Affiliations: Department of General Internal Medicine, University Hospital Berne, Switzerland | Department of Psychiatry, University of California, San Diego, USA | Department of Medicine, University of California, San Diego, USA | White Mountain Research Station and Department of Medicine, University of California, San Diego, USA
Note: [] Corresponding author: Joel E. Dimsdale, MD, Department of Psychiatry, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0804, USA. Tel.: +1 619 543 5592; Fax: +1 619 543 5462; E-mail: jdimsdale@ucsd.edu.
Abstract: Hemostatic changes might contribute to the increased risk of cardiovascular and cerebrovascular events in patients with obstructive sleep apnea (OSA). We investigated the effect of a short-term isocapnic hypoxic challenge on coagulation activation markers thrombin/antithrombin III complexes (TAT) and D-dimer in OSA. Thirty-two OSA patients (mean age 48±11 years) inhaled a gas mixture containing 10% O2 and 90% N2 and further adjusted to yield pulse oximetry saturation of 80–85% for 5 minutes. Plasma levels of TAT and D-dimer were measured immediately before and immediately after the hypoxic challenge. The hypoxic challenge provoked a significant increase in TAT (p<0.001) and in D-dimer (p=0.037). Mean nocturnal oxygen saturation from the sleep recordings correlated with D-dimer increase (r=−0.37, p=0.041). Also, OSA patients with a history of hypertensive parents had greater D-dimer increase in response to hypoxia than patients having normotensive parents (p=0.035). Parental hypertension independently explained 15% of the variance in D-dimer increase after hypoxia (p=0.035). Oxygen desaturation during sleep may predispose OSA patients, in particular those with a parental history of hypertension, to a hypercoagulable state providing one explanation for the increased risk of atherothrombotic events in this population.
