Collaterals dramatically alter stroke risk in intracranial atherosclerosis

Abstract

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.

Figure 1

Protective effect of collateral circulation offsets risk of territorial stroke in severe stenoses. (A) Cerebellar hemispheric collaterals from posterior inferior cerebellar territory to the superior cerebellar territory provide flow downstream from a proximal basilar stenosis. (B) Leptomeningeal collaterals from anterior and posterior cerebral augment flow beyond a proximal middle cerebral artery stenosis.

Figure 2

Collaterals avert stroke in severe stenosis yet may be a marker of hemodynamic impairment and elevated stroke risk in moderate stenoses. (A) Robust collaterals in severe MCA stenosis prevent stroke whereas (B) brisk collateral filling in a moderate distal vertebral stenosis may be an ominous marker.

Figure 3

Kaplan-Meier curves for the endpoint of stroke in the territory of the symptomatic intracranial stenosis based on collateral status for severe stenoses. The presence of good collaterals diminishes risk of territorial stroke.

Figure 4

Kaplan-Meier curves for the endpoint of stroke in the territory of the symptomatic intracranial stenosis based on collateral status for moderate stenoses. The presence of any collaterals, good or poor, serve as an ominous marker of future stroke in cases of moderate stenosis.