Hemodynamic Consequences of Cerebral Vasospasm on Perforating Arteries

Abstract

Background and Purpose-Hemodynamics of cerebral vasospasm after subarachnoid hemorrhage remain unclear, and the discrepancy between ultrasonographic or angiographic evidence of arterial narrowing and neurological ischemic deficit is still debated. Most blood flow studies have been involved with large arteries, and thus, very little is known regarding the hemodynamic behavior of small perforating vessels. Patients with symptomatic vasospasm, however, often present with neurological signs suggesting involvement of deep-sited areas of the brain supplied by perforating arteries. Methods-A pulsatile pump was set to provide an outflow of 350 mL/min through a 10-mm-diameter C-flex tube at a perfusion pressure of 130/80 mm Hg. The perfusion fluid used was prepared to approximate blood viscosity. Perforating arteries were simulated by a 1-mm tube connected to the parent tube at a 90°angle. Cylindrical stenotic devices of decreasing diameters were then introduced into the parent tube at the level of the aperture of the secondary tube and 1.5 diameters upstream of it. Velocity profiles both proximal and distal to the stenosis in the parent tube were obtained with a newly developed ultrasonographic flowmeter that allows for high spatial resolution. Results-Increasing stenosis resulted in decreased outflow in the main tube, although it was significant only with severe stenosis. Whenever the simulated stenosis was placed upstream of the secondary tube, flow reduction was associated with a progressive change in the velocity profile, which gradually changed from laminar conditions to a jet stream limited to the center of the lumen. Further diameter reduction was responsible for the occurrence of flow separation with retrograde flow velocities in the periphery of the lumen. In the secondary tube, flow reduction was much more pronounced and began at a lesser degree of stenosis. Increasing fluid viscosity and decreasing perfusion pressure enhanced flow separation and prominently affected the outflow in the secondary tube. Conversely, whenever the simulated stenosis involved the branching area of the secondary tube, there was a slightly progressive decrease in the relative flow in the main tube as the stenosis became tighter. When the stenosis equaled the diameter of the secondary tube, the relative contribution of the secondary tube increased markedly at the expense of the main tube outflow. Conclusions-The present results show that local cerebral vasospasm induces changes in postvasospastic velocity profile affecting the shear rate and may eventually lead to flow separation. This phenomenon may, in turn, result in a venturi-like effect over the aperture of perforating arteries branching out of the postvasospastic portion of the affected parent artery. These alterations of cerebral hemodynamics may account for at least part of the vasospasm symptomatology, especially in the vertebrobasilar system, where vasospasm is commonly focal rather than diffuse. Furthermore, these changes proved to be affected significantly by manipulations ...

Impairment of Cerebral Perfusion and Infarct Patterns Attributable to Vasospasm After Aneurysmal Subarachnoid Hemorrhage

“…As a result of a venturi-like effect leading to flow separation in poststenotic vessel segments, the orifices of perforating arteries are affected ( Figure 2B). 26 Therefore, circumscribed ischemia in deep-sited areas of the brain supplied by perforating arteries originating from the proximal vessel segments may be a likely consequence of the pressure collapse at the perforator apertures. In contrast, in 7 (44%) of the 16 focal band-like infarcts with adjacent thick sulcal clots, DSA showed none or only mild CVS suggesting a different underlying pathophysiological mechanism.…”

Basilar Artery Vasospasm and Delayed Posterior Circulation Ischemia After Aneurysmal Subarachnoid Hemorrhage

“…BA-VS might result in reduced perfusion to the perforating arteries feeding the BS. Using a phantom model designed to simulate the anatomy of the perforating arteries, Soustiel et al 23 showed that with significant narrowing of the parent vessel, perforating vessel flow is significantly impaired. As the narrowing in the parent vessel worsens or extends in length, perforating vessel flow is not only reduced, but flow separation appeared in the parent vessel, which, in turn, produced a Venturi-like effect responsible for pressure collapse at the aperture of the perforating vessels.…”

“…As the narrowing in the parent vessel worsens or extends in length, perforating vessel flow is not only reduced, but flow separation appeared in the parent vessel, which, in turn, produced a Venturi-like effect responsible for pressure collapse at the aperture of the perforating vessels. Soustiel et al 23 suggested that this phenomenon could exist in the vertebrobasilar system and can result in reduced flow to the perforating arteries. This is consistent with the finding that patients with very elevated BA-MFVs (Ͼ115 cm/s) are at higher risk (57.6%) for developing BS hypoperfusion.…”

Impact of Basilar Artery Vasospasm on Outcome in Patients With Severe Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage

“…Because BS perfusion occurs mainly through the perforating arteries, VS in the BA might result in reduced perfusion to the perforating arteries that feed the BS through Venturi effects, as was suggested by Soustiel et al 19 Nevertheless, a Venturi-like effect may not necessarily explain reduced perfusion in cases where BA narrowing is Ͻ50%. We should consider that VS of the perforating artery contributes to hemodynamic impairments.…”

“…Although VS after aSAH was described Ͼ50 years ago and has been uniformly recognized by the neurosurgical community for Ͼ20 years, many questions remain unanswered regarding the clinical significance of posterior circulation VS. 18,19 Should the posterior circulation be monitored for VS? Does BAVS lead to reduced collateral perfusion to affected anterior circulation territories, or does it reduce perforating arterial flow to the BS?…”