title: The incremental effect of obstructive sleep apnoea syndrome on arterial stiffness in newly diagnosed essential hypertensive subjects.
abstract: OBJECTIVE
  Although obstructive sleep apnoea syndrome (OSAS) is accompanied by an increased atherosclerotic cardiovascular disease burden, its relationship with arterial stiffness is not yet well determined. We investigated whether essential hypertensive individuals with OSAS are characterized by increased arterial stiffness.
  
  
  METHODS
  Our study population consisted of 46 consecutive patients with newly diagnosed untreated stage I-II essential hypertension suffering from OSAS (35 men, aged 49 +/- 8 years) and 53 hypertensive individuals without OSAS, matched for age, sex, and smoking status. All subjects underwent polysomnography, echocardiography and aortic stiffness evaluation by means of carotid-femoral pulse wave velocity (c-fPWV) measurements.
  
  
  RESULTS
  Hypertensive subjects with OSAS [apnoea/hypopnoea index (AHI)>or =5] compared with hypertensive subjects without OSAS (AHI < 5) demonstrated increased levels of body mass index (31.4 +/- 4 versus 29.3 +/- 4 kg/m2, P = 0.015), office systolic/diastolic blood pressure (151/99 versus 145/94 mmHg, respectively, P < 0.05, for both cases) and relative wall thickness (RWT; 0.46 +/- 0.06 versus 0.42 +/- 0.07, P=0.010). Hypertensive subjects with OSAS compared with those without OSAS had significantly increased c-fPWV by 9% (8.56 +/- 0.49 versus 7.85 +/- 0.93 m/s, P=0.001) and this difference remained significant even after adjustment for confounders (P=0.04). In the total study population, c-fPWV was correlated with age (r=0.35, P=0.015), office systolic blood pressure (r=0.30, P=0.007), RWT (r=0.30, P=0.03), logAHI (r=0.389, P=0.0001) and minimum oxygen saturation (r=-0.418, P=0.0001).
  
  
  CONCLUSIONS
  OSAS has a significant incremental effect on aortic stiffening in the setting of middle-aged essential hypertensive subjects. This finding suggests that the presence of OSAS in a hypertensive patient accelerates vascular damage, increasing cardiovascular risk.
authors.affiliation: Department of Cardiology, Hippokration Hospital, Athens, Greece. ktsioufis@hippocratio.gr
authors.forename: Costas
authors.initials: C
authors.lastname: Tsioufis
authors.forename: Konstantinos
authors.initials: K
authors.lastname: Thomopoulos
authors.forename: Kyriakos
authors.initials: K
authors.lastname: Dimitriadis
authors.forename: Anastasia
authors.initials: A
authors.lastname: Amfilochiou
authors.forename: Dimitris
authors.initials: D
authors.lastname: Tousoulis
authors.forename: Manos
authors.initials: M
authors.lastname: Alchanatis
authors.forename: Christodoulos
authors.initials: C
authors.lastname: Stefanadis
authors.forename: Ioannis
authors.initials: I
authors.lastname: Kallikazaros
mesh_terms: D000328:Adult; D001794:Blood Pressure; D002318:Cardiovascular Diseases / Q000209:etiology*; D002339:Carotid Arteries / Q000000981:diagnostic imaging* / Q000503:physiopathology; D016022:Case-Control Studies; D004548:Elasticity; D005260:Female; D005263:Femoral Artery / Q000000981:diagnostic imaging* / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000000981:diagnostic imaging* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D017286:Polysomnography; D011673:Pulsatile Flow; D012307:Risk Factors; D012720:Severity of Illness Index; D020181:Sleep Apnea, Obstructive / Q000150:complications / Q000000981:diagnostic imaging* / Q000503:physiopathology; D014463:Ultrasonography