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Collaterals dramatically alter stroke risk in intracranial atherosclerosis
David S Liebeskind1, George A Cotsonis, Jeffrey L Saver
1UCLA Stroke Center, Los Angeles, CA 90095, USA. davidliebeskind@yahoo.com
Insights
Collateral circulation significantly impacts stroke risk in intracranial atherosclerosis. Good collaterals protect against stroke in severe stenosis, while poor collaterals indicate higher risk in milder stenosis.
Area of Science:
- Neurology
- Vascular Medicine
- Radiology
Background:
- Intracranial atherosclerosis is a major cause of stroke.
- The degree of arterial stenosis correlates with stroke risk.
- The role of collateral circulation in modifying this risk is not well understood.
Purpose of the Study:
- To investigate the role of collateral circulation in modifying stroke risk in patients with intracranial atherosclerosis.
- To assess the impact of collaterals on subsequent stroke characteristics.
Main Methods:
- Collateral flow was graded from baseline angiograms in 287 patients from the Warfarin--Aspirin Symptomatic Intracranial Disease (WASID) trial.
- Patients had stenoses ranging from 50-99% and adequate collateral views.
- Statistical models predicted stroke risk based on collateral grade, stenosis percentage, and other covariates.
Main Results:
- Collateral extent predicted stroke risk across all stenoses (P < 0.0001).
- Extensive collaterals reduced stroke risk in severe stenoses (70-99%, P = 0.0427).
- Collaterals were associated with increased stroke likelihood in milder stenoses (50-69%, P < 0.0001).
Conclusions:
- Collateral circulation is a critical factor in determining stroke risk in intracranial atherosclerosis.
- Collaterals offer protection in severe stenoses but may indicate instability in milder stenoses.
Objective:
Stroke risk due to intracranial atherosclerosis increases with degree of arterial stenosis. We evaluated the previously unexplored role of collaterals in modifying stroke risk in intracranial atherosclerosis and impact on subsequent stroke characteristics.
Methods:
Collateral flow was graded in blind fashion on 287 of 569 baseline angiograms (stenoses of 50-99% and adequate collateral views) in the Warfarin--Aspirin Symptomatic Intracranial Disease (WASID) trial. Statistical models predicted stroke in the symptomatic arterial territory based on collateral flow grade, percentage of stenosis, and previously demonstrated independent covariates.
Results:
Across all stenoses, extent of collaterals was a predictor for subsequent stroke in the symptomatic arterial territory (hazard ratio [HR] none vs good, 1.14; 95% confidence interval [CI], 0.39-3.30; poor vs good, 4.36; 95% CI, 1.46-13.07; p < 0.0001). For 70 to 99% stenoses, more extensive collaterals diminished risk of subsequent territorial stroke (HR none vs good, 4.60; 95% CI, 1.03-20.56; poor vs good, 5.90; 95% CI, 1.25-27.81; p = 0.0427). At milder degrees of stenoses (50-69%), presence of collaterals was associated with greater likelihood of subsequent stroke (HR none vs good, 0.18; 95% CI, 0.04-0.82; poor vs good, 1.78; 95% CI, 0.37-8.57; p < 0.0001). In multivariate analyses, extent of collaterals was an independent predictor for subsequent stroke in the symptomatic arterial territory (HR none vs good, 1.62; 95% CI, 0.52-5.11; poor vs good, 4.78; 95% CI, 1.55-14.7; p = 0.0019).
Interpretation:
Collateral circulation is a potent determinant of stroke risk in intracranial atherosclerosis, demonstrating a protective role with severe stenoses and identifying more unstable milder stenoses.
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