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Chest. 2003 Nov;124(5):1956-67.

Hemostatic alterations in patients with obstructive sleep apnea and the implications for cardiovascular disease.

Author information

1
Institute for Behavioral Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland. roland.vonkaenel@ifv.gess.ethz.ch

Abstract

STUDY OBJECTIVES:

Patients with obstructive sleep apnea (OSA) are at increased risk for coronary artery and cerebrovascular diseases. Numerous studies suggest that a hypercoagulable state is prospectively related to atherothrombotic events. This review explores whether changes in hemostasis may constitute one biological link between OSA and vascular disease.

DESIGN:

Ten studies on hemostatic variables in OSA were located by electronic library search and descriptively reviewed. Work on hemostatic function with physiologic conditions similar to those found in OSA (hypoxemia and hyperactivity of the sympathetic nervous system) was considered to discuss potential molecular mechanisms of procoagulant disturbances in OSA.

MEASUREMENTS AND RESULTS:

The reviewed data suggest that, as compared to non-OSA control subjects, patients with OSA have elevated plasma fibrinogen levels, exaggerated platelet activity, and reduced fibrinolytic capacity. Although not consistently shown, severity of OSA (ie, apnea-hypopnea index) and plasma epinephrine were independent predictors of platelet activity, and average minimal oxygen saturation was an independent predictor of fibrinogen. In some studies, treatment with continuous positive airway pressure decreased platelet activity, plasma fibrinogen levels, and activity of clotting factor VII.

CONCLUSIONS:

There is some evidence for a hypercoagulable state in OSA, which might help explain the increased prevalence of vascular diseases in this population. To further confirm such a notion, future studies need to be performed on sufficiently large samples to be able to control for confounders of hemostatic activity. Prospective studies are needed to examine the association between hemostasis molecules and strong vascular end points.

PMID:
14605073
DOI:
10.1378/chest.124.5.1956
[Indexed for MEDLINE]

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