Arterial Stiffness Increases During Obstructive Sleep Apneas SLEEP AND BREATHING

OBSTRUCTIVE SLEEP APNEA (OSA) APPEARS TO BE AN INDEPENDENT RISK FACTOR FOR DIURNAL SYSTEMIC HYPERTENSION,1-3 although the biologic markers for this association have not been well worked out. Acute systemic blood pressure (BP) perturbations have been well described in association with obstructive events in patients with OSA,4-8 but arterial vasomotor activity, which may influence BP activity in this setting, has not. Therefore, defining the effects of obstructive apneas during sleep on arterial vascular response continues to be of great physiologic and clinical interest. Arterial stiffness, a measure of arterial vessel resistance to deformation, is determined functionally by neurohumoral components, including endothelial relaxation factors, and by structural components, including collagen and elastin. Increased arterial stiffness is associated with increased pulse wave velocity and subsequent early wave reflection in systole.9-13 Increased vascular stiffness and an associated augmented sympathetic milieu may precede the onset of elevated BP.14,15 Arterial stiffness has not, however, heretofore been measured in association with obstructive apnea in patients with OSA, nor related to BP activity in this setting. The arterial augmentation index (AAI), derived from arterial wave reflection analysis and defined as the ratio of augmented systolic pressure (due to the late systolic peak in the pressure waveform) to pulse pressure, has been well-validated as a noninvasive measure of arterial stiffness.12,13 We hypothesized that the AAI may be utilized as a sensitive and noninvasive measure of arterial vasomotor perturbation during obstructive events in patients with OSA and, specifically, that 1) arterial stiffness, measured by the AAI, increases acutely in association with obstructive apnea and hypopnea and 2) such increased stiffness may occur in the absence of concomitant acute BP increase in this setting.