Association of Myeloperoxidase and Granulocyte Colony-Stimulating Factor With Intracranial Atherosclerosis Presence and Progression From a Community-Based Study.

BACKGROUND

Myeloperoxidase may promote plaque instability, while granulocyte colony-stimulating factor may aggravate inflammation. We investigated their associations with intracranial artery plaque, stenosis, atherosclerotic burden, and plaque progression.

METHODS

This analysis included 3059 participants from the PRECISE (Polyvascular Evaluation for Cognitive Impairment and Vascular Events) study in China. Intracranial artery plaque, stenosis, and intracranial atherosclerotic burden were assessed using 3.0-T magnetic resonance imaging at baseline (2017-2019) and 2 follow-ups (2019-2022 and 2022-2024). Logistic regression and restricted cubic spline models were used to evaluate associations between biomarkers and intracranial atherosclerosis.

RESULTS

Participants had a median age of 61 years, and 53.4% were women. Restricted cubic spline analyses indicated linear associations of higher myeloperoxidase and granulocyte colony-stimulating factor levels with intracranial atherosclerosis. Each 1-SD increase in myeloperoxidase was associated with intracranial artery plaque (odds ratio [OR], 1.12 [95% CI, 1.02-1.23]), stenosis (OR, 1.19 [95% CI, 1.02-1.39]), and higher intracranial atherosclerotic burden (common OR, 1.12 [95% CI, 1.02-1.23]) at baseline, as well as plaque progression at wave 2 (OR, 1.18 [95% CI, 1.07-1.30) and wave 3 (OR, 1.13 [95% CI, 1.02-1.26). Continuous granulocyte colony-stimulating factor levels were not significantly associated with these outcomes; however, its highest tertile was associated with baseline intracranial artery plaque and higher intracranial atherosclerotic burden versus the lowest tertile (P for trend<0.05).

CONCLUSIONS

Elevated myeloperoxidase and granulocyte colony-stimulating factor levels were associated with intracranial atherosclerosis and plaque progression over ≈4.7 years, highlighting the role of neutrophil-driven inflammation.