Otherwise healthy patients who have obstructive sleep apnea (OSA) demonstrate an increase in arterial stiffness in relation to the severity of their sleep-disordered breathing, according to a study in the May 1 issue of the journal Sleep.
Compared to study participants with the least severe OSA, those with the most severe cases of OSA show an increase of 8 percent in evening measures of the aortic augmentation index. The authors state that this difference is equivalent to about eight years of aging.
The augmentation index is a means of quantifying the augmentation of central aortic pressure and of determining the level of arterial stiffness, according to background information in the article. Arterial stiffness increases both with age and in people with certain diseases that tend to be associated with cardiovascular risk.
Craig Phillips, BSc, of the Woolcock Institute of Medical Research at the University of Sydney, Australia, and his colleagues suggest that measuring arterial stiffness and central blood pressure may be more effective than the traditional measure of peripheral blood pressure in detecting cardiovascular risk.
In fact, their findings suggest that an increase in arterial stiffness may precede the development of overt high blood pressure, which is an important predictor of cardiovascular risk.
“Arterial stiffness and central blood pressure may be superior predictors of cardiovascular disease than peripheral blood pressure because they represent a more precise measure of the load on the heart,” said Phillips.
“Depending upon the degree of arterial stiffness, there can be marked differences in central systolic blood pressure that will not be appreciated with a peripheral measurement.”
The study also reveals an overnight change in arterial stiffness that is independent of OSA severity. A marked increase in morning arterial stiffness is shown relative to evening measures, regardless of the presence or absence of sleep-disordered breathing. This results in an overnight increase in central systolic blood pressure, although early morning peripheral systolic pressure remains unchanged.
“Clearly there is still much to be elucidated about how the sleep process influences vascular function and different blood pressures,” said Phillips.
While they find the results of their study to be promising, the authors state that further study needs to be made of central blood pressure over a 24-hour period and in population groups that do not have OSA.
It also needs to be seen if the elimination of OSA with continuous positive airway pressure (CPAP) therapy reduces central blood pressure and the arterial stiffness associated with OSA.
The study involved 57 male nonsmokers, between 17 and 65 years of age, who had been referred for a routine diagnostic sleep study but had no medical history of cardiovascular disease or diabetes. In the early evening (5 to 7 p.m.) before and morning (5 to 6 a.m.) after an overnight sleep study, they underwent a noninvasive assessment known as pulse wave analysis (PWA) to determine central aortic pressures.
Readings were done in triplicate, and testing was performed at least three times, resulting in a minimum of nine PWA readings for each session. A mean evening and morning score was then calculated for each subject. A standard measure of peripheral blood pressure was also taken before the PWA readings as a means for comparison.
This study was supported by a grant from the National Health and Medical Research Council.
The journal Sleep is the official publication of the Associated Professional Sleep Societies, LLC, a joint venture of the American Academy of Sleep Medicine and the Sleep Research Society.