Introduction: Cerebral small vessel disease (SVD) is considered as precursor lesion of many clinical outcomes including stroke and dementia. It is well established that obstructive sleep apnea or chronic obstructive pulmonary disease is an independent risk factor of stroke. However, there are few studies about the association between pulmonary function and the presence of cerebral small vessel disease.
Purpose: This study aims to investigate the association between pulmonary function and cerebral SVD in healthy adults.
Methods: We conducted a cross-sectional study of 1,528 neurologically healthy people (mean age 56.0±9.0; 847 men), who underwent brain MRI and pulmonary function tests (forced vital capacity (FVC), forced expiratory volume in the first second (FEV1)). Risk factors, anthropometric parameters and clinical information were obtained. For evaluating cerebral SVD, the presence of small silent infarction (SSI) and the volume of white matter hyperintensity (WMH) were assessed through axial T2 fluid-attenuated inversion recovery (FLAIR) sequences MRI. Cerebral microbleeds (CMBs) were evaluated through T2-weighted gradient-recalled echo MRI.
Results: The prevalence of SSI and CMBs were 9.6% (147 subjects) and 4.1% (63 subjects), respectively. The mean volume of WMH was 2.8±6.2mm3. In multiple regression analysis that controlled for age, sex, and smoking status, FVC had a significant negative correlation with WMH volume (R2=0.005, β=-0.109, p=0.002), and FEV1/FVC ratio had a significant correlation with WMH volume (R2=0.006, β=0.083, p=<0.001). In multivariable logistic analysis, after adjusting age, gender, hypertension, and glucose, FVC was negatively associated with the presence of SSI (adjusted OR 0.63, 95% CI 0.44-0.91), and FEV1/FVC ratio was positively associated with the presence of SSI (adjusted OR 1.05, 95% CI 1.02-1.08). The presence of CMBs was not associated with any factor of pulmonary function tests.
Conclusions: The results from our study suggest that lower pulmonary function, especially FVC, was found to be an independent risk factor of cerebral SVD in neurologically healthy adults.