Intracranial collateralization determines hemodynamic forces for carotid plaque disruption
Brajesh K Lal1, Kirk W Beach, David S Sumner
1Center for Vascular Diagnostics, Department of Vascular Surgery, University of Maryland, Baltimore, MD 21201, USA. blal@smail.umaryland.edu
Insights
Incomplete circle of Willis collateralization increases disruptive forces on carotid plaques, making diameter reduction an inaccurate stroke risk predictor. Assessing flow rates and collateral circulation offers better risk assessment for carotid atherosclerosis.
Area of Science:
- Cardiovascular Science
- Neurology
- Biomedical Engineering
Background:
- Carotid atheroembolism risk assessment using percent diameter reduction is imperfect.
- Stroke from carotid stenosis often results from plaque disruption due to hemodynamic forces.
- The study investigates the impact of circle of Willis (COW) collateralization on these forces.
Purpose of the Study:
- To predict the effect of incomplete intracranial collateralization via the COW on disruptive hemodynamic forces acting on carotid plaques.
- To evaluate the accuracy of diameter reduction in assessing stroke risk.
- To explore alternative methods for refining stroke risk estimation.
Main Methods:
- A circuit model simulating intra- and extracranial arterial pathways and COW collaterals was developed.
- Pressure-flow relationships were modeled using fluid mechanics principles.
- Pressure drops across carotid stenosis were computed for scenarios with and without COW collateralization.
Main Results:
- Higher flow rates and velocities across carotid plaques were observed with a disconnected COW compared to an intact COW.
- Pressure drops across similar stenoses were significantly higher with a disconnected COW.
- Despite stenosis, mean brain blood flow was sustained, but achieved differently based on COW status.
Conclusions:
- Incomplete COW collateralization leads to increased shear stress on carotid plaques, elevating stroke risk.
- Percent diameter reduction is an inaccurate measure of atheroembolic stroke risk.
- Assessing carotid flow rates, velocities, and COW collateral status can improve stroke risk prediction in asymptomatic carotid atherosclerosis.
Introduction:
Percent diameter reduction provides an imperfect assessment of the risk for stroke from carotid atheroembolism. Stroke associated with atherosclerotic carotid stenosis commonly results from plaque disruption brought about by hemodynamic shear stress and Bernoulli forces. The aim of the present study was to predict the effect of incomplete intracranial collateralization through the circle of Willis (COW) on disruptive hemodynamic forces acting on carotid plaques.
Methods:
A simple circuit model of the major pathways and collaterals that form and supply the COW was developed. We modeled the intra- and extracranial arterial circuits from standard anatomic references, and the pressure-flow relationships within these conduits from standard fluid mechanics. The pressure drop caused by (laminar and turbulent) flow along the internal carotid artery path was then computed. Carotid circulation to the brain was classified as being with or without collateral connections through the COW, and the extracranial carotid circuit as being with or without severe stenosis. The pressure drop was computed for each scenario. Finally, a linear circuit model was used to compute brain blood flow in the presence/absence of a disconnected COW.
Results:
Pressure drop across a carotid artery stenosis increased as the flow rate within the carotid conduit increased. Poststenotic turbulence from a sudden expansion distal to the stenosis resulted in an additional pressure drop. Despite the stenosis, mean brain blood flow was sustained at 4.15 mL/s bilaterally. In the presence of an intact (collateralized) COW, this was achieved by enhanced flow in the contralateral (normal) carotid artery. However, in a disconnected COW, this was achieved by sustained systolic and enhanced diastolic flow through the stenosed artery. For a similar degree of stenosis, flow and velocity across the plaque was much higher when the COW was disconnected compared with an intact COW. Furthermore, the pressure drop across a similar stenosis was significantly higher with a disconnected COW compared with an intact COW.
Conclusions:
Incomplete intracranial collateralization through the COW results in increased flow rates and velocities, and therefore large pressure drops across a carotid artery stenosis. This exerts large disruptive shear stress on the plaque compared with patients with an intact COW. Percent diameter reduction provides an inaccurate assessment of risk for atheroembolic stroke. An assessment of carotid flow rates, flow velocities, and the intracranial collateral circulation may add independent information to refine the estimation of stroke risk in patients with asymptomatic carotid atherosclerosis.
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