Discussion

Here we present a case of apical HCM with focal hyperenhancement of the non-hypertrophic basal lateral segment of the left ventricle. Germans et al5 showed that in HCM carriers who have not yet developed overt hypertrophy, cardiac MRI can detect crypts in the inferoseptal left ventricular wall, even when echocardiography and ECG are normal. Their location is similar to the typical location of the delayed contrast enhancement in HCM patients, which suggests that crypts, as well as formation of focal replacement fibrosis–the histological counterpart of late contrast enhancement–might both reflect two different stages of the same disease process that ultimately results in manifest HCM. In general, hyperenhancement can occur not only in collagenous scar tissue, but also in any condition accompanied by a larger volume of distribution of gadolinium, such as disruption of cellular membrane, oedema, and increased blood volume. Therefore, hyperenhancement in HCM may be related not only to fibrosis but also to other conditions, such as disarray, inflammation, myolysis, and necrosis. 6, 7 A recent study8 found that 9 out of 53 patients (17%) showed delayed enhancement in segments with normal wall thickness, either as an isolated finding or associated with perfu-