Abstract

Obstructive sleep apnea (OSA) is gaining recognition as a cardiovascular and cerebrovascular risk factor. Sleep apnea is now implicated in the etiopathogenesis of stroke, coronary artery disease, hypertension, and congestive heart failure. OSA exerts its negative cardiovascular consequences through its unique pattern of intermittent hypoxia and arousals. The putative mechanisms involved in the pathogenesis of cardiovascular disease in OSA include fibrinolytic imbalance, endothelial dysfunction, oxidative stress, and inflammation. This study discusses the known cellular and molecular processes that promote atherogenesis and vascular dysfunction in patients with OSA, and their implications for cardiovascular disease and prevention in that patient population. Neurologists should familiarize themselves with the symptoms and signs of OSA and the pathophysiology of the association between untreated OSA and cardiovascular disease, including stroke. OSA should be ruled out in patients with cardiovascular disease and be regarded as an important modifiable risk factor. Knowledge of this association is of prime public health importance and can result in primary and secondary prevention of cardiovascular events. This study will also help neurologists in providing patient education and treatment.

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