Two more Cases of Takotsubo Stress Cardiomyopathy

Two more Cases of Takotsubo Stress Cardiomyopathy

Case 1.

This is the ECG of a 50 yo old woman who collapsed, was found to have a pulse, but then found to be in ventricular tachycardia. She was shocked into sinus rhythm. She presented to the ED comatose.
There is marked ST elevation especially in leads V3 to V6, as will as limb leads I and II, with no reciprocal ST depression. The cath lab was activated for STEMI, but the patient had clean coronaries. Before initiating therapeutic hypothermia, a head CT was done and showed fatal subarachnoid hemorrhage.
Case 2.

This 81 yo was found comatose.
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There is ST elevation in V1-V3 with hyperacute T-waves and Q-waves in V2 and V3. This is highly suspicious for acute anterior STEMI. However, she was found to have a fatal pontine hemorrhage and had a maximum troponin I, at 12 hours after presentation, of 2.0 ng/ml. Echocardiogram showed an anteroapical wall motion abnormality. In this case, since no angiogram was done, it is not proven that she did not have a simultaneous anterior STEMI, but with a low maximum troponin and alternative explanation, it is highly unlikely.
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These cases demonstrate that SCM can present with STEMI pseudoinfarction patterns.

Takostubo Stress Cardiomyopathy, with Echocardiogram

Takostubo Stress Cardiomyopathy, with Echocardiogram

This case was posted on the www.hqmeded.com ultrasound site, of which this ECG blog is a part. However, only the first ECG was shown, and it was recorded before the patient became ill.

I refer you to the video case presentation by one of my colleagues, Dr. Rob Reardon (who has, by the way, a fantastic collection of ED ultrasound cases).
http://www.hqmeded.com/node/107

Briefly, this woman without significant cardiac history went into pulmonary edema with respiratory failure. Her ED echo is diagnostic of apical ballooning, also known as "stress cardiomyopathy" (SCM) or "takostubo cardiomyopathy" (because the heart, with its apical ballooning, resembles the Japanese octopus trap called a "takostubo"). The contraction at the base of the heart remains intact, while contraction of the distal or apex is very poor.

Here is the first ECG after the patient became ill.

There is sinus tach with some anterior ST elevation, however not an alarming amount.

Several hours later, she had this ECG recorded:Theere is anterior T-wave inversion and very long QTc (680 ms). These are classic SCM findings after the hyperacute phase.


This ECG was recorded the following day:

The QTc is even longer now, at > 700 ms. T-waves are bizarre.

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The coronaries were clean, the troponin had a small bump, and the patient recovered. The apparent trigger was stress from losing custody of children.

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SCM may happen from a wide variety of psychological or physiological stresses, including respiratory failure (although in this case a psychological stress led to poor myocardial function and then pulmonary edema, then respiratory failure) and intracranial bleeding.

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In this case, the ECG never mimicked a STEMI. I will proceed to post a couple cases in which SCM does mimic STEMI.