Northbrook, IL - A diagnosis of obstructive sleep apnea (OSA) isn't needed for sleep disturbances to have an adverse effect on markers of cardiovascular risk, suggests a prospective study that links some more common sleep disruptions to increased levels of clotting factors and other molecules involved in hemostasis [1].

According to polysomnographic data from 135 generally healthy volunteers without diagnosed sleep disorders, poor sleep efficiency—defined as reduced sleep time compared with overall time in bed—and more frequent arousal from sleep independently predict increased concentrations of soluble tissue factor (sTF) and von Willebrand factor (VWF), respectively. The study also found that arousal frequency and apnea-hypopnea index (AHI) correlated with levels of the antifibrinolytic molecule plasminogen-activator-inhibitor 1 (PAI-1), report Dr Roland von Känel (University Hospital Berne, Switzerland) and associates in the March 2007 issue of Chest.

"Our findings suggest that sleep disruptions, even in a relatively healthy population, are associated with a prothrombotic state that might contribute to coronary artery disease," say the authors, who observed that "apnea may not be the only 'toxic' component of disturbed sleep."

Many physicians and most of our patients believe strongly that sleep is a vital sign.

The study indicates that nonapneics with sleep disturbances can have increased procoagulant activity, but "the clearest evidence for increased cardiovascular risk is in patients with likely obstructive sleep apnea," coauthor Dr Joel E Dimsdale (University of California, San Diego) told heartwire. "Our observations on sleep disruption push this envelope more broadly, but we need further extensive replication in studies before asserting that the relationship is established."

The participants, who had been recruited from the community, who averaged 37 years of age and were free of potentially confounding comorbidities and medications, underwent overnight polysomnographic studies and assessment of hemostasis factors.

In analyses that adjusted for age, sex, ethnicity, body-mass index, blood pressure, and smoking history, direct correlations were observed between the following:

• Total arousal index, based on the frequency of EEG-defined arousals, and VWF levels (p=0.011).
• Total time awake after the onset of sleep and sTF concentrations (p=0.023).
• AHI and levels of PAI-1 (p=0.034).
• Time at an oxyhemoglobin saturation <90% and PAI-1; after adjustment for AHI, the correlation fell short of significance (p=0.053).

The findings support other research suggesting that increased procoagulant activity accounts for some of the elevated cardiovascular risk in patients with OSA, according to the group. "The present study extends these findings, in that we found evidence that apnea and desaturation during sleep might exert antifibrinolytic properties even in patients whose sleep disruption may not yet 'qualify' for a diagnosis of sleep apnea," they write.

To heartwire, Dimsdale said, "Many physicians and most of our patients believe strongly that sleep is a vital sign. We should be asking patients routinely about their sleep."