Abstract

Objective: Obstructive sleep apnea syndrome (OSAS) is caused by physical constriction of the upper airway during sleep. When breathing is resumed from the closed apnea state, the brain becomes a waking state, sleep is temporarily suspended. And blood pressure increase by sympathetic nervous system activation. OSAS is sympathetic is activated to repeat the pattern of these apnea and respiratory resumed, blood pressure fluctuation will persist. Decreasing of blood pressure is low at night, or in the case that shows the increase in blood pressure at night, that the risk of cardiovascular disease is higher has been demonstrated. CPAP is known to be an effective treatment of SAS. We therefore examined the blood pressure variation after the introduction of the CPAP hypertension patients complicated with SAS. Design and method: Uncontrolled hypertension (SBP> = 140 or DBP> = 90) with SAS were enrolled from outpatient. We examine the Polysomnography (PSG) in patients who was suspected SAS from the symptoms. And we started CPAP treatment for patients who have been diagnosed with moderate (AHI> = 20) OSAS. All patients were investigated with untreated or in medication for hypertension and well-controlled SAS. All other treatment including antidiabetic and antihypertensive medication has not been changed through out the study period. Heart rate and BP were measured in our office and/or by self monitoring just after wake up at home. Ankle/brachial index (ABI), pulse wave velocity (PWV), and intima media thickness (IMT) were evaluated before and after every 3 months of CPAP treatment. And blood samples were obtained every 6 months for measurements of biochemical markers, including lipid and glucose metabolism. Results: After the treatment, SBP and DBP(p < 0.001), PWV and IMT(p < 0.05) were decreased significantly. This study shows that the treatment with CPAP in hypertension patients with SAS improved the control of hypertensive state as well as the profile of arterial stiffness. Conclusions: Treatment with CPAP improved office and home blood pressure, endothelial dysfunction and arterial stiffness in hypertensive patients with SAS. It's possibly due to inhibit the over-excitement of the SNS by regulating the release of NE, and via its potent hypotensive as well as anti-atherosclerotic properties.

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