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Original Research: SLEEP MEDICINE |

Association Between Polysomnographic Measures of Disrupted Sleep and Prothrombotic Factors*

Roland von Känel, MD; José S. Loredo, MD, FCCP; Sonia Ancoli-Israel, PhD; Paul J. Mills, PhD; Loki Natarajan, PhD; Joel E. Dimsdale, MD
Author and Funding Information

*From the Department of General Internal Medicine (Dr. von Känel), University Hospital Berne, Switzerland; and the Departments of Psychiatry (Drs. Mills, Dimsdale, and Ancoli-Israel) and Medicine (Dr. Loredo), and Division of Statistics, Department of Family and Preventive Medicine (Dr. Natarajan), University of California San Diego, La Jolla, CA.

Correspondence to: Joel E. Dimsdale, MD, Department of Psychiatry, University of California San Diego, 9500 Gilman Dr, La Jolla, CA 92093-0804; e-mail: jdimsdale@ucsd.edu



Chest. 2007;131(3):733-739. doi:10.1378/chest.06-2006
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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 (β = 0.25, p = 0.011, ΔR2 = 0.045), and longer wake after sleep onset was associated with higher levels of sTF (β = 0.23, p = 0.023, ΔR2 = 0.038). More nighttime spent at mean oxygen saturation < 90% (β = 0.20, p = 0.020, ΔR2 = 0.029) and higher apnea-hypopnea index (AHI) [β = 0.19, p = 0.034, ΔR2 = 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 (β = 0.28, p = 0.005, ΔR2 = 0.056) and WASO (β = 0.25, p = 0.017, ΔR2 = 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.


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