elikowski et al — with similar suggestion of this ECG pattern in the June 24, 2014 and September 4, 2018 posts in Dr. Smith's ECG Blog).

  • So, the Echo in today's case is not what we'd expect for "Reverse" Takotsubo (because hypokinesis was limited to the anterior basal segment). That said — perhaps the "moderate-to-severe concentric hypertrophy" that was found on Echo might have had an effect on contractility that altered results — and/or — perhaps the Echo pattern was in process of evolving ...

Use of the "Mirror" Test:
Since the anatomic abnormalities encountered with "Reverse" Takotsubo are in a sense, a mirror-image of what we expect to see with typical Takotsubo Cardiomyopathy (ie, basal rather than apical akinesis with compensatory hyperkinesis of other areas) — I thought it might be interesting to produce a mirror-image ECG (in which I invert the inferior and lateral chest leads, which are those leads that view the LV apex).
  • I reproduce the initial ECG on today's case in the TOP tracing shown below in Figure-1. Doesn't this initial tracing present a striking picture of diffuse ST depression with large terminal T wave positivity and a markedly prolonged QT interval?

  • After inverting the infero-lateral leads (BOTTOM tracing in Figure-1) — Doesn't the ECG picture this produces now look much more like the ECG picture of typical Takotsubo?

BOTTOM LINE — I completely agree with Drs. Longerstaey and Meyers that acute MI is an unlikely explanation for today's presentation. Serial ECGs in today's case are also not as expected for typical Takotsubo. For this reason — the most logical explanation for the overall clinical picture in today's case seems most consistent with some unusual form of Takotsubo Cardiomyopathy.
  • Although not perfect — I thought clinical features in today's case come closest to being consistent with the "Reverse" form of Takotsubo Cardiomyopathy.

  • I wish we had a definitive answer ...

Figure-1: Comparison of the initial ECG (TOP) — with superimposed mirror-image pictures of the inferior and lateral chest leads (BELOW).

Figure-2: ECG Findings in the "typical" form of Takotsubo Cardiomyopathy — adapted from Namgung in Clin Med Insights Cardiol (See text).

No comments:

Post a Comment

DEAR READER: I have loved receiving your comments, but I am no longer able to moderate them. Since the vast majority are SPAM, I need to moderate them all. Therefore, comments will rarely be published any more. So Sorry.

Recommended Resources