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PurposeGender related differences in left ventricular (LV) remodelling in aortic stenosis (AS) have previously been reported, though functional differences have not been identified. We assessed torsion and global longitudinal strain (GLS) with three dimensional transthoracic echocardiography (3DE), and LV mass and fibrosis with cardiac magnetic resonance (CMR) imaging in age and velocity-matched men and women with moderate-severe AS.Methods: 71 AS patients (56 men) underwent comprehensive transthoracic echocardiography (TTE) assessment, including 3DE, and a CMR scan at 1.5T including late gadolinium enhancement (LGE). The two cohorts were matched for age, blood pressure and transvalvular velocity (Males 67±16 yrs, SBP 130± 23 mmHg, DBP 76±11 mmHg, Peak aortic velocity 3.6±0.5ms-1, Females 71±13yrs, SBP 132±16 mmHg, DBP 76±7 mmHg, velocity 3.5±0.7 ms-1, all p>0.05). Patients with a previous history of confirmed myocardial infarction or LGE with a typical infarct pattern were excluded from the analysis. The TTE and CMR images were analysed independently by two blinded operators. LV mass was analysed using standard protocols. LGE absence or presence was agreed upon by two independent observers. Strain analysis was carried out from the 3DE volume loops using TomTech imaging systems software to measure GLS and torsion (‘twist’).Results: Men had significantly increased myocardial mass index (88 v 73.8 gm-2 p= 0.003), significantly increased torsion (11 v 7o p=0.002) and increased likelihood of patchy LGE (p=0.05) compared to female patients. There was no difference in GLS between the two groups (p=0.47).Conclusions: Our results confirm gender differences in the LV remodelling processes associated with AS. Male patients with AS have increased patchy fibrosis, global torsion and LV mass index compared to their female counterparts, despite similar degrees of AS. The increased torsion in the male hearts may represent an adaptive mechanism to maintain LV ejection fraction despite increased workload and fibrotic disruption of myocardial architecture.