Endothelial Function in Obstructive Sleep Apnea and Response to Treatment

Abstract

Impaired endothelium-dependent vascular relaxation is a prognostic marker of atherosclerosis and cardiovascular disease. We evaluated endothelium-dependent flow-mediated dilation (FMD) and endothelium-independent nitroglycerin (NTG)-induced dilation of the brachial artery with Doppler ultrasound in 28 men with obstructive sleep apnea (OSA) and 12 men without OSA. Subjects with OSA (apnea-hypopnea index; mean +/- SD, 46.0 +/- 14.5) had lower FMD compared with subjects without OSA (5.3 +/- 1.7% vs. 8.3 +/- 1.0%, p < 0.001), and major determinants of FMD were the apnea-hypopnea index and age. There was no significant difference in NTG-induced dilation. Subjects with OSA were randomized to nasal continuous positive airway pressure (nCPAP) or observation for 4 weeks. Subjects on nCPAP had significant increase in FMD, whereas those on observation had no change (4.4% vs. -0.8%, difference of 5.2%, p < 0.001). Neither group showed significant change in NTG-induced vasodilation. Eight subjects who used nCPAP for over 3 months were reassessed on withdrawing treatment for 1 week. On nCPAP withdrawal, FMD became lower than during treatment (p = 0.02) and were similar to baseline values. Our findings demonstrated that men with moderate/severe OSA have endothelial dysfunction and treatment with nCPAP could reverse the dysfunction; the effect, however, was dependent on ongoing use.

Independent Association Between Obstructive Sleep Apnea and Noncalcified Coronary Plaque Demonstrated by Noninvasive Coronary Computed Tomography Angiography

“…Furthermore, there is evidence that treatment of OSA with nasal CPAP therapy improves endothelial function and reduces the risk for fatal and nonfatal cardiovascular events. 31 The possibility of OSA causing or accelerating atherosclerosis has been supported by data from several studies. 32 -35 Obstructive sleep apnea being an independent risk factor for atherosclerosis is further supported by a randomized controlled trial in which intervention by CPAP resulted in significant reduction in carotid intima-media thickness.…”

Effects of long-term treatment for obstructive sleep apnea on pulse wave velocity

“…Several experimental and clinical studies have shown that nocturnal hypopnea induces increases in blood pressure levels 6,19 and the progression of arterial stiffness. 18,19 Endothelial dysfunction 4,[20][21][22] and disturbances of sympathetic activity 5,23 are recognized clinical features in OSA patients that increase vascular tone and accelerate the progression of arterial stiffness. 7 Chronic intermittent hypoxia causes dyslipidaemia and initiates the development of atherosclerosis, both of which contribute to arterial stiffness.…”

“…1,2 Atherosclerosis is a progressive disease that is also a pivotal risk factor for these cardiovascular disorders. OSA induces systemic HT, inflammation, 3 endothelial dysfunction 4 and disturbances in sympathetic activity, 5 all of which are known to accelerate the development of atherosclerosis. It has been shown that continuous positive airway pressure (CPAP) treatment improves these risk factors for atherosclerosis.…”

“…It has been shown that continuous positive airway pressure (CPAP) treatment improves these risk factors for atherosclerosis. [3][4][5][6] Arterial stiffness, an indicator of worsening atherosclerosis, has been shown in OSA patients, with the degree of arterial stiffness correlated with the severity of OSA. 7,8 Pulse wave velocity (PWV) reflects arterial stiffness associated with cardiac events, and thus the severity of atherosclerosis.…”

Gender Differences on Brachial Flow‐mediated Dilation and Carotid Intima‐media Thickness for Prediction of Spontaneous Cardiovascular Events

“…Brachial artery FMD: Patients were studied in the fasting state and all vasoactive medications were withheld for at least 12 h before the study. As previously described, 10,11 longitudinal scans of the brachial artery were obtained at rest, and then FMD was induced by inflation of a pneumatic tourniquet placed on the forearm to a pressure of 250 mm Hg for 5 min. The cuff was then released and serial imaging of the brachial artery was recorded for 5 min.…”