TURBULENT STRESSES DOWNSTREAM OF 3 MECHANICAL AORTIC-VALVE PROSTHESESIN HUMAN-BEINGS

High levels of turbulent stresses resulting from disturbed blood flow may cause damage to red blood cells and platelets. The purpose of this study was to evaluate the spatial distribution and temporal developme nt of turbulent stresses downstream of three mechanical aortic valve p rostheses in human subjects: the St. Jude Medical, the CarboMedics, an d the Starr-Edwards silicone rubber ball. Blood velocity measurements were taken at 17 measuring points in the cross-sectional area of the a scending aorta 5 to 6 sm downstream of the aortic anulus with the use of a perivascular pulsed Doppler ultrasound system. Turbulence analysi s was done for each of the 17 measuring points by calculating the radi al Reynolds normal stresses within 50 msec overlapping time windows du ring systole. By coordinating the calculated Reynolds normal stress va lues for each time window and for all measuring points, computerized t wo-dimensional color-coded mapping of the turbulent stress distributio n during systole was done. For the St. Jude Medical valves the highest Reynolds normal stress (27 to 63 N/m(2)) were found along the central slit near the vessel walls. The temporal development and spatial dist ribution of Reynolds normal stresses for the CarboMedics valves were q uite similar to those of the St. Jude Medical valves with maximum Reyn olds normal stress values ranging from 19 to 72 N/m(2). The typical Re ynolds normal stress distribution for the Starr-Edwards silicone rubbe r ball valves was asymmetric, revealing the highest Reynolds normal st resses, (11 to 56 N/m(2)) at various locations in the annular region b etween the ball and the vessel wall. The spatial distribution and temp oral development of turbulent stresses downstream of the three investi gated mechanical aortic valve prostheses correlated well with the supe rstructure of the valves. The maximum Reynolds normal stresses for the three valve types were in the same order of magnitude with exposure t imes sufficient to cause sublethal damage to red blood cells and plate lets.