Frontiers in Neurology · Nov 6, 2026
Effect of Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitor Use on Early Neurological Deterioration in Branch Atheromatous Disease: A Retrospective Study
By Lili Zhu, Ying Zhang, Jiarong Li et al.
Introduction: Branch atheromatous disease (BAD) is a unique type of cerebral infarction, caused by perforating artery disease with vessel diameters of 200–800 μm. In this study, BAD was defined as ischemic stroke occurring in either the lenticulostriate‑artery territory (infarct involving ≥3 horizontal levels on diffusion‑weighted imaging [DWI]) or the paramedian pontine‑artery territory (infarct abutting the ventral pontine surface near the midline without midline crossing on DWI), with exclusion of patients exhibiting ≥50% stenosis of the parent artery. Patients with BAD are prone to early neurological deterioration (END) and exhibit a poor prognosis. Current treatment regimens for BAD are suboptimal, and fewer than one-third of patients achieve the target low-density lipoprotein cholesterol (LDL-C) level with statin monotherapy. We aimed to explore the combined effect of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors and statins on END incidence and LDL-C levels in patients with BAD, and to identify independent risk factors for END. Methods: This retrospective study involved 1,020 patients with BAD (aged 47–89 years; mean age, 61.2 ± 9.5 years; 64.0% men [661/1,020]) from seven Zhengzhou medical centers (January 2020– April 2025). Based on PCSK9 inhibitor use, patients were divided into PCSK9 inhibitor (n=380) and regular groups (n=640). The median time from symptom onset to PCSK9 inhibitor administration was 3 h (IQR, 2–4 h).Propensity score matching (PSM) was used to eliminate general differences between the groups, yielding 324 matched pairs. We focused on comparing the incidence of END and related indicators such as LDL-C levels in patients. Results: Following PSM, 648 patients (409 men and 239 women; age, 61.2±9.5 years) remained. Hospitalization duration was significantly lower in the PCSK9 inhibitor group than in the regular group (P<0.05); END incidence was lower in the PCSK9 inhibitor group than in the regular group (P<0.05). Multivariate logistic analysis revealed that C-reactive protein level and PCSK9 inhibitor use (both P<0.05) were associated with END occurrence. Discussion: Treating patients with BAD using PCSK9 inhibitors significantly reduced END occurrence and LDL-C levels.