Neurogenic Retrograde Arterial Flow During Obstructive Sleep Apnea: A Novel Mechanism for Endothelial Dysfunction?

Abstract

To the Editor: Patients with obstructive sleep apnea (OSA) exhibit impaired brachial artery flow-mediated dilation during wakefulness, a phenomenon that has been attributed to a carryover into the awake state of the consequences of recurrent cycles of hypoxia and reperfusion during sleep, resulting in decreased NO bioavailability and vascular inflammation.1 However, recent prospective studies have failed to identify clearly an independent predictive relationship between markers of oxidative stress and endothelial function.2 Our unanticipated detection of retrograde arterial flow during spontaneous obstructive apnea in an experimental subject who fell asleep when studied during the daytime leads us to propose a novel, additional mechanism for the development of this marker of endothelial dysfunction. A 67-year–old man (blood pressure: 142/84 mm Hg; heart rate: 49 bpm) with known severe untreated OSA (apnea-hypopnea index: 63 events per hour) and treated hypertension (40 mg of fosinopril), whose apneas precipitated …