The interesting study by Stanton et al of 30 patients with left ventricular hypertrabeculation (LVHT), or noncompaction, raises the following concerns. What were the diagnostic criteria the 9 patients excluded after initially having been diagnosed with LVHT did not fulfill? How many of the 39 echocardiograms would have fulfilled the diagnostic criteria used by other investigators? Stanton et al should explain why a ratio <2:1 between noncompacted and compacted layers does not represent LVHT. This ratio is strongly dependent on the location where it is measured, and so far there is no consensus on the optimal location for measurement. The presence of a 2-layer structure might already be a strong indicator supporting the diagnosis of LVHT. Information should be provided as to whether interobserver variability studies were carried out for measuring the thickness of the compacted and noncompacted layers, because, as shown in Figure 1 of the report, determination of the border between the 2 layers is often not easy and is thus arbitrary. It should be mentioned whether previous echocardiographic recordings were reviewed for acquired LVHT, which has been observed in single patients.

Information is missing concerning co-morbidities in patients with LVHT. Depending on the group of patients, LVHT is associated with neuromuscular disorders in up to 80% of cases, with a number of chromosomal disorders, and also with extracardiac co-morbidities. How many of the patients presented with morphologic features of neuromuscular or chromosomal disorders? For how many patients were family members also investigated for LVHT? Familial occurrence of LVHT has been occasionally reported, but there has been no systematic study of the screening of family members to date.

Oral anticoagulation (OAC) as primary stroke prevention in patients with neither atrial fibrillation nor systolic dysfunction is highly questionable in light of previous studies, which showed no increased stroke rate in these patients with LVHT. Nine of the included patients received OAC. What were the indications for OAC in these patients? How many received OAC for primary and how many for secondary stroke prevention? Did the number of patients receiving OAC increase during follow-up? Did all patients with atrial fibrillation receive OAC?

In 1/3 of the patients, implantable cardioverter-defibrillator (ICDs) were implanted. How many of the patients received ICDs for primary and how many for secondary prevention of sudden cardiac death? In how many were ICDs combined with cardiac resynchronization therapy? Because none of the ICDs discharged appropriate shocks in Stanton et al’s study, and ICD implantation has its inherent risks, the indications for ICDs should be reassessed.

How many patients experienced improvements in cardiac function during follow-up? Did the investigators find any patient in whom LVHT disappeared? Were any of the patients listed for heart transplantation? Did LVHT change in extension during follow-up? What were the causes of death in the 3 patients with LVHT who died?

On the basis of an increasing amount of evidence that predictors of mortality in LVHT are reduced systolic function, atrial fibrillation, and ventricular arrhythmias, the treatment of patients with LVHT should be focused at optimizing pharmacotherapy in those with heart failure, considering cardiac resynchronization therapy in those with heart failure despite pharmacotherapy, the application of OAC in those with atrial fibrillation and/or systolic dysfunction, and the implantation of an ICD if ventricular tachycardia is documented. LVHT in the absence of any co-morbidities or complications is, as far as we know, no indication for preventive measures, including ICDs.