The aortic valve area was calculated with the continuity equation using the time velocity integral at the aortic valve and left ventricular outflow tract level. Transaortic mean PG was measured by using multiple transducer positions, i.e. apical 5 or 3 chamber, subcostal, right parasternal and suprasternal notch view. Each measurement was averaged for three cardiac cycles for patients in sinus rhythm and five cardiac cycles in atrial fibrillation. Global LV hemodynamic load was estimated using valvuloarterial impedance, calculated as /stroke volume index. Stroke volume index, measured by Doppler echocardiography with the continuity equation, was used to calculate ZVA. Body surface area was calculated using the Mosteller formula and the AVA was divided by the BSA to calculate indexed AVA. All echocardiograms were interpreted by one cardiologist unaware of the purpose of the study, the patient��s condition and treatment, and blinded to the CMR measurements. Since recently published studies showed that the trabeculations and papillary muscle could account for a substantial proportion of the LV mass, we also measured total LV mass with incorporation of the trabeculations and papillary muscle, and the overall statistical analysis was repeated to confirm the robustness of the original results. This is one of the first reports to use CMR to investigate both the gender-specific difference of the hypertrophic and remodeling CMPDA response and the interaction of these parameters with the hemodynamic parameters BPIPP observed in AS patients. We demonstrated the gender-specific differences in the association between AS severity and the LVMI or LVRI. More specifically, the LVMI and LVRI were significantly associated with transaortic mean PG, indexed AVA, and valvuloarterial impedance in both genders. More importantly, there was a significant interaction between genders and the regression coefficients, suggesting that the LV remodeling process differs between the two genders. In addition, independent predictors of LVMI were male gender and transaortic mean PG, whereas significant predictors of LVRI were male gender, transaortic mean PG and valvuloarterial impedance, even after adjusting with baseline characteristics including hypertension, height, and BMI. The incorporation of the LV trabeculations and papillary muscle into the total LV mass did not alter the overall results regarding the gender-specific differences in LV hypertrophy and remodeling patterns. To summarize, although males are associated with more LVH and a higher LV remodeling index even with a similar degree of AS severity or global LV hemodynamic load, females showed a more exaggerated LV remodeling response with increased severity of AS and hemodynamic loads.