Silent left ventricular apical ballooning and Tako-tsubo cardiomyopathy and it's prevalence in the ICU

I have published already on Tako - tsubo cardiomyopathy (LVAB or TCC ) . If you go in the search engine you will find that post  , it was presented as a MC question.( Differentiating between the three morphological types.

I know, I may be boring you to death, but my suspicion after looking at multiple echos of various institutions, I was surprised on the high prevalence of this disorde , without its classic risk factors, consistent with what's being reported in the literature

Recent studies have reported a variable, but surprisingly high,incidence of undiagnosed LVAB in some intensive care settings. An incidence of 28% in medical ICU patients was reported in a South Korean study that screened 92 consecutive patients by echocardiography and 5.6% of the medical ICU patients who required echocardiography for clinical and hemodynamic reasons. Harm was caused by using inotropes with worse outcomes.

A more recent study in  the September issue of  The European Society Cardiology Heart Failure .the incidence of silent LVAB suggestive of TCC was substantially lower in this study than recently reported in other international ICU settings .A total of 116 patients were enrolled of whom four had LVAB (3.5%,95% confidence interval 0.9–8.6%). The authors conclusion was: a larger, multi-centre study, prospectively screening for LVAB may help understand any variation between centers and regions, with important implications for ICU management.

I think this number is probably to low and as shown on the diagram,  so many risk factors now are identified that most likely none of the studied population groups are similar in risk factor pofile;  they will have a different pre- test probabilities for risk of LVAB. Also regional /geographic /ethnic factors may play a role.It's a little bit of a similar story with ATTR- amyloidosis,  which is grossly under diagnosed, and patient are not being treated with new drugs directed at transthyretin tetramer folding and deposition in the myocardium.

Nevertheless, when I was still doing bedside medicine no patient came in the ICU/CCU  without getting an immediate echocardiogram ( complete study with TDI) ,  particularly if there was any evidence of hemodynamic instability. It's truely not all about fluids and vaspressors only.

We know there is a substantial population we will harm with blindly throwing them on vasopressors/inotropes as discussed above  . One specific example  were excessive doses of epinephrine causes harm, for  example is the Kounis Syndrome  ( Kounis syndrome and Epinephrine; the ATAK Complex )  ATAK constitutes a challenging contemporary complex in anaphylaxis associated with TCC. It is vital to use epinephrine correctly and monitor vital signs and ECGs for patients with acute anaphylaxis.(see Kounis syndrome link above)

It also makes me wonder if high and repeated doses of epinephrine are truly the right therapy for example in PEA arrest  or could they be more harmful ?

Reference images :Current state of knowledge on Tako-tsubo syndrome: a position statement from the task force on Takotsubo syndrome of the Heart Failure Association of the European Society of
Cardiology