- WITH THE OBESITY EPIDEMIC, THE PREVALENCE OF OBSTRUCTIVE SLEEP APNEA (OSA) IS ALMOST CERTAINLY ON THE RISE.1 MANY HAVE THEORIZED THAT repetitive hypoxemia and sympathetic surges, which characterize OSA, can lead to oxidative stress, systemic inflammation, endothelial dysfunction, and, ultimately, cardiovascular disease.2–4 OSA causes hypertension5,6 and has been associated with other cardiovascular sequelae, such as stroke,7 ischemic heart disease, heart failure,8 and arrhythmias.9 Physiologic studies of OSA and cardiovascular disease have been of predominantly male populations with comorbid conditions who present to sleep clinics. Often, data from patients with OSA from sleep clinics are matched with those obese control subjects from the general population or from primary care clinics. Studies that include patients referred to sleep clinics with suspected OSA, however, may have a referral bias. We sought, therefore, to study the effect of OSA on an obese but healthy population recruited primarily from the community to assess OSA effects. Because we wanted to assess subclinical effects of OSA in an obese population without comorbidities, we limited our study to correlates of cardiovascular endpoints, such as flow-mediated dilation (FMD), arterial stiffness, and skin microvascular reactivity. FMD is a measure of endothelial function derived by comparing arterial vessel dilation before and after hyperemic ischemia.10–14 Dysfunctional endothelium results in decreased arterial vessel dilation after hyperemic ischemia due to reduced endothelial nitric oxide production, likely a harbinger of atherosclerosis.15 Arterial stiffness is likely a composite measure of arterial elasticity, endothelial function, and sympathetic tone.16,17 Although important distinctions exist between various metrics of arterial stiffness (e.g., augmentation index [AIx] and pulse wave velocity),22,23 a number of studies have shown increases in OSA and improvements with treatment with continuous positive airway pressure.12,18,19,44 Finally, skin microvascular reactivity has been associated with poor wound healing and increased insulin resistance in diabetes, but the effect of OSA is unknown.24–26 We hypothesized that OSA would have an effect in this obese population on both macrovascular and microvascular reactivity and arterial stiffness (as estimated by the AIx). Furthermore, because age is a strong predictor of both endothelial function and arterial stiffness, we predefined a subgroup of younger subjects (< 50 years) for further analyses. We theorized that the effect of OSA on vascular function may be modulated by age and that such influences may be differentially expressed among our vascular measurements.27 As a result, we speculated that the effects of OSA on vascular function would be most pronounced in younger participants.