Mechanistic Underpinnings of Mitral Regurgitation in Patients With Takotsubo Syndrome

Silverio et al¹ reported on acute mitral regurgitation (MR) in 1,025 patients with takotsubo syndrome (TTS), from the Takotsubo Italian Network multicenter registry, 186 (18.2%) of whom had developed MR; the authors found that the patients with MR had higher rates of acute heart failure, cardiogenic shock, and mortality at a median of 29 months follow-up, than the patients without MR, with the coexistence of MR and left ventricular (LV) outflow tract obstruction (LVOTO), imparting further increase in the acute heart failure and cardiogenic shock rates. Considering the role of the transient LVOTO in the emergence of MR in patients with TTS, and the possible pathogenetic overlap of TTS, hypertophic cardiomyopathy, and segmental LV hypertrophy of the “sigmoid septum” variety, in “LV ballooning”,2, 3, 4, 5 I have some questions for the authors. 1) Did the patients with MR and LVOTO had a shorter time interval between onset of symptoms and echocardiography, than the patients with MR without LVOTO, or the patients without MR? 2) Are there any data about the in-hospital/follow-up of LVOTO recovery time? 3) Did serial echocardiography reveal transient/persistent septal hypertophy or sigmoid septum in any patients? 4) Were there any structural mitral valve, chordae tendineae, or pupillary muscle changes on echocardiography? 5) Could inotropic agents and/or implementation of the inta-aortic balloon counterpulsation have played a role in the emergence of LVOTO? 6) Is it possible that transient LVOTO and/or MR were present early in the TTS clinical course, with both subsequently disappearing, or the latter ameliorated to mild MR by the time of echocardiography evaluation? 7) Are there any LV size echocardiography measurements indicative of “small LV size” phenotype? 8) Were any patients eventually diagnosed with hypertophic cardiomyopathy?