The electrocardiographic signature of post–myocardial infarction chronic akinesia or dyskinesia (ventricular aneurysm [VA]) is persistent ST-segment elevation, which has been attributed to either myocardial ischemia at the boundary of normal muscle and the VA or to an abnormal mechanical stretch due to the systolic paradoxical motion of the VA territory, deforming the ST segment on the electrocardiogram. Takotsubo syndrome (TTS), which is primarily characterized by a transient apical akinesia or dyskinesia (“ballooning”), lasting a few days to weeks, is associated with ST-segment elevation, T-wave inversions, and corrected QT interval prolongation. Although such ST-segment elevation in TTS is modest in magnitude, occasionally, very large ST-segment elevations are noted, particularly during the hours to 2 days after admission to the hospital. As a rule, ST-segment elevation is seen only transiently, and it is replaced by T-wave inversions, which increase in depth and persist for many days, weeks, or even months, although they decrease in depth at their later stage.

The cause and the exact pathophysiology of TTS are still unknown, although it appears that a state of myocardial stunning, with problems affecting the microcirculation, is at play. Myocardial edema, which also appears to be an associated pathologic condition, has been detected by cardiac magnetic resonance imaging and persists for a few weeks, along with the inverted T waves, long after the myocardial stunning has completely resolved and left ventricular function has been restored to the baseline state. The ST-segment elevation in TTS is implicitly attributed to myocardial ischemia, along the current conceptualization of its mechanism in acute coronary syndromes. It is conceivable that ST-segment elevation in TTS is partially (or even totally) due to the dyskinesia displayed by the apical “ballooning,” along the pathophysiologic paradigm of VA. Not every patient with TTS presents with ST-segment elevation on electrocardiography. As cases of TTS are reported, a possible association of ST-segment elevation with dyskinesia could be explored using the routinely performed initial transthoracic 2-dimensional echocardiography, by documenting apical and midventricular systolic stretching in combination with basal hyperkinesia. According to this reasoning, patients with apical and midventricular systolic hypokinesia or akinesia would be expected not to show contemporaneously ST-segment elevation on electrocardiography.