Abstract
Plasma von Willebrand factor (VWF), produced in and released from vascular endothelial cells by various stimuli including hypoxia, induces platelet aggregation under high shear stress and plays dual pivotal roles in hemostasis and thrombosis within arterioles, that are regulated by the size of VWF multimers (Ms).
Patients with obstructive sleep apnoea (OSA) have increased risk of thrombotic cardiovascular events, but the pathogenesis is unclear. We examined the relationship between VWF and OSA by measuring VWF antigen, VWFMs, VWF collagen binding activity (VWF:CB), and ADAMTS13. Fifty-eight OSA patients were enrolled. Blood samples were collected before sleep, after sleep, and after one night of nasal continuous positive airway pressure (CPAP) therapy.
Based on VWFM analysis, OSA patients were classified into 3 groups; consistently normal VWFM (Group 1, n=29), increased high molecular weight (HMW)-VWFM at 6 am (Group 2, n=18), and decreased or absent HMW-VWFM at 6 am (Group 3, n=11). Patients in Group 3 had significantly worse apnoea-hypopnoea index; VWF:CB followed a similar pattern. We observed a significant decrease in platelet count between 9 pm and 6 am in OSA patients, potentially associated with reduced larger VWFMs together with decreased VWF antigen levels. Severe OSA may contribute to an arterial pro-thrombotic state.
- ERS