With the increasing accuracy of cardiac imaging techniques, new findings, not or rarely observed before, come to light. In particular, the improvement in high spatial resolution of a multiplanar imaging technique such as cardiac magnetic resonance (CMR), associated with its increased contrast between blood and endocardial border surface of current cine images, led the appreciation of subtle left ventricular (LV) wall structural features, not seen or neglected by 2-dimensional echocardiography. This is the case of myocardial clefts, described both in hypertrophic cardiomyopathy (HCM) and in healthy volunteers, thus providing another hot potato to the hands of the clinical cardiologist. Article see p 259 These myocardial invaginations have been variably called clefts, crypts, fissures, crevices, and atypical LV noncompaction. Although the etiopathogenesis remains a matter of debate, it is a common belief that they represent a failure to resorb the trabeculated part of ventricular wall during normal embryological development, as seen in isolated LV noncompaction.1,2 Before the development of coronary circulation, the myocardium consists of a spongy meshwork of interwoven myocardial fibers organized into trabeculae with deep recesses, the latter communicating with the LV cavity and enabling a direct blood supply to the myocardium. Myocardial crypts have been described within the LV wall of patients with HCM since early postmortem studies.3–5 In particular, to the best of our knowledge, the first pathological description of a myocardial cleft dates back to 1958, in the historical publication of Donald Teare.3 Noteworthy, Teare …