title: The hypercoagulable state in sleep apnea is related to comorbid hypertension.
abstract: OBJECTIVE
  Obstructive sleep apnea (OSA) is associated with increased prevalence of atherosclerotic disease. A hypercoagulable state thought to underly atherosclerosis has been described in both OSA and systemic hypertension. We wondered about the respective contribution of apnea and hypertension to a hypercoagulable state.
  
  
  METHODS
  Eighty-seven subjects with symptoms suggestive of OSA, mean age 47 years (range 32-64 years), underwent polysomnography and blood pressure (BP) screening. OSA was diagnosed when respiratory disturbance index (RDI) > or = 15. Subjects having systolic BP (SBP) > 140 mmHg and/or diastolic BP (DBP) > 90 mmHg were classified as having hypertension. Three hypercoagulability markers were measured: thrombin/antithrombin III complex (TAT), fibrin D-dimer (DD), and von Willebrand factor antigen (vWF:ag).
  
  
  RESULTS
  Analysis of variance and multiple linear regression were performed on the following four subject groups: (1) normotensive non-apneics (n = 19), (2) normotensive apneics (n = 38), (3) hypertensive non-apneics (n = 11), and (4) hypertensive apneics (n = 19). OSA (groups 2 and 4) had no significant main effect on hemostasis. Hypertensives (groups 3 and 4) had higher plasma levels of TAT (median/inter-quartile range, 148/59-188 versus 77/53-108 pmol/l; P = 0.009) and of DD (376/265-721 versus 303/190-490 ng/ml; P = 0.040) than normotensives (groups 1 and 2). Across all subjects, SBP was the only significant predictor of TAT (P = 0.001) and of DD (P = 0.004), whereas DBP was the only significant predictor of vWF:ag (P = 0.029). These findings persisted even after controlling for gender, age, body mass index, RDI, mean SaO2, and hematocrit.
  
  
  CONCLUSIONS
  Hypercoagulability in OSA is mediated by comorbid hypertension and might account for high cardiovascular morbidity in OSA in general.
authors.affiliation: Department of Psychiatry, University of California, San Diego 92093-0804, USA.
authors.forename: R
authors.initials: R
authors.lastname: von Känel
authors.forename: D T
authors.initials: DT
authors.lastname: Le
authors.forename: R A
authors.initials: RA
authors.lastname: Nelesen
authors.forename: P J
authors.initials: PJ
authors.lastname: Mills
authors.forename: S
authors.initials: S
authors.lastname: Ancoli-Israel
authors.forename: J E
authors.initials: JE
authors.lastname: Dimsdale
mesh_terms: D000328:Adult; D000941:Antigens / Q000032:analysis; D000990:Antithrombin III / Q000032:analysis; D001778:Blood Coagulation Disorders / Q000209:etiology* / Q000503:physiopathology; D001794:Blood Pressure; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010447:Peptide Hydrolases / Q000032:analysis; D012891:Sleep Apnea Syndromes / Q000150:complications* / Q000503:physiopathology; D013599:Systole; D014841:von Willebrand Factor / Q000276:immunology
chemical_list: D000941:Antigens; D005338:Fibrin Fibrinogen Degradation Products; C029417:Von Willebrand antigen; C046193:antithrombin III-protease complex; D014841:von Willebrand Factor; D000990:Antithrombin III; D010447:Peptide Hydrolases