Association between polysomnographic measures of disrupted sleep and prothrombotic factors.
BACKGROUND
Subjective sleep disturbances have been associated with increased risk of coronary artery disease (CAD). We hypothesized that disrupted sleep as verified by polysomnography is associated with increased levels of prothrombotic hemostasis factors previously shown to predict CAD risk.


METHODS
Full-night polysomnography was performed in 135 unmedicated men and women (mean age +/- SD, 36.8 +/- 7.8 years) without a history of sleep disorders. Morning fasting plasma levels of von Willebrand Factor (VWF) antigen, soluble tissue factor (sTF) antigen, d-dimer, and plasminogen activator inhibitor (PAI)-1 antigen were determined. Statistical analyses were adjusted for age, gender, ethnicity, body mass index, BP, and smoking history.


RESULTS
Higher total arousal index (ArI) was associated with higher levels of VWF (beta = 0.25, p = 0.011, DeltaR(2) = 0.045), and longer wake after sleep onset was associated with higher levels of sTF (beta = 0.23, p = 0.023, DeltaR(2) = 0.038). More nighttime spent at mean oxygen saturation < 90% (beta = 0.20, p = 0.020, DeltaR(2) = 0.029) and higher apnea-hypopnea index (AHI) [beta = 0.19, p = 0.034, DeltaR(2) = 0.024] were associated with higher PAI-1. There was a trend for a relationship between mean oxygen desaturation < 90% and PAI-1 (p = 0.053), even after controlling for AHI. Total ArI (beta = 0.28, p = 0.005, DeltaR(2) = 0.056) and WASO (beta = 0.25, p = 0.017, DeltaR(2) = 0.042) continued to predict VWF and sTF, respectively, even after controlling for AHI.


CONCLUSIONS
Polysomnographically verified sleep disruptions were associated with prothrombotic changes. Measures of sleep fragmentation and sleep efficiency were related to VWF and sTF, respectively. Apnea-related measures were related to PAI-1. Our findings suggest that sleep disruptions, even in a relatively healthy population, are associated with potential markers of prothrombotic cardiovascular risk.
von Känel
Roland
R
Department of General Internal Medicine, University Hospital Berne, Switzerland.
Loredo
José S
JS
Medicine, University of California San Diego, La Jolla, CA.
Ancoli-Israel
Sonia
S
Departments of Psychiatry, University of California San Diego, La Jolla, CA.
Mills
Paul J
PJ
Department of General Internal Medicine, University Hospital Berne, Switzerland.
Natarajan
Loki
L
Division of Statistics, Department of Family and Preventive Medicine, University of California San Diego, La Jolla, CA.
Dimsdale
Joel E
JE
Departments of Psychiatry, University of California San Diego, La Jolla, CA. Electronic address: jdimsdale@ucsd.edu.
D000328:Adult; D000941:Antigens / Q000097:blood*; D001143:Arousal / Q000502:physiology; D003328:Coronary Thrombosis / Q000097:blood* / Q000209:etiology; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D017286:Polysomnography; D012307:Risk Factors; D020181:Sleep Apnea, Obstructive / Q000097:blood* / Q000150:complications; D012892:Sleep Deprivation / Q000097:blood; D012894:Sleep Stages / Q000502:physiology; D019851:Thrombophilia / Q000097:blood* / Q000209:etiology; D013925:Thromboplastin / Q000378:metabolism*; D014841:von Willebrand Factor / Q000276:immunology
D000941:Antigens; D005338:Fibrin Fibrinogen Degradation Products; D017395:Plasminogen Activator Inhibitor 1; C051321:SERPINE1 protein, human; C029417:Von Willebrand antigen; C036309:fibrin fragment D; D014841:von Willebrand Factor; D013925:Thromboplastin; D010100:Oxygen