Biomedical subjects

D N Ku

Publications and source records attributed to D N Ku.

57 records · Page 4Linked to original sources

PubMedDate not supplied

Pulsatile flow in a model carotid bifurcation.

Pulsatile flow in an in vitro model of the human carotid bifurcation was studied by flow visualization using hydrogen bubble techniques. A glass model was constructed after determining an average geometry from 57 biplanar angiograms of 22 subjects ranging from 34 to 77 years of age. The flow pulse used was a half-sine wave superimposed upon a mean flow. Maximum and minimum values of the instantaneous Reynolds number were 1200 and 400, respectively, based upon conditions in the common carotid model artery; the frequency parameter was 6.0. The division of flow into the internal external branches was 70:30. Visualization by hydrogen bubbles demonstrated significant deviations from steady flow behavior. Flow separated in the carotid sinus over the entire cycle, but the location and extent of separation varied strongly. The direction of flow near the walls of the model changed sharply during the cycle except for the region near the apex of the bifurcation where the orientation of streaklines was more nearly unidirectional at all times. Bubbles entering the separated flow region tended to remain entrapped there for several cycles. Rapid dispersion of bubbles occurred in the internal branch near the end of systole, suggesting the presence of flow disorder. The location of low wall shear stresses, directionally varying stresses, and longer residence times for fluid elements appears to coincide with the localization of early atheromatous plaques in human carotid specimens.

Adult↗

PubMedDate not supplied

Pulsatile flow and atherosclerosis in the human carotid bifurcation. Positive correlation between plaque location and low oscillating shear stress.

Fluid velocities were measured by laser Doppler velocimetry under conditions of pulsatile flow in a scale model of the human carotid bifurcation. Flow velocity and wall shear stress at five axial and four circumferential positions were compared with intimal plaque thickness at corresponding locations in carotid bifurcations obtained from cadavers. Velocities and wall shear stresses during diastole were similar to those found previously under steady flow conditions, but these quantities oscillated in both magnitude and direction during the systolic phase. At the inner wall of the internal carotid sinus, in the region of the flow divider, wall shear stress was highest (systole = 41 dynes/cm2, diastole = 10 dynes/cm2, mean = 17 dynes/cm2) and remained unidirectional during systole. Intimal thickening in this location was minimal. At the outer wall of the carotid sinus where intimal plaques were thickest, mean shear stress was low (-0.5 dynes/cm2) but the instantaneous shear stress oscillated between -7 and +4 dynes/cm2. Along the side walls of the sinus, intimal plaque thickness was greater than in the region of the flow divider and circumferential oscillations of shear stress were prominent. With all 20 axial and circumferential measurement locations considered, strong correlations were found between intimal thickness and the reciprocal of maximum shear stress (r = 0.90, p less than 0.0005) or the reciprocal of mean shear stress (r = 0.82, p less than 0.001). An index which takes into account oscillations of wall shear also correlated strongly with intimal thickness (r = 0.82, p less than 0.001). When only the inner wall and outer wall positions were taken into account, correlations of lesion thickness with the inverse of maximum wall shear and mean wall shear were 0.94 (p less than 0.001) and 0.95 (p less than 0.001), respectively, and with the oscillatory shear index, 0.93 (p less than 0.001). These studies confirm earlier findings under steady flow conditions that plaques tend to form in areas of low, rather than high, shear stress, but indicate in addition that marked oscillations in the direction of wall shear may enhance atherogenesis.

Adult↗

PubMedDate not supplied

Effect of stenosis on wall motion. A possible mechanism of stroke and transient ischemic attack.

The mechanism by which atherosclerotic plaque causes stroke and transient ischemic attack is not fully understood. One possibility is that the plaque stenosis may set up hemodynamic conditions causing local arterial wall collapse. Arterial wall collapse may, in turn, affect the integrity of the plaque. This study was designed to define the effects of stenosis on the production of arterial wall collapse using a latex tube model. Stenoses ranging up to 81% by diameter were tested in a Starling resistor chamber under pulsatile pressure conditions upstream of the tube. Increasing the degree of stenosis progressively decreased the external pressure necessary to produce collapse, from 37 mm Hg with the 0% stenosis to 24 mm Hg for the 81% stenosis. The stenoses greater than 70% produced a new phenomenon of "systolic wall collapse" just distal to the stenosis. The maximum diameter decrease was 2.83 mm from the baseline diameter of 6.41 mm. Cyclic wall motion just downstream of the stenosis increased with the increased degree of stenosis from 0.34 mm at 0% stenosis to -1.28 mm at 75% stenosis. The phenomena are discussed in terms of simplified Bernoulli pressure drops. We conclude that local arterial stenosis can produce conditions favorable for wall collapse and increased wall motion at physiologic pressure and flow. This collapse may be important in the development of atherosclerotic plaque fracture and subsequent thrombosis or distal embolization.

Arteriosclerosis↗