Left Ventricular Diverticulum Associated with Takotsubo Cardiomyopathy

Case Description
We report the case of a 61-year-old female with atypical chest pain associated with electrocardiographic (ECG) changes (T-wave inversion in V2–V6 and I–II–aVL) (Figure 1) with left ventricular apical dysfunction on transthoracic echocardiography and normal cardiac enzymes. The coronary angiogram was normal. Left ventriculography confirmed apical akinesia and was associated with the presence of a large anterobasal left ventricular outpouching (Figure 2, arrows). On cardiac magnetic resonance (CMR) performed 7 days after admission, the dyskinetic dysfunction disappeared completely and there was no evidence of delayed enhancement suggestive of fibrosis due to previous myocardial infarction or inflammation. CMR also confirmed the presence of an antero-basal left ventricular trabeculated diverticulum (40 x 43 x 15 mm) communicating with the left ventricle by a large “collar” and exhibiting a synchronous contraction with the left ventricle and normal thinning of the wall during cardiac cycles (Figures 3A and B, arrows). No paradoxical systolic expansion was appreciated.1 The patient was empirically treated with atenolol (50 mg/d), enalapril (10 mg/d) and aspirin (100 mg/d) and was discharged 3 days after admission.

At a 2-month follow-up visit, the patient complained of no symptoms, her ECG was normal, and a new CMR confirmed complete apical dyskinetic dysfunction disappearance, whereas the anterobasal diverticulum remained unchanged.

For the purpose of role-out, a microcirculation problem such as Syndrome X, no subendocardial hypoperfusion under pharmacologic adenosine stress testing using CMR was appreciated.2

Conclusion

This case is compatible with a form of Takotsubo cardiomyopathy with the unusual concomitant presence of a large anterobasal diverticulum, probably of congenital origin.3 CMR was crucial in defining the localization and morphology of the left ventricular diverticulum. CMR was also important in detecting and defining the transitory dyskinetic apical area without evidence of delayed enhancement and without perfusion disturbances under adenosine perfusion at follow up. This fact does not support the hypothesis of microvascular disease at least as detectable by CMR under adenosine perfusion.4