Turbulent stresses downstream of three mechanical aortic valve prostheses in 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 development of turbulent stresses downstream of three mechanical aortic valve prostheses in human subjects: the St. Jude Medical, the CarboMedics, and the Starr-Edwards silicone rubber ball. Blood velocity measurements were taken at 17 measuring points in the cross-sectional area of the ascending aorta 5 to 6 cm downstream of the aortic anulus with the use of a perivascular pulsed Doppler ultrasound system. Turbulence analysis was done for each of the 17 measuring points by calculating the radial Reynolds normal stresses within 50 msec overlapping time windows during systole. By coordinating the calculated Reynolds normal stress values for each time window and for all measuring points, computerized two-dimensional color-coded mapping of the turbulent stress distribution during systole was done. For the St. Jude Medical valves the highest Reynolds normal stress (27 to 63 N/m2) were found along the central slit near the vessel walls. The temporal development and spatial distribution of Reynolds normal stresses for the CarboMedics valves were quite similar to those of the St. Jude Medical valves with maximum Reynolds normal stress values ranging from 19 to 72 N/m2. The typical Reynolds normal stress distribution for the Starr-Edwards silicone rubber ball valves was asymmetric, revealing the highest Reynolds normal stresses (11 to 56 N/m2) at various locations in the annular region between the ball and the vessel wall. The spatial distribution and temporal development of turbulent stresses downstream of the three investigated mechanical aortic valve prostheses correlated well with the superstructure of the valves. The maximum Reynolds normal stresses for the three valve types were in the same order of magnitude with exposure times sufficient to cause sublethal damage to red blood cells and platelets.