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Hemodynamic Consequences of Cerebral Vasospasm on Perforating Arteries

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Presentation on theme: "Hemodynamic Consequences of Cerebral Vasospasm on Perforating Arteries"— Presentation transcript:

1 Hemodynamic Consequences of Cerebral Vasospasm on Perforating Arteries
by Jean F. Soustiel, Eli Levy, Roni Bibi, Sergei Lukaschuk, and Dan Manor Stroke Volume 32(3): March 1, 2001 Copyright © American Heart Association, Inc. All rights reserved.

2 A, Schematic of the phantom model.
A, Schematic of the phantom model. B, Detail of the bifurcation zone in the model with the location of the ultrasound probes upstream and downstream of stenosis. C, Intrastenosis perforating artery model. Jean F. Soustiel et al. Stroke. 2001;32: Copyright © American Heart Association, Inc. All rights reserved.

3 Changes in velocity profile upstream and downstream of stenosis.
Changes in velocity profile upstream and downstream of stenosis. Each diagram depicts the envelope of the flow velocity vectors in a longitudinal section of the parent tube, defining the velocity profile. Positive velocities are depicted as an upward signal. Color coding is used for signal intensity, with brighter tones indicating higher-intensity signal. Although they do not appear in the figure, the tube walls stand longitudinally on either side of the velocity profile. As evidenced here, increasing stenosis corrupted the poststenotic laminar flow (right column) into a sharp and narrow velocity jet limited to the center of the lumen. At 80% stenosis, no flow could be detected near the tube boundaries, whereas further diameter reduction eventually caused flow separation in the periphery of the lumen with negative flow velocities (zero velocity indicated by dashed line). These negative flow-velocity vectors represent a retrograde flow that may account for circulation collapse in the secondary tube. As depicted in the left column, upstream flow-velocity profiles remained almost unchanged until 60% diameter reduction was achieved. At that point, a progressive flattening of the profile was observed. Jean F. Soustiel et al. Stroke. 2001;32: Copyright © American Heart Association, Inc. All rights reserved.

4 Changes in time-collected flow in the parent and secondary tubes in response to increasing stenosis of the parent tube. Changes in time-collected flow in the parent and secondary tubes in response to increasing stenosis of the parent tube. As expected, reduction in the parent-tube diameter resulted in flow reduction in both tubes. In the parent tube (upper trace), however, this flow reduction was only moderate and occurred at 70% stenosis and above. In the secondary tube (lower trace), the flow reduction occurred at earlier stages of the stenosis and was much more pronounced than in the parent tube. Jean F. Soustiel et al. Stroke. 2001;32: Copyright © American Heart Association, Inc. All rights reserved.

5 Effect of perfusion pressure on relative outflows in the parent tube and the secondary tube in a model of severe narrowing (80% stenosis). Effect of perfusion pressure on relative outflows in the parent tube and the secondary tube in a model of severe narrowing (80% stenosis). As anticipated, elevation of the perfusion pressure in the system by increasing the pump output resulted in elevation of the gradient pressure across the parent-tube stenosis and therefore in time-collected flows in both tubes. These changes, however, were much more pronounced in the secondary tube, whose relative contribution to the system total flow increased up to 75% when the mean perfusion pressure was elevated from 56 to 123 mm Hg. Jean F. Soustiel et al. Stroke. 2001;32: Copyright © American Heart Association, Inc. All rights reserved.

6 Changes in velocity profile of a 70% stenosis as a response to increasing fluid viscosity.
Changes in velocity profile of a 70% stenosis as a response to increasing fluid viscosity. Each diagram depicts the envelope of the flow-velocity vectors in a longitudinal section of the parent tube, defining the velocity profile. Positive velocities are depicted as an upward signal. Color coding is used for signal intensity, with brighter tones indicating higher-intensity signal. Increasing viscosity of the fluid mixture used from 2.1 to −2 · cm2 · s−1 through a 70% stenosis in the parent tube resulted in marked changes in the poststenotic velocity profile, which gradually turned into a sharp and thin velocity jet. As viscosity reached values usually obtained in clinical situations with blood hematocrit of 40% and above, flow separation occurred with increasing retrograde flow velocities near the vessel walls (zero line indicated by dashed line). Jean F. Soustiel et al. Stroke. 2001;32: Copyright © American Heart Association, Inc. All rights reserved.

7 Changes in velocity profile induced by increasing viscosity correlated with changes in flow distribution in the system with relative rerouting of the fluid stream into the parent tube and progressive decrease of the percentage of the total outflow delivered by the secondary tube. Changes in velocity profile induced by increasing viscosity correlated with changes in flow distribution in the system with relative rerouting of the fluid stream into the parent tube and progressive decrease of the percentage of the total outflow delivered by the secondary tube. Retrograde flow velocities in the periphery of the lumen may be responsible for a venturi-like effect over the aperture of the secondary tube and may account for the relative decrease in its outflow. The x axis indicates viscosity values. Jean F. Soustiel et al. Stroke. 2001;32: Copyright © American Heart Association, Inc. All rights reserved.

8 Changes in flow distribution in increasing stenosis involving the aperture of the secondary tube.
Changes in flow distribution in increasing stenosis involving the aperture of the secondary tube. Unlike in the previous situation (Figure 3), increasing stenosis produced a moderate and progressive increase in secondary-tube outflow. At 90% stenosis, flow distribution abruptly changed in favor of the secondary tube, probably owing to a relatively significant increase in the peripheral resistance of the stenosis compared with unchanged resistance in the secondary tube. This may account for the higher incidence of cortical ischemic lesions after aneurysmal SAH compared with hypothalamic lesions. Because vasospasm is most often diffuse in anterior circulation, flow in end arteries is likely to be more significantly reduced than in proximal perforating hypothalamic arteries. Jean F. Soustiel et al. Stroke. 2001;32: Copyright © American Heart Association, Inc. All rights reserved.


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