Progression of Intracranial Artery Stenosis and Cerebral Small Vessel Disease and Associations Between the Two Entities: A Prospective Community-based Cohort Study
Ziang Pan1, Fei Han1, Yicheng Zhu1
1Department of Neurology, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science
Objective:
To investigate the risk factors for intracranial artery stenosis (ICAS) and cerebral small vessel disease (CSVD) progression and their associations in a community population.
Background:
Both ICAS and CSVD can cause heavy socioeconomic burdens. However, their longitudinal changes remain controversial.
Design/Methods:
This longitudinal analysis included 756 participants who underwent both baseline and follow-up brain magnetic resonance imaging (MRI) and magnetic resonance angiography from Shunyi cohort. The follow-up duration was 5.58±0.49 years. Incident ICAS was defined as new stenosis occurring in at least one artery or increased severity of the original artery stenosis. CSVD markers included lacunes, cerebral microbleeds (CMB), and white matter hyperintensities (WMH).
Results:
Of the 756 participants (aged 53.7±8.0 years, 34.9% men), 8.5% had incident ICAS. Body mass index (BMI) and diabetes mellitus are independent risk factors for ICAS. Hypertension is an independent risk factor for incident lacunes and CMB, whereas WMH progression is primarily affected by BMI. Higher LDL cholesterol level independently protects against WMH progression. Baseline ICAS burden predicted an increased risk of incident lacunes (odds ratio [OR] = 2.17, 95% confidence interval [CI] = 1.10–4.29, p = 0.025) after adjusting for age, sex, follow-up time, vascular risk factors, and baseline lacunes burden. Incident ICAS was also significantly associated with incident lacunes (OR = 3.29, 95% CI = 1.61–6.72, p = 0.001). No significant correlation was identified between ICAS and CMB or WMH.
Conclusions:
Patients with ICAS and CSVD progression had different modifiable risk factor profiles. The disparate association between ICAS and progressions of different MRI markers of CSVD imply vital differences of their underline mechanism.