And we proposed additional explanations that in patients with dilated LVNC, the increased ventricular end-diastolic pressure and wall tension due to cardiac dilation could stimulate natriuretic peptide secretion, resulting in generally elevated BNP/NT-proBNP levels, and that when hospitalized for HF, the symptoms of dilated LVNC patients (more often NYHA III/IV) were usually more severe than isolated LVNC patients. The gene discussed is NPPB; the disease is left ventricular noncompaction.