Introduction:
Leptomeningeal collaterals are native (pre-existing) anastomoses that cross-connect a small number of distal-most arterioles within the crowns of the cerebral artery trees. We seek to identify potentially modifiable determinants associated with variability in leptomeningeal collateral status in patients with acute ischemic stroke.
Methods:
Data is from the Keimyung Stroke Registry, a prospectively collected dataset of patients with acute ischemic stroke from Daegu, South Korea. Patients with M 1 segment middle cerebral artery (MCA) +/- intracranial internal carotid artery (ICA) occlusions on baseline CT-angio from May 2004 to July 2009 were included in the study.Baseline and follow-up imaging was analyzed at the imaging core lab of the Calgary Stroke Program. Two readers blinded to all clinical information assessed leptomeningeal collaterals on baseline CT-angio by consensus using the regional leptomeningeal score (rLMC).
Results:
Of 206 patients[mean age66.9±11.6 years, median baseline NIHSS 14 (IQR11-20), median stroke symptom onset to CT-angio time 166 minutes (IQR 96-262)], 133 patients (64.6%) had poor collateral status at baseline (rLMC score 11-20). On univariate analyses, patients with poor collateral status at baseline were older, hypertensive, had higher blood glucose values, higher white blood cell count at baseline, higher D-dimer and serum uric acid levels (measured next day morning) and were more likely to have metabolic syndrome as per ATP III criteria. Multivariable modeling identified metabolic syndrome (OR 3.22 95% CI 1.69-6.15, p<0.001), raised serum uric acid (per 1mg/dl OR 1.35 95% CI 1.12-1.62, p<0.01) and age (per year, OR 1.03 95% CI 1-1.05, p=0.03) as independent predictors of poor leptomeningeal collateral status at baseline.
Conclusion:
Metabolic syndrome and hyperuricemia are modifiable determinants associated with poor leptomeningeal collateral status in patients with acute ischemic stroke. This knowledge could potentially help in focusing research on appropriate therapeutic strategies for modulating function of leptomeningeal collaterals.