• Kannan Ramar and Sean M Caples.
• Mayo Clinic, Center for Sleep Medicine, Division of Pulmonary, Sleep & Critical Care Medicine, Mayo Clinic, Rochester, MN, USA. ramar.kannan@mayo.edu
• Future Cardiol. 2011 Mar 1; 7 (2): 241-9.

AbstractVascular changes related to obstructive sleep apnea (OSA) can lead to chronic cardiovascular consequences such as hypertension. The cardiovascular consequences are owing to nocturnal perturbations related to intrathoracic pressure changes, intermittent hypoxia, sympathetic neural activation, endothelial dysfunction, oxidative stress and systemic inflammation. Intermittent hypoxia due to sleep-related events in OSA activates the renin-angiotensin system and increases the levels of endothelin-1. Intermittent hypoxia also results in oxidative stress, as evidenced by elevated levels of xanthine oxidoreductase, lipid peroxidation and the presence of reactive oxygen species. There is also evidence for a decrease in antioxidant capacity. Patients with OSA may have endothelial dysfunction that resolves with continuous positive airway pressure. OSA is a state of inflammation as evidenced by elevated levels of C-reactive protein, IL-6, NF-κB, TNF-α, ICAM-1, VCAM-1 and E-selectin. This may suggest that OSA is a predisposing factor for atherogenesis. This article will discuss the role of nocturnal perturbations consequent to OSA resulting in endothelial dysfunction, oxidative stress, and inflammation and how they may subsequently play a causative role in cardiovascular disorders.

14 keywords...

hide…