Obstructive sleep apnea: the new cardiovascular disease. Part I: Obstructive sleep apnea and the pathogenesis of vascular disease

Abstract

Obstructive sleep apnea (OSA) is increasingly recognized as a novel cardiovascular risk factor. OSA is implicated in the pathogenesis of hypertension, left ventricular dysfunction, coronary artery disease and stroke. OSA exerts its negative cardiovascular consequences through its unique pattern of intermittent hypoxia. Endothelial dysfunction, oxidative stress, and inflammation are all consequences of OSA directly linked to intermittent hypoxia and critical pathways in the pathogenesis of cardiovascular disease in patients with OSA. This review will discuss the known mechanisms of vascular dysfunction in patients with OSA and their implications for cardiovascular disease.

Fig. 1

A fragment from a full night sleep study recording (polysomnography) of a patient with severe OSA. Channels from top: LOC: left eye electrooculogram, ROC: right eye electrooculogram, Chin EMG: Electromyogram of the chin, C3-A2 and O2-A1: recordings of two Electroencephalogram leads used for scoring sleep; EKG: Electrocardiogram, Air flow: measured by nasal pressure cannula; Abdomen and chest effort measured by respiratory inductance plesythmography belts, SaO2: Pulse oximetry. Note the recurrent episodes of cessation of flow with persistent respiratory effort (obstructive apneas). Each episode is associated with hypoxia, and is terminated by an arousal and subsequent restoration of the patency of the airway and airflow

Fig. 2

A schema of potential mechanisms of oxidative stress-mediated endothelial dysfunction. IH: intermittent hypoxia, ADMA: asymmetrical dimethlarginine, BH4: tetrahydrobiopterin, eNOS: endothelial nitric oxide synthase, NO: nitric oxide, O2: oxygen ONOO-: peroxynitrite