Carotid atherosclerosis progression in patients with Parkinson's disease: a prospective cohort study

Evidence regarding the association between Parkinson's disease (PD) and cardio-cerebrovascular risk remains conflicting, and it is unclear whether the dynamic progression of carotid atherosclerosis in PD patients differs from that in non-PD individuals. This study aimed to compare the progression of carotid atherosclerosis over a 1-year follow-up between PD patients and matched controls, and to investigate whether PD influences this progression independently of traditional cardiovascular risk factors.

This prospective cohort study ultimately included 61 PD patients and 59 age- and sex-matched non-PD controls. Carotid ultrasound was performed at baseline and at the 1-year follow-up. The primary outcome was the annual change in total plaque area (ΔTPA), with plaque progression defined as ΔTPA ≥ 0.05 cm². Multivariable logistic regression models, adjusting for diabetes, smoking, total cholesterol, and low-density lipoprotein cholesterol (LDL-C), were used to assess the independent association between PD status and plaque progression.

At baseline, carotid intima-media thickness and TPA were significantly lower in the PD group than in the control group (both P < 0.05). After 1 year, ΔTPA was significantly smaller in the PD group (P < 0.001), and the incidence of plaque progression was 6.56% in PD patients versus 25.42% in controls. Multivariable regression analysis showed that PD status was a protective factor against atherosclerosis progression (adjusted OR = 0.27, 95% CI: 0.074-0.984, P = 0.047). Within the PD group, no significant associations were observed between plaque progression and disease-specific factors such as disease duration, motor severity, or levodopa equivalent daily dose.

Carotid atherosclerosis progression is significantly slower in PD patients than in non-PD individuals, and this effect is independent of traditional cardiovascular risk factors. These findings suggest that PD patients may exhibit a "vascular protective phenotype," and that a unique shared regulatory network may exist between neurodegenerative processes and peripheral vascular homeostasis.