Many risk factors for OSA are also known risk factors for cardiovascular disease, such as age, male gender, and obesity. In addition, OSA is associated with numerous conditions that are known to increase the risk for cardiac disease, such as diabetes mellitus and hypertension.
Episodes of sleep-disordered breathing cause pathologic vascular changes and dysfunction, both of which can cause and contribute to cardiovascular disease, independent of confounding factors. The adverse effects that OSA imposes on cardiovascular function are thought to arise from several overlapping mechanisms. Apneic events, intermittent hypoxia, and the resulting arousals result in an increased sympathetic tone and endothelial dysfunction.
Recurrent arousals resulting from episodic apneic episodes cause repetitive catecholamine surges and a marked increase in sympathetic tone. The increase in vascular sympathetic nerve activity and circulating catecholamine’s subsequently lead to increased peripheral vascular resistance, episodic elevations in nocturnal blood pressure, and propagation of atherosclerosis. Daytime hypertension develops secondary to the persistently elevated sympathetic state. Intermittent hypoxia that follows these apneic events can further add to vascular dysfunction. Hypoxic vasoconstriction and hypoxia-reperfusion oxidative stresses lead to vascular remodeling and the release of pro-inflammatory mediators .