Background: Lacunar infarcts, caused by occlusion of small penetrating arteries, account for approximately 25% of ischemic strokes. Despite mild presentations, up to 30% of patients experience early neurological deterioration (END). While several mechanisms have been implicated, the influence of anatomical variants in the Circle of Willis (CoW) and major intracranial arteries on END risk remains uncertain. This study assessed whether specific vascular configurations are associated with END in patients with lacunar infarction. Methods: We retrospectively analyzed 245 patients with acute lacunar infarcts attributed to small vessel disease, admitted to a tertiary care center between 2020–2024. Vascular imaging (CTA or MRA) and clinical, laboratory, and imaging data were obtained from institutional stroke registries. END was defined as a ≥2-point increase in the NIHSS within 72 hours, without alternative explanation. Vascular anatomical variants, including fetal PCA and PCA presence and laterality (unilateral vs. bilateral), ACA and vertebral artery hypoplasia or aplasia were assessed. Univariate and multivariable logistic regression analyses were used to identify predictors of END. Results: Of 245 patients, 50 (20.4%) experienced END. Compared to those without END, affected patients had significantly higher rates of fetal PCA, unilateral PCA, peripheral artery disease (PAD), larger infarct volumes, higher pulse pressure, and more frequent ataxia (Table 1). To avoid collinearity and enhance interpretability, PCA laterality was selected over fetal PCA presence due to its more granular anatomical distinction. In the final model, PAD (aOR = 7.65, 95% CI: 1.76–33.37, p = 0.007), infarct volume (aOR = 2.21, 95% CI: 1.28–3.80, p = 0.004), and ataxia (aOR = 2.79, 95% CI: 1.25–6.26, p = 0.01) remained independently associated with END. PCA laterality (aOR = 1.81, 95% CI: 0.82–4.00, p = 0.14) and pulse pressure (aOR = 1.01, 95% CI: 0.99–1.03, p = 0.19) were not significant in adjusted models (Table 2). Conclusions: In lacunar infarction, END was associated with vascular comorbidities (PAD), clinical signs (ataxia), and infarct burden, but not with intracranial arterial variants in adjusted models. While fetal PCA was significant in univariate analysis, its overlap with PCA laterality precluded inclusion in multivariable models. These findings suggest END in small vessel stroke is more likely driven by local ischemic burden than by upstream vascular anatomy.
Khasiyev et al. (Thu,) studied this question.