Acute myocardial infarction triggering Takotsubo syndrome, and the need to search for its prevalence.

To the Editor

The interesting report by Redfors, et al.[1] in the June issue of the Journal of Geriatric Cardiology, about an 88-year-old woman who presented with chest pain, found on echocardiography (ECHO) to have transient left ventricular apical akinesis with a hypercontractile base, and an occluded first diagonal coronary branch with suspected acute plaque rupture, on coronary angiography, treated with a percutaneous coronary intervention, for which the authors concluded that the observed extent of akinesis was disproportionally large for the occluded coronary lesion, letting them to deduce that the acute myocardial infarction (AMI) caused the episode of Takotsubo syndrome (TTS), reminds me of a similar case of an AMI due to stent thrombosis and a resultant associated TTS.[2],[3] The troponin T release was higher than what would be expected from TTS, and reflected mainly the preceding AMI, with a possible lower contribution from the associated TTS. Both ECHO and contrast ventriculography revealed transient apical akinesis, as shown by the ECHO three days later which detected resolution of the apical akinesis, with the left ventricular function found to be completely normal, at the 6-months follow-up ECHO. This is surprising considering the electrocardiographic (ECG) findings of widened QRS complexes, with Q-waves suggestive of previous myocardial infarction(s), in leads 1, -aVR, 2, aVF, and V3-V6, except if all these were transient ECG changes reflective of the TTS; subsequent ECG could provide an answer to this inquiry. I agree with the authors that “the somatic stress associated with AMI may have caused Takotsubo cardiomyopathy (TCM) in this patient”, and their proposal “that TCM and AMI may not be mutually exclusive conditions, and that they may be intertwined in ways we have yet to discover”. The prevalence of TTS complicating AMI needs to be investigated further. Instead of episodic reporting of cases showing the simultaneous occurrence of AMI and TTS, clinicians with access of large databases of patients presenting with acute coronary syndromes should try to evaluate this new “angle”; for example in a recent paper based on a “1875 patients admitted (with suspected ST-elevation AMI), 17 patients (all female) with mean age of 69 ± 11.9 years were identified to have clinical features of typical TTC, thus giving an overall prevalence of 0.9% in primary percutaneous coronary interventions (PPCI) admissions (3.2% prevalence in women).[4] Thus such databases reports should include cases of AMI, TTS, and AMI associated with TTS. It is conceivable that the later occurrence could be detected with contrast ventriculography, and frequent ECHOs revealing rarely classic cases, like the one reported by Redfors, et al,[1] and more frequently myocardial transient regional contraction abnormalities, in the contralateral to the AMI, myocardial plane.[5] This is the reason why combinations of AMI and TTS have been included as plausible occurrences, in recently proposed diagnostic criteria of TTS.[6]