Takotsubo syndrome (TTS) is characterized by severe left ventricular (LV) dysfunction that gradually recovers, thus leading to the commonly accepted belief that it is a transient and self-limiting condition. Histologically, TTS can be accompanied by severe morphological alterations potentially resulting from catecholamine excess followed by microcirculatory dysfunction and direct cardiotoxicity. The affected myocardium, however, has a high potential of structural reconstitution which correlates with the rapid functional recovery. The lack of persistent morphological changes in TTS has been confirmed by original CMR studies which pointed out that the acute phase of the disease is characterized only by remarkable myocardial edema with no evidence of significant late gadolinium enhancement. Indeed, the absence of LGE in TTS patients has become a common diagnostic criterion in most CMR centers. Although some studies have challenged this notion by reporting delayed hyper-enhancement in TTS patients, the intensity and extent of LGE in the acute phase of TTS are less than usually reported in studies of myocardial infarction. The long-term clinical and functional consequences of an acute episode of TTS are still unclear. A recent spectroscopic investigation has shown that long-term (\>1 year) abnormalities in cardiac energetic persist after an acute episode of TTS. Also, a few patients with residual wall motion abnormality in whom LGE fails to resolve (suggesting the acute event resulted in frank infarction) have been reported. However, how often persistent morphologic abnormalities are present after the index episode remains undefined. The possibility exists that fibrosis was undetected at follow-up CMR studies using conventional LGE threshold methods due to the fact that myocardial injury is subtler and there are no confidently recognizable reference regions of normal myocardium. Newer echocardiographic tools (i.e. tissue Doppler) have now the potential to detect persistence of post-TTS LV function abnormalities.
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Left ventricular systolic dysfunction
Timeframe: Up to 5 years