Briefly, this woman without significant cardiac history went into pulmonary edema with respiratory failure. Her ED echo (not shown) 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:
Several hours later, she had this ECG recorded:
There 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.
The coronaries were clean, the troponin had a small bump, and the patient recovered. The apparent trigger was stress from losing custody of children.
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.
In this case, the ECG never mimicked a STEMI. I will proceed to post a couple cases in which SCM does mimic STEMI.
Why would the ICH be related to the SCM? Would you expect more tachycardia from the SCM?
ReplyDeleteThis is the general understading of the pathophysiology: ICH results in massive catecholamine surge in the myocardium, which leads to diffuse myocardial ischemia. (Not the other way around.)
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