Fig. 1.

The value of CMR tissue characterisation in distinguishing the underlying cause for LVH phenotypes. Panel a shows a patient with familial HCM caused by a pathogenic MYBPC3 mutation. There is asymmetric septal hypertrophy and extensive diffuse and patchy LGE in the hypertrophied segments with corresponding high native myocardial T₁ in these areas of fibrosis. Panel b shows a male patient with LVH secondary to myocardial glycosphingolipid accumulation in Fabry disease as a result of which myocardial T₁ times are low and there is the classic patch of subepicardial fibrosis in the inferolateral wall. b/m/aSAX basal/mid/apical short axis, 4/2C 4/2-chamber, HCM hypertrophic cardiomyopathy, LGE late gadolinium enhancement, LVH left ventricular hypertrophy, MOCO motion-corrected, MOLLI modified Look-Locker inversion recovery, MYBPC3 myosin-binding protein C3, PSIR phase-sensitive inversion recovery, ShMOLLI shortened MOLLI, SSFP steady-state free precession