Abstract / Summary
Abstract Background Acute ischemic stroke (AIS) is characterized by substantial biological and clinical heterogeneity, in which systemic inflammation, neurological impairment, cardiovascular risk,carotid artery metabolism dysregulation and lifestyle-related factors may contribute differently to the overall phenotype. This study investigated the inflammatory profile of patients with AIS and its relationships with neurological-functional severity and documented alcohol status. Methods A retrospective observational study included 71 patients with acute ischemic cerebrovascular events treated in a neurological department in Romania. Systemic inflammatory and biological status was assessed using C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), fibrinogen, and hemoglobin (HGB), while neurological and functional status was characterized using the National Institutes of Health Stroke Scale (NIHSS), modified Rankin Scale (mRS), and Gugging Swallowing Screen (GUSS). Principal component analysis (PCA) and categorical principal component analysis (CATPCA) were used to identify latent biological-clinical structures. Patients were subsequently compared according to documented alcohol status using non-parametric analysis, and the association with log-transformed CRP was examined using unadjusted and multivariable linear regression. Results Biological PCA identified a single systemic inflammatory-biological component dominated by ESR and fibrinogen, explaining 56.1% of biological variance. Incorporation of NIHSS, mRS, and GUSS produced a two-component solution explaining 71.1% of total variance and distinguished a neurological-functional severity component from an inflammatory-biological component. CATPCA extended this structure to the broader patient profile, identifying an Inflammatory-Neurological Severity Dimension and an Age-Cardiovascular Profile Dimension. Documented alcohol status contributed only modestly to these latent dimensions, indicating that it was not a major determinant of the overall multidimensional phenotype. Targeted comparison nevertheless identified CRP as the only investigated biological or clinical variable differing significantly between alcohol-status categories (Mann–Whitney U = 293.5, p = 0.026). The alcohol-status coefficient remained significant after adjustment for age, sex, obesity, and metabolic disease (B = 0.732, 95% CI 0.071–1.394, p = 0.031), although the adjusted model had limited explanatory capacity (R² = 0.086) and was not statistically significant overall (p = 0.307). Conclusions AIS was characterized by related but distinguishable inflammatory-biological and neurological-functional domains embedded within a broader multidimensional clinical phenotype. Documented alcohol status did not define this global structure but showed a selective association with CRP that persisted after adjustment for selected demographic and metabolic factors. These findings suggest that alcohol-related characteristics may be linked to a specific component of systemic inflammatory activity rather than to generalized inflammation or greater neurological-functional severity. Prospective studies with quantitative assessment of alcohol exposure and longitudinal inflammatory profiling are required to confirm this association.