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Background Fabry disease (FD) is a rare X-linked lysosomal disorder characterized by deficient or absent α-galactosidase A activity due to mutations in the GLA gene. This results in build-up of globotriaosylceramide (GB3), causing progressive, multisystem tissue damage. Migalastat is an oral chaperone therapy that stabilises defective enzyme in those with amenable mutations, including the most common form N215S in the United Kingdom. Although Migalastat improves enzyme activity in some, there remains debate about real world impact. Cardiovascular involvement is characterised by left ventricular hypertrophy (LVH) but real-world results of treatment are mixed, largely due to reliance on echocardiography to quantify LV mass. The aim of this study was to assess impact of Migalastat on LVH measured by cardiac magnetic resonance imaging (CMR).Methods This was an observational, retrospective, single-centre study of all FD patients prescribed Migalastat at University Hospital Birmingham (UHB). Patients attending this clinic underwent routine assessments including blood sampling and CMR. Data relating to patient demographics, comorbidities and FD-specific therapy were extracted from the electronic health record. Contrast-enhanced CMR (1.5 T Avanto, Siemens Healthcare, Erlangen, Germany) was performed in line with standard protocols. Data were extracted for the CMR before the start of Migalastat and the final study before discontinuation or censored at end of December 2020. Paired t-test was used to examine differences in CMR parameters before and after Migalastat treatment.Results In total, 85 FD patients were commenced on migalastat between 2016-2020, including 31 females and 54 males with a median age of 59 at point of prescription (mean 58, range 14-82 years). Most patients (71/85: 84%) had an N215S mutation. A minority were treated with enzyme replacement therapy before starting Migalastat (22/85: 26%). The average time from treatment to repeat CMR was 3 years (range 46-2812 days). There were 45 patients with CMR before and after Migalastat therapy as per the study flow chart. There was no difference in indexed left ventricular mass (LVMi), end diastolic volume (LVEDVi) or stroke volume (SVi) between these two timepoints. There was an increase in T1 time (ms) which was driven differences in the male subgroup. Although there was a decrease in left ventricular end systolic volume (LVESVi) and ejection fraction (EF) in males the mean values remained within the normal range.Conclusion These data suggest that, over a mean follow-up of 3 years, that LV mass does not increase in Fabry patients treated with Migalastat. This contrast with our previous data indicating a consistent increase in mass over a similar time period on enzyme replacement.