RT Journal Article
SR Electronic
T1 Reduced larger von Willebrand factor multimers at dawn in OSA plasmas reflect severity of apnoeic episodes
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 657
OP 664
DO 10.1183/09031936.00186210
VO 40
IS 3
A1 Noriko Koyama
A1 Masanori Matsumoto
A1 Shinji Tamaki
A1 Masanori Yoshikawa
A1 Yoshihiro Fujimura
A1 Hiroshi Kimura
YR 2012
UL http://erj.ersjournals.com/content/40/3/657.abstract
AB 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 haemostasis and thrombosis within arterioles, which are regulated by the size of vWF multimers (VWFMs). 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 (VWF:Ag), VWFMs, VWF collagen binding activity (VWF:CB) and a disintegrin-like, metalloproteinase, and thrombospiondin type 1 motifs 13. A total of 58 OSA patients were enrolled. Blood samples were collected before sleep, after sleep, and after one night of nasal continuous positive airway pressure therapy. Based on VWFM analysis, OSA patients were classified into three groups; consistently normal VWFMs (group 1, n=29), increased high molecular weight (HMW)-VWFMs at 06:00 h (group 2, n=18), and decreased or absent HMW-VWFMs at 06:00 h (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 21:00 h and 06:00 h in OSA patients, potentially associated with reduced larger VWFMs together with decreased VWF:Ag levels. Severe OSA may contribute to an arterial pro-thrombotic state.