Objective:

We hypothesized that thrombocytosis, an acute inflammatory marker, is associated with poor leptomeningeal collateral recruitment in patients with large-vessel occlusive (LVO) stroke.  

Background:

Leptomeningeal collaterals protect brain tissue from ischemia when direct blood flow is compromised in LVO stroke. Robust collateral flow improves stroke outcomes following reperfusion via IV thrombolysis or thrombectomy, yet little is known about whether systemic inflammation may impair collateral recruitment.

Design/Methods:

Consecutive patients presenting with acute LVO stroke confirmed on computed topography angiography (CTA) and underwent thrombectomy at a single center from 2012 to 2020 were included. Collaterals were categorized as good (≥50% retrograde collaterals supply in the occluded territory) or poor (<50% filling). Thrombocytosis was defined as platelets ≥350,000 cell/mcL. Baseline characteristics including vascular risk factors, hemodynamics, laboratory markers, initial NIHSS were compared by thrombocytosis status. Odds ratios (OR) of poor collaterals were estimated using multivariable logistic models adjusting for age, sex, race, smoking, hypertension, diabetes and atrial fibrillation. All tests were two-sided and considered nominally significant when P<0.05.

Results:

A total of 244 patients were identified. Mean age of 70±15 years, 43.4% were women, 77.5% were white and median NIHSS was 18. Twelve of 244 (4.9%) had thrombocytosis, and the mean platelet counts in those with or without thrombocytosis were 402±37 cells/mcL vs 210±59 cells/mcL. Patients with thrombocytosis were more likely to be younger, female sex, have lower blood pressure, lower hemoglobin, and higher white blood count (P<0.05). Poor collaterals were observed in 55.3%. There was a significant association between poor collateral circulation and thrombocytosis with an adjusted OR 5.90 (95% CI 1.27-27.6; p=0.024). 

Conclusions:

We found that in patients with acute LVO stroke, thrombocytosis is associated with nearly 6-fold increased odds of having poor collaterals. Additional studies would be of interest to see if treating thrombocytosis in patients with LVO improves collateral circulation and perhaps clinical outcomes.