Noncompaction of the ventricular myocardium is a disease characterized by an increase of the ventricular trabecular meshwork caused by arrest of the normal endomyocardial morphogenesis (Figs. 1, 2, 3). In accordance with the normal human anatomy, the left ventricular wall is well compacted with a few thin trabeculae; on the contrary, the normal right ventricular wall is furrowed by many trabeculae (the trabecula of the marginal septum as well as other ones). For this reason, the term ‘‘noncompaction’’ usually refers to an exclusive or prevalent disease of the left ventricle [1–16]. Recently Song and Aragona et al. [1–3] reported two cases of isolated right-ventricular noncompaction. According to the data coming from scientific literature and from our own experience, in some patients noncompaction is biventricular [5, 6], and an increase of the right ventricular meshwork is often evident in such cases, even more so than on the left side. The main diagnostic criterion of noncompaction, that is, the only one that is accepted and recognized, is evaluation of the ratio between the spongiosus and the compact thickness of the ventricular wall, which must be [2 [6–16]. This ratio is easy to calculate for the left ventricle; on the contrary, it is more difficult to calculate for the right ventricle. Only one case of right-ventricular noncompaction has been reported in the literature [7, 8]. In our personal clinical experience, we have found that many cases of biventricular noncompaction are reported in the register of Italian Society of Cardiovascular Echocardiography. Recently two patients with an inexplicable dilatation of the right ventricle caught our attention: Both of them showed a more prominent trabecular meshwork on