A better understanding of the etiology of discrete subaortic stenosis (SAS) would be useful in identifying patients at risk and in surgical decision making since the onset, progression, and recurrence of SAS are difficult to predict. Previous studies have shown that congenital defects and morphologic abnormalities associated with SAS (such as steepened aortoseptal angle [AoSA]) cause significant, localized elevations in peak wall shear stress and the wall shear stress gradient (WSSG). High WSSG has been associated with cellular changes in the endothelium. Since the magnitude of wall shear stress varies thoughout the cardiac cycle, we addressed the hypothesis that these morphologic abnormalities have similar effects on the time-averaged shear stress and WSSG. Methods: A finite element model of the left ventricular outflow tract was implemented on the Cray C90 at the Pittsburgh Supercomputing Center for typical pulsatile flow conditions. AoSA was varied between 120 and 150 degrees, maximum aortic velocities from 0.5 to 1 m/s, and aortic diameter from 1 to 1.5 cm. Shear stress and WSSG were directly calculated from the velocity field at discrete points in time. The time-averaged wall shear stress and WSSG at the location of the peak was determined. Results: At an aortic velocity of 1 m/s, the peak and time-averaged shear stress increased with steeper AoSA by 52% and 49.5% respectively. WSSG was more sensitive to changes in AoSA with the peak WSSG increasing by 217%, compared to the time-averaged WSSG which increased by 225%. Conclusions: Geometric variables had similar effects on both the peak and mean shear stress and WSSG. Although the progression and recurrence of SAS may be dependent on time-varying exposure to shear stress, this exposure may be quantified using either a peak or a mean value.