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Left ventricular (LV) twist is increased in aortic stenosis (AS) and is ascribed as a compensatory mechanism. However, the mechanisms by which such derangement occurs are not fully characterized. Our objective was to assess the relationship between LV twist and various factors which mirror LV morphology and function in the setting of severe AS (SAS) (≤ 0.6 cm2/m2) and preserved LV ejection fraction (LVEF) (> 50%).Methods: 46 consecutive patients (pts) (72 ± 10 years, 48% women, LVEF 69 ± 10 %) with isolated SAS (0.44 ± 0.12 cm2/m2) underwent prospectively a comprehensive transthoracic Doppler echocardiography including 2D strain and LV twist by speckle tracking echocardiography, and coronary flow reserve (CFR) measurement in the distal part of the left anterior descending artery using intravenous adenosine infusion. Clinical and plasma NT-proBNP were also assessed. Twenty normal subjects matched for age, gender, and LVEF served as a control group. LV twist was assessed using the parasternal basal and apical short-axis planes, and defined as the net difference in degrees of apical (Ar) and basal rotation (Br).Results: When compared to controls, pts with SAS had a similar Br, a higher Ar and LV twist (24 ± 7 vs. 20 ± 7 °), LV mass/m2, E/Ea, pulmonary artery systolic pressure, and a lower global longitudinal strain (GLS), (all, p < 0.05). Furthermore, in pts with SAS, there was a significant correlation between LV twist and GLS, LV end-systolic volume, LVEF, aortic valve area/m2, relative LV wall thickness, NT-proBNP (log) (all, p < 0.05), but not between LV twist and CFR (p = NS). Furthermore, asymptomatic SAS pts (n = 16) had a higher LV twist when compared to symptomatic pts (27.5 ± 8 vs. 21.5 ± 6 °, p =0.01). In multivariate analysis, besides LVEF, the main independent predictor of LV twist was relative LV wall thickness (all, p < 0.05).Conclusion: LV twist seems to be a compensatory mechanism in SAS, and in addition to LV systolic function, is significantly linked to LV hypertrophic remodeling but not to CFR.