Takotsubo: the myth of rapid and complete recovery

As the youngest diagnostic entity in cardiology, Takotsubo has made a rapid transition from an initial curiosity proposed in Japan by Sato in 1990 to a reasonably frequent diagnosis in any cardiology department. This neuro-cardiac condition is an acute form of left ventricular dysfunction which mimics a myocardial infarction in its presentation with chest pain, ECG changes, and biomarker release. In contrast to a myocardial infarction patients have non-obstructed coronary arteries and a typical area of dyskinesia initially described as ‘myocardial ballooning’, which typically, is disproportionately larger than the cardiac troponin leak would suggest. The close resemblance of this peculiar left ventricular shape with a Japanese octopus-fishing pot gave it the name of ‘Takotsubo’, and it has also been widely presented in the media by the resonant layman term of ‘broken heart syndrome’.

Takotsubo has been widely recognized as a strong, if not the strongest psycho-somatic interaction described in medicine, because the hallmark of this condition is that it is often precipitated by an intense episode of emotional or physical stress Although acute mortality and morbidity has been recognized, Takotsubo patients demonstrate a natural process of spontaneous recovery. Whilst this is of course very encouraging, it has led cardiologists to assume further, generally viewing Takotsubo as a self-limiting condition with rapid and complete recovery.

I started to review these patients in a dedicated clinic in 2011, mainly in an attempt to objectively demonstrate this complete recovery and understand the time frame for it. Before long, I learned that a significant number of patients with prior Takotsubo continued to suffer 3–4 months after their acute event: most were complaining of general fatigue, breathlessness, fleeting episodes of chest pain but mostly not being able to physically engage at the same level of activity as they had previously. Since the restoration of the left ventricular ejection fraction in these patients had been reinforced by the concept of general absence of scar on cardiac magnetic resonance,1 what could be the mechanisms of such protracted recovery?