Obstructive sleep apnea (OSA) is characterized with recurrent collapse of upper airway during sleep and may result in chronic intermittent hypoxia and sleep fragmentation, which is associated with the increase risk of cardiovascular diseases, metabolic disorders and neurocognitive dysfunctions. The cardiovascular complications attributed to OSA patients included hypertension, coronary artery disease, heart failure and stroke. Our data showed that among 599 moderate-severe OSA patients (AHI �d15/hr)， 44.5% had cardiovascular disease, which include 41.4% having hypertension，7% having CAD and 2.4% having congestive heart failure。.
Sleep apnea (AHI�d10/hr) is found in 40% hypertensive subjects and in 50% treated but uncontrolled hypertensive subjects. About 40% of OSAS patients are hypertensive while awake. Community-based epidemiologic studies show sleep apnea is independently associated with hypertension. The influence of sleep apnea on hypertension is more pronounced in younger and middle aged men than in older men. The apnea-hypopnea index (AHI) and degree of desaturation (%Time SpO2<90%, lowest desaturation) are independent predictors of hypertension irrespective of confounders. The sympathetic hyperactivity induced by chronic intermittent hypoxia attributes to cardiovascular consequences in OSA. The sympathetic hyperactivity in OSA include hypercatecholaminemia and elevated sympathetic tone of peripheral nerve system (PNS) and both contribute to hypertension in OSA.
So far, continuous positive airway pressure (CPAP) is the standard treatment for patients with OSAS. CPAP effectively improves airway patency and eliminate the hypoxic episodes and abolish sympathetic hyperactivity. CPAP also can lower the levels of inflammatory mediators, catecholaine and insulin resistance in OSAS patients. Therefore, CPAP can improve objectively and subjectively measured daytime sleepiness, functional status, blood pressure, metabolic abnormalities and quality of life.
|
