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Is Surgical Removal of the Noncompacted Layer the Clue to Treat Left Ventricular Hypertrabeculation/Noncompaction?

Dear Editor, With interest we read the article by Gan et al. about surgical restoration as possible treatment for left ventricular hypertrabeculation/noncompaction (LVHT). We have the following questions: It would be interesting to know if progressive exercise intolerance was attributable only to cardiac dysfunction or any extracardiac disease, in particular a neuromuscular disorder with which LVHT is frequently associated, if the patient was investigated neurologically and if cardiac or muscle disease was present in any of the relatives. Information should be given, if heart failure developed suddenly or symptoms progressed slowly, and if echocardiographic recordings were available to assess if LVHT was congenital or acquired. Did the electrocardiogram show any abnormalities? Since it remains unclear if mitral regurgitation was due to a valvular or ventricular problem, we would like to know inmore detail themorphology of themitral valves, the chordae tendineae, and the papillary muscles, especially if LVHT also affected the papillary muscles. Speckle-tracking is a new technique with inherent limitations. Was it decided to surgically remove LVHT preoperatively or intraoperatively, based only on the reduced early diastolic strain-rate or were other indicators for diastolic dysfunction considered, like Doppler sonography or cardiac catheterization? It should be clarified whether diastolic dysfunction was due to impaired relaxation or restriction. There is a discrepancy between the echocardiographic image showing trabeculations protruding into the left ventricular cavity and the diagram showing horizontal trabeculations crossing the left ventricular cavity. Were all segments of noncompacted myocardium removed or did some segments remain? The histological appearance of the resected trabeculations should be described. Were the trabeculations associated with subendocardial fibrosis, a frequent finding in LVHT? The postoperative pharmacotherapy of the patient, including anticoagulation therapy, would be interesting to know. The authors mention another case of LVHT in whom the left ventricular cavity was partially excluded. Both cases, so far reported, recovered well after surgery. It remains unclear, however, whether in the present case clinical improvement was due to correction of the mitral regurgitation or due to the resection of LVHT. Since the etiology and pathogenesis of LVHT is largely unknown we do not know if the trabecular meshwork is a compensatory, adaptive attempt of the failing myocardium or the reason for heart failure. In view of the limited therapeutic options for LVHT patients with severe heart failure and disadvantages of cardiac transplantation due to shortage of donor organs and necessity for lifelong immunosuppression, we consider further investigations about LVHT resection useful, preferentially starting in genetically engineered mouse models.