Wednesday, July 24, 2019

Bizarre T-wave inversions, with Negative U-waves and Very long QT. And a myocardial viability study.

This 60-something year old male was admitted and his hospital course complicated by GI bleed, hemodynamic instability, and a nadir hemoglobin less than 5 g/dL.  An ECG was relatively normal.

The next AM, his potassium was measured at 2.9 mEq/L, so another ECG was recorded.

He was asymptomatic.
The previous ECG from one week prior had been relatively normal.

There are bizarre inverted T-waves and also inverted U-waves (see the 2nd inverted bump?)
The QT is incredibly long
There is some subtle STE in inferior leads but also STE in I, aVL.
There is STE before the bizarre TU inversion in leads V3-V6.

There are some artifacts that look similar to this.  

Bizarre (Hyperacute??) T-waves

Inverted U-waves are very strongly associated with LAD occlusion.

Besides the Nonspecific T-wave Inversion in aVL, What Else is Abnormal on this ECG?

Bizarre T-wave inversion with long QT is typical of takotsubo.

Bizarre T-wave Inversions in a Patient without Chest Pain

I thought he either had acute MI of the LAD, or takotsubo stress cardiomyopathy.  The team obtained an immediate cardiology consult, a stat formal echo, and serial troponins.

Troponin I was 4.2 ng/mL.
Echo showed: 
Low normal left ventricular systolic function with an ejection fraction of 52%.
Regional wall motion abnormality--akinesis of the apical anterior, mid-anteroseptal, apical septal, apical inferior, and apical lateral segments.
Regional wall motion abnormality--hypokinesis of the mid anterolateral and anterior segments.
Hyperdynamic basal segments.

This is consistent w/ wraparound LAD occlusion or takotsubo; the ECG is consistent with both.

Cardiology consult elicited some brief episodes of chest pain while in the hospital, squeezing, lasting 10 minutes.

The patient went for an angiogram.

Impression and recommendation:
Severe multivessel CAD involving the ostial LAD.
Occlusion of the apical LAD resulting in inferior infarction, chronicity uncertain - decreasing troponin would suggest that occlusion is more than 24-48 hours old.

Given the distal LAD occlusion of uncertain chronicity, TIMI III flow in other vessels and patient restlessness, as above, intervention was deferred.

Here is the ECG after the angiogram:
Some interesting evolution

After all this, it was not certain whether there was ACS (type I MI), type II MI due to GI bleed with anemia and hemodynamic instability, or takotsubo.

Further, if it was MI, was it:
1) a large MI with downtrending troponin or
2) a previous large MI due to the previous LAD occlusion, with superimposed small acute MI, or
3) a small acute MI with a large area of myocardial stunning (large wall motion abnormality)?

Absence of Q-waves on the ECG should argue strongly against a large irreversible infarction.  This was almost certainly a small infarction or takotsubo.

A Thallium Myocardial Viability Study was done.

--Myocardium may not contract because of "hibernation" or stunning, which are reversible, as well as by irreversible infarction.
--This may be assessed by Thallium scintigram myocardial viability study.
--Details of this are beyond the scope of this article, but may be found here (full text, 2019).

Review of the rest/redistribution 3 plane SPECT reconstructed scintigram demonstrate normal perfusion on the immediate scintigram except for a small area of reduced perfusion in the apical inferior and mid segments consistent with absence of infarct and normal viability in all vascular
distribution. The 24-hour/redistribution image shows reduced uptake in the apical and mid inferior wall adjustment to significant subdiaphragmatic tracer uptake most consistent with ramp filter artifact.

1. Normal viability of the anterior, anterolateral, septal, and inferolateral walls.
2. High probability of viability in the inferior wall.

This answered the above questions:

Thus, it was not a large infarction with downtrending troponins, or an old infarction with acute MI superimposed.

It had to be either a small infarction (type 1 or type 2), or takotsubo.  And this is evident from the ECG.


  1. I thought all findings are consistent with hypoK including STE. Why not repeat ECG after correction of HypoK as patient dint have chest pain( for better ECG interpretation)??

    1. This is not what hypokalemia looks like. Search for it on my blog and look at the many examples.

  2. Many thanks again Steve for the posts !
    In "The enigmatic sixth wave of the EKG : the U wave" by Andrès Ricardo Pérez Riera.QU prolongation and prominent U waves can be seen with some drugs : Class IA antiarrhythmic (quinidine, disopyramide and procainamide)and Phenothiazines.
    Class III antiarrhytmic drugs (amiodarone, dofetilide and sotalol) : prominent U waves only


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