Abstract

Background and Purpose: Acute leptomeningeal collateral flow is vital to maintain blood perfusion to penumbral tissue in acute ischemic stroke due to large vessel occlusion (LVO). However, the degree of this collateral flow differs among patients. Patient premorbid factors as well as factors caused by the mechanisms of stroke are expected to be associated with this collateral flow. We aimed to investigate the clinical determinants of acute leptomeningeal collateral flow in embolic LVO. Methods: Among consecutive stroke patients caused by acute embolic anterior circulation LVO, we retrospectively reviewed 108 patients who underwent evaluation of acute leptomeningeal collateral status (CS) on pretreatment CTA admitted from January 2015 to December 2019. Both premorbid information including cerebrovascular risk factors and leukoaraiosis evaluated by the total white matter (WM) Fazekas score on MRI, which was calculated as periventricular plus deep WM scores, and stroke related information including stroke subtypes, severity, time course, and occlusive thrombus characteristics were collected. Among thrombus characteristics, thrombus length was measured by tracing the filling defect of contrast on CTA. The clinical determinants of good leptomeningeal CS (> 50% collateral filling of the occluded territory) were analyzed. Results: CS was good in 67 patients (62%). On multivariate logistic regression analysis, cardioembolic stroke subtype was negatively related (OR, 0.170; 95% CI, 0.022-0.868), and mild leukoaraiosis (total WM Fazekas scores of 0-2) was positively related (OR, 9.57; 95% CI, 2.49-47.75) to good CS. On subgroup analysis limited to 82 patients with cardioembolic stroke, shorter thrombus length (OR, 0.913 per mm increase; 95% CI, 0.819-0.999) as well as mild leukoaraiosis (OR, 5.79; 95% CI, 1.40-29.61) were independently related to good CS. Conclusions: Premorbid leukoaraiosis and cardioembolic etiology are determinants of acute leptomeningeal collateral flow in embolic LVO. In addition, thrombus length is also a determinant of collateral flow in cardioembolic LVO. These findings indicate that a combination of chronic cerebrovascular damage and acute embolic mechanisms could determine the degree of leptomeningeal collateral flow.

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