Endothelial function and arterial stiffness in minimally symptomatic obstructive sleep apnea.
BACKGROUND
Moderate-severe obstructive sleep apnea (OSA) is associated with endothelial dysfunction, increased arterial stiffness, and hypertension. It is not known whether minimally symptomatic OSA is also associated with impaired vascular function.


OBJECTIVE
To determine whether minimally symptomatic OSA is associated with impaired vascular function.


METHODS
In 64 patients (7 females) with minimally symptomatic OSA (oxygen desaturation index, 23.1 [SD, 15.6]; Epworth Sleepiness Scale score, 8 [SD, 3.8]), and 15 matched control subjects without OSA, endothelial function was assessed by ultrasonographic measurement of flow-mediated dilatation, and by applanation tonometry-derived pulse wave analysis (forearm ischemia and salbutamol-induced changes in augmentation index, AI(x)). Arterial stiffness was assessed by AI(x) and ambulatory blood pressure (ABP) was measured over 1 week.


RESULTS
In patients with OSA, flow-mediated dilatation was significantly lower than in control subjects (5.0% [SD, 2.7%] and 7.5% [SD, 3.3%], respectively; P = 0.003). AI(x) was significantly higher in the OSA group compared with the control group (26.0% [interquartile range (IQR), 19.0-29.5%] and 21.0% [IQR, 8.0-27.0%], respectively; P = 0.04). Change in AI(x) after both forearm ischemia and salbutamol was significantly smaller in patients with OSA (-2.0% [IQR, -5.0 to +4.0%] and -3.0% [IQR, -7.0 to 0.0%], respectively), than in control subjects (-6.0% [IQR, -8.0 to -5.0%] and -7.0% [IQR, -10.0 to -3.0%]; P = 0.005 and P = 0.04, respectively). ABP was similar (97.6 mm Hg [SD, 7.9 mm Hg] and 94.8 mm Hg [SD, 7.4 mm Hg], OSA and control groups, respectively; P = 0.21).


CONCLUSIONS
In patients with minimally symptomatic OSA, diverse properties of endothelial function are impaired and arterial stiffness is increased. Although this was not associated with a significantly increased ABP, the findings suggest that patients with minimally symptomatic OSA are at increased cardiovascular risk.
Kohler
Malcolm
M
Oxford Centre for Respiratory Medicine, Churchill Hospital, Headington, Oxford OX3 7LJ, UK. malcolm.k@bluewin.ch
Craig
Sonya
S
Nicoll
Debby
D
Leeson
Paul
P
Davies
Robert J O
RJ
Stradling
John R
JR
D000368:Aged; D001794:Blood Pressure; D001916:Brachial Artery / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D002318:Cardiovascular Diseases / Q000209:etiology / Q000503:physiopathology; D003430:Cross-Sectional Studies; D042783:Endothelial Cells / Q000000981:diagnostic imaging*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology; D008297:Male; D008365:Manometry / Q000379:methods; D008875:Middle Aged; D011673:Pulsatile Flow; D012307:Risk Factors; D012720:Severity of Illness Index; D020181:Sleep Apnea, Obstructive / Q000150:complications* / Q000503:physiopathology; D014463:Ultrasonography