Possible Atherogenic Effects of Hypoxia During Obstructive Sleep Apnea

Dean, Roger T.; Wilcox, Ian

doi:10.1093/sleep/16.suppl_8.s15

Cited by 125 publications

(70 citation statements)

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“…12,27 -29 Several studies have looked at the mechanism of endothelial damage secondary to OSA. 25,26,30 These studies suggest that endothelial damage occurs due to increased endothelial oxidative stress, inflammation, and reduced endothelial-repair capacity. 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.…”

Section: Discussionmentioning

confidence: 97%

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

Sharma

Gebregziabher

Parker

et al. 2012

Clinical Cardiology

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Background: Coronary artery atherosclerosis has been associated with obstructive sleep apnea (OSA). However, the type and severity of plaque formation have not been characterized. This study evaluated the association of coronary noncalcified plaques and severity of stenosis in patients with OSA. Hypothesis:Methods: This study was a retrospective analysis of 81 patients, 49 with OSA and 32 without OSA, who had undergone multidetector-row helical computed tomography scanning. The board-certified radiologist was blinded to the diagnosis of OSA and reviewed the scans for plaque characterization, severity of stenosis, and number of vessels involved. Results: Of the 81 patients reviewed, the mean apnea-hypopnea index in the OSA group was 42.2 vs 7.5 in the non-OSA group. The groups did not significantly differ in the distribution of comorbid conditions. We found that among the patients with OSA, 63% had noncalcified/mixed plaques, as opposed to 16% in the non-OSA group (P< 0.0001), with unadjusted odds ratio of 9.3 (3.0, 28.4). After adjustment for other risk factors such as age, sex, race, hypercholesterolemia, and history of smoking, the association remained strong, with an odds ratio of 7.0 (1.9, 26.5; P < 0.05). Conclusions: Our study finds that the frequency of noncalcified/mixed plaques is much higher in patients with OSA than in non-OSA patients. Patients with OSA also have more severe stenosis and a higher number of vessels involved. This study adds to a growing body of data regarding our understanding of the association of OSA and atherosclerosis.

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Section: Discussionmentioning

confidence: 97%

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

Sharma

Gebregziabher

Parker

et al. 2012

Clinical Cardiology

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“…Mechanisms have been postulated to account for possible increased atherogenesis in OSAS [26], and it has recently been reported that patients with coexisting CHD and OSAS are at increased risk of apnoeaassociated ischaemic events [27]. An association of snoring and OSAS is also reported with stroke and possibly stroke prognosis [28], though studying patients following stroke is made difficult by the fact that stroke itself may induce or worsen OSAS.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular risk factors in patients with obstructive sleep apnoea syndrome

Kiely¹,

McNicholas²

2000

Eur Respir J

164

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Cardiovascular disorders are common in patients with obstructive sleep apnoea syndrome (OSAS) but there is debate as to whether OSAS is an independent risk factor for their development, since OSAS may be associated with other disorders and risk factors that predispose to cardiovascular disease.In an effort to quantify the risk of OSAS patients for cardiovascular disease arising from these other factors, the authors assessed the future risk for cardiovascular disease among a group of 114 consecutive patients with established OSAS prior to nasal continuous positive airway pressure therapy, using an established method of risk prediction employed in the Framingham studies.Patients were 100 males, aged (meanSD) 529.0 yrs, and 14 females, aged 5110.4 yrs, with an apnoea/hypopnoea index of 4522 . h -1 . Based on either a prior diagnosis, or a mean of three resting blood pressure recordings >140 mmHg systolic and/or 90 diastolic, 68% of patients were hypertensive. Only 18% were current smokers, while 16% had either diabetes mellitus or impaired glucose tolerance, and 63% had elevated fasting cholesterol and/or triglyceride levels. The estimated 10-yr risk of a coronary heart disease (CHD) event in males was (meanSEM) 13.90.9%, 95% confidence interval (95% CI) 12.1±16.0, and for a stroke was 12.31.4%; 95% CI 9.4± 15.1, with a combined 10 yr risk for stroke and CHD events of 32.92.7%; 95% CI 27.8±38.5 in males aged >53 yrs.These findings indicate that obstructive sleep apnoea syndrome patients are at high risk of future cardiovascular disease from factors other than obstructive sleep apnoea syndrome, and may help explain the difficulties in identifying a potential independent risk from obstructive sleep apnoea syndrome.

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“…21 Biosynthesis of NO from L-arginine is an oxygendependent process, and hypoxia might influence NO formation in vascular beds directly. 22,23 The endothelial cell re- …”

Section: Potential Mechanisms Of Endothelial Dysfunction In Patients mentioning

confidence: 99%

Impairment of Endothelium-Dependent Vasodilation of Resistance Vessels in Patients With Obstructive Sleep Apnea

et al. 2000

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Background —Patients with obstructive sleep apnea (OSA) experience repetitive episodic hypoxemia with consequent sympathetic activation and marked blood pressure surges, each of which may impair endothelial function. We tested the hypothesis that patients with OSA have impaired endothelium-dependent vasodilation, even in the absence of overt cardiovascular disease. Methods and Results —We studied 8 patients with OSA (age 44±4 years) and 9 obese control subjects (age 48±3 years). Patients with OSA were newly diagnosed, never treated for OSA, on no medications, and free of any other known diseases. All obese control subjects underwent complete overnight polysomnographic studies to exclude occult OSA. Resistance-vessel function was tested by use of forearm blood flow responses to intra-arterial infusions of acetylcholine (a vasodilator that stimulates endothelial release of nitric oxide), sodium nitroprusside (an exogenous nitric oxide donor), and verapamil (a calcium channel blocker). Conduit-vessel function was also evaluated by ultrasonography. Brachial artery diameter was measured under baseline conditions, during reactive hyperemia (with flow increase causing endothelium-dependent dilatation), and after sublingual administration of nitroglycerin (an endothelium-independent vasodilator). Patients with OSA had a blunted vasodilation in response to acetylcholine ( P <0.007), but responses to sodium nitroprusside and verapamil were not significantly different from those of control subjects. No significant difference in conduit-vessel dilation was evident between OSA patients and obese control subjects. Conclusions —Patients with OSA have an impairment of resistance-vessel endothelium-dependent vasodilation. This may be implicated in the pathogenesis of hypertension and heart failure in this condition.

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Possible Atherogenic Effects of Hypoxia During Obstructive Sleep Apnea

Cited by 125 publications

References 0 publications

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

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

Cardiovascular risk factors in patients with obstructive sleep apnoea syndrome

Impairment of Endothelium-Dependent Vasodilation of Resistance Vessels in Patients With Obstructive Sleep Apnea

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