Chest
Original ResearchAssociation Between Polysomnographic Measures of Disrupted Sleep and Prothrombotic Factors
Section snippets
Study Participants
All subjects gave informed written consent on the study protocol approved by the University of California San Diego Institutional Review Board. Participants consisted of employed (≥ 30 h/wk) men and women recruited from the community by advertisement, by word of mouth, or by referral from local medical practitioners to participate in a study on BP, cardiovascular physiology, and sleep as described in more detail elsewhere.30, 31Recruitment strategies yielded a total of 385 individuals who
Subject Characteristics
Table 1 provides the demographic and sleep characteristics as well as plasma levels of hemostasis factors of the entire sample of 135 subjects. Nineteen subjects (14%) were found to have an AHI > 15 events/h and were considered to have OSA.
Bivariate Associations Between Subject Characteristics and Hemostasis
Levels of d-dimer correlated with age (r= 0.26, p = 0.002) and were higher in women than in men (341 ± 318 ng/mL vs 223 ± 147 ng/mL, p < 0.001) and in African Americans than in whites (328 ± 315 ng/mL vs 233 ± 155 ng/mL, p = 0.011). PAI-1 correlated with BMI (
Discussion
The aim of this study was to examine the notion that disrupted sleep may confer a prothrombotic state. We found that poor general sleep efficiency (longer WASO and lower sleep efficiency) predicted sTF. Measures that relate to perturbed sleep architecture and increased sleep fragmentation (less percentage of SWS and more arousals) were related to higher VWF. Measures reflecting apnea severity (higher AHI and more nighttime spent with Spo2< 90%), were related to PAI-1. Different types of sleep
References (38)
- et al.
Role of thrombotic and fibrinolytic factors in acute coronary syndromes
Prog Cardiovasc Dis
(2004) - et al.
The effects of nasal continuous positive airway pressure on platelet activation in obstructive sleep apnea syndrome
Chest
(2004) - et al.
Hemostatic alterations in patients with obstructive sleep apnea and the implications for cardiovascular disease
Chest
(2003) - et al.
Insomnia and heart disease: a review of epidemiologic studies
J Psychosom Res
(1999) - et al.
Sleep and cardiovascular disease
Curr Probl Cardiol
(2005) Thrombogenic risk factors for atherothrombosis
Rev Cardiovasc Med
(2006)Overview of hemostatic factors involved in atherosclerotic cardiovascular disease
Lipids
(2005)Hemostatic risk factors for atherothrombotic disease: an epidemiologic view
Thromb Haemost
(2001)- et al.
Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study
Am J Respir Crit Care Med
(2001) - et al.
Sleep-disordered breathing and coronary artery disease: long-term prognosis
Am J Respir Crit Care Med
(2001)
Respiratory disturbance index: an independent predictor of mortality in coronary artery disease
Am J Respir Crit Care Med
A path model of chronic stress, the metabolic syndrome, and coronary heart disease
Psychosom Med
Fibrinogen levels and obstructive sleep apnea in ischemic stroke
Am J Respir Crit Care Med
Morning increase of whole blood viscosity in obstructive sleep apnea syndrome
Clin Hemorheol Microcirc
Blood viscosity and platelet function in patients with obstructive sleep apnea syndrome treated with nasal continuous positive airway pressure
Clin Hemorheol Microcirc
Circulating cardiovascular risk factors in obstructive sleep apnoea: data from randomised controlled trials
Thorax
In vivoplatelet activation is increased during sleep in patients with obstructive sleep apnea syndrome
Respiration
Platelet function and fibrinolytic activity in hypertensive and normotensive sleep apnea patients
Sleep
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This research was supported in part by National Institutes of Health grants HL44915, AG08415, M01 RR00827, HL36005, and K23 HL04056–01.
The authors have no financial or other potential conflicts of interest to disclose.