No abstract

The specific features of turbulent flow that are likely to be damaging to the blood cells and platelets are the stresses which are intrinsic to turbulence, known as Reynolds stresses. These include normal stresses as well as shear stresses. The purpose of this study is to determine the magnitude of the turbulent stresses that may occur during ejection in the vicinity of normal and diseased aortic valves near normal pulmonary valves. Both Reynolds normal stresses and Reynolds shear stresses were calculated from velocities obtained in vitro with a laser Doppler anemometer in the region of two severely stenotic and regurgitant human aortic valves. Reynolds normal stresses were also calculated from velocities obtained with a hot-film anemometer in 21 patients in the region of normal and diseased aortic valves. In seven of these patients, it was calculated in the region of the normal pulmonary valve. The Reynolds normal stress in patients with combined aortic stenosis and insufficiency was prominently higher than in patients with normal valves. In the former, the Reynolds normal stress during ejection transiently reached 18,000 dynes/cm2. This was in the range of the Reynolds normal stress observed in vitro. The Reynolds shear stress measured in vitro transiently reached 11,900 dynes/cm2 during ejection. Because the Reynolds normal stresses in the presence of the severely stenotic and regurgitant valves were comparable in vitro and in patients, it is likely that the Reynolds shear stress in patients is also comparable to values measured in vitro. These values were well above the stresses which, when sustained, have been shown to have a damaging effect upon blood cells and platelets.

The purpose of this investigation is to describe our preliminary observations of the overall pattern of flow in a mold of the left coronary artery of a pig. Flow in the coronary mold was visualized by the injection of dye into the sinus of Valsalva. Studies were performed during steady flow at rates of 100, 200, 300, 400, and 500 mL/min. Studies were also performed during pulsatile flow, using a pulse duplicator that simulated the magnitude and phasic pattern of coronary flow at rest and during reactive hyperemia. At conditions that simulated rest, mean coronary flow was adjusted to 121 mL/min of which 24 mL/min (20 percent) was systolic. During simulated reactive hyperemia, mean flow was 440 mL/min. Visualization of flow revealed the absence of disturbances of turbulence during both steady and pulsatile flow in the left anterior descending (LAD) and left circumflex (CIRC) coronary arteries throughout the entire range of flow studied. Prominent spiraling of flow occurred during steady and pulsatile flow. Spiraling of flow was not observed in the LAD at rest during pulsatile flow, but developed during simulated reactive hyperemia. Helical flows were observed in the CIRC both during simulated rest and reactive hyperemia. These observations suggest that helical flows may be characteristic features of flow in the left coronary artery; whereas turbulence may not be a feature of this flow field. Whether the spiraling of flow that we observed related to the spiral distribution of early atheroma reported by others, is undetermined.

A comparison was made between turbulence calculated by subtracting an ensemble average from the instantaneous velocity and calculations made with a high pass digital filter. Velocity was measured with a laser Doppler anemometer in vitro in the region of a normal porcine aortic valve and in patients with a hot film anemometer in the region of normal aortic valves. From the velocity obtained in patients, the absolute turbulence intensity calculated using an ensemble average of 50 beats was nearly twice the turbulence intensity calculated using a digital filter. Individual beats sometimes showed differences of 150% compared to calculations based upon the use of a digital filter. Inspection showed that the ensemble average varied widely from the actual nonfluctuating velocity. Studies in vitro showed less beat to beat variation than occurred in patients. The absolute turbulence intensity measured in vitro, when calculated using an ensemble average, was only 20% greater than calculations using a digital filter. The differences were due primarily to beat-to-beat variations of the nonfluctuating velocity, but these beat-to-beat variations were less prominent than occurred in patients. These observations suggest that ensemble averaging may not be appropriate for the calculation of turbulence, particularly in patients.

No abstract