Left ventricular aneurysm formation as a complication of Takotsubo syndrome: Mechanistic and clinical implications

Dear Editor,

Left ventricular (LV) aneurysm formation in the context of Takotsubo syndrome (TTS) has been regarded as an extremely rare phenomenon.^{[1, 2]} The recent report by Yılmaz et al.^[1] has described an interesting case of giant apical LV aneursym formation following an emotionally-triggered TTS episode in a middle-aged male patient. Accordingly, we would like to highlight further aspects of LV aneurysm formation in the setting of TTS based on this interesting case:

First, TTS evolution, besides traditionally attributed to catecholamine toxicity at the myocardial level, may also arise due to acute LV outflow tract or midventricular obstruction (MVO) leading to supply-demand mismatch and subsequent stunning in the apical territories particularly in patients with certain myocardial conditions including hypertrophic cardiomyopathy (HCM), hypertensive heart disease or ventricular septal bulge.^{[2, 3, 4]} This specific form of TTS was previously named as "mechanically-triggered TTS" which might usually arise in the presence of mild LV hypertrophy, and has a particular predisposition to mechanical TTS complications including LV rupture largely due to the extremely high levels of apical intraventricular pressure during the TTS course.^[4]

Similarly, LV apical aneurysm formation may be particularly associated with a mechanically-triggered TTS episode presenting with a relatively persistent intraventricular obstruction.^[2] In general, this form of LV aneurysms may not present with severe myocardial wall thinning and fibrosis, and is more likely to present with the persistence of TTS-related apical ballooning pattern (as in the present case).^[1] In this context, we wonder whether the patient^[1] had any of the aforementioned myocardial conditions presenting with a significant intraventricular gradient at rest on echocardiogram. Did the authors^[1] also plan to perform advanced diagnostic tests including magnetic resonance imaging (MRI) for the evaluation of these possible myocardial conditions?

Second, intraventricular obstruction in this context may not be evident at rest, and may exclusively be provoked with certain maneuvers (including Valsalva maneuver) or provocation tests including dobutamine stress echocardiogram.^[4] We wonder about the authors’ attitude towards the diagnostic use of provocation tests for their patient. Management of significant intraventricular gradient (at rest or provoked) may prevent recurrent TTS episodes that might possibly be complicated with LV apical aneurysm formation or even myocardial rupture in the long-term.^[4]

Finally, LV aneursym formation in the setting of TTS may also be attributable to pre-existing myocardial conditions including HCM with a chronic MVO or may arise as a consequence of co-existing acute coronary syndromes (due to spontaneous coronary artery dissection or coronary embolism originating from the myocardial territories with severe ballooning, etc.).^{[2, 3]} Of note, these LV aneurysms are characterized by significant myocardial wall thinning and fibrosis (with late gadolinium enhancement on MRI).^[2] However, histopathological examination excluded these factors as potential triggers of LV aneurysm formation in the patient.^[1]

In conclusion, LV apical aneursym formation following a TTS episode may potentially suggest the presence of subtle or overt intraventricular obstruction mostly arising as part of certain pre-existing myocardial conditions. Timely diagnosis and management of these myocardial conditions and associated intraventricular obstruction may prevent recurrent TTS episodes and possible complications including LV aneurysm formation.