Atherosclerosis and Obstructive Sleep Apnea in Patients with Ischemic Stroke

Dziewas, Rainer; Ritter, Martin; Usta, Nesrin; Boentert, Matthias; Hor, Hyon; Dittrich, Ralf; Schäbitz, Wolf Rüdiger; Ringelstein, E. B.; Young, Peter

doi:10.1159/000103611

Cited by 43 publications

(14 citation statements)

References 49 publications

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“…Intermittent hypoxemia also has been shown in mice models to induce the hepatic enzyme, stearoyl coenzyme desaturase, leading to dyslipidemia and atherosclerotic lesions (24). The potential importance of OSA in increasing stroke risk through atherogenic pathways is consistent with the reported higher prevalence of internal carotid artery atherosclerotic lesions in stroke patients with compared with those without OSA (25). Carotid ultrasonography also has demonstrated that severity of OSA correlates with increased degrees of intimal medial thickness, a marker of subclinical atherosclerosis (26,27).…”

Section: Discussionmentioning

confidence: 65%

Obstructive Sleep Apnea–Hypopnea and Incident Stroke

Redline¹,

Yenokyan

Gottlieb³

et al. 2010

Am J Respir Crit Care Med

1,119

494

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Rationale: Although obstructive sleep apnea is associated with physiological perturbations that increase risk of hypertension and are proatherogenic, it is uncertain whether sleep apnea is associated with increased stroke risk in the general population. Objectives: To quantify the incidence of ischemic stroke with sleep apnea in a community-based sample of men and women across a wide range of sleep apnea. Methods: Baseline polysomnography was performed between 1995 and 1998 in a longitudinal cohort study. The primary exposure was the obstructive apnea-hypopnea index (OAHI) and outcome was incident ischemic stroke. Measurements and Main Results: A total of 5,422 participants without a history of stroke at the baseline examination and untreated for sleep apnea were followed for a median of 8.7 years. One hundred ninety-three ischemic strokes were observed. In covariate-adjusted Cox proportional hazard models, a significant positive association between ischemic stroke and OAHI was observed in men (P value for linear trend: P 5 0.016). Men in the highest OAHI quartile (.19) had an adjusted hazard ratio of 2.86 (95% confidence interval, 1.1-7.4). In the mild to moderate range (OAHI, 5-25), each one-unit increase in OAHI in men was estimated to increase stroke risk by 6% (95% confidence interval, 2-10%). In women, stroke was not significantly associated with OAHI quartiles, but increased risk was observed at an OAHI greater than 25. Conclusions: The strong adjusted association between ischemic stroke and OAHI in community-dwelling men with mild to moderate sleep apnea suggests that this is an appropriate target for future stroke prevention trials.Keywords: sleep apnea; stroke; epidemiology Approximately 15.3 million strokes occur annually worldwide, and about one-third of these are fatal (1). Stroke is not only the second leading cause of death globally, but it also accounts for significant disability, institutionalization, and health care costs (2). Because stroke rates increase exponentially with advancing age, the public health importance of strokes is likely to increase as the population ages. The risk of stroke is particularly high in African Americans, American Indians, and elderly women (2). Numerous studies have identified risk factors for stroke, including hypertension, atrial fibrillation, diabetes, and smoking (2-5). Even after considering these well-recognized risk factors, there is substantial variation in stroke rates and stroke-related outcomes.Emerging data implicate obstructive sleep apnea (OSA) in the pathogenesis of risk factors associated with ischemic stroke (i.e., hypertension, coronary heart disease, diabetes, and atrial fibrillation) (6). These associations are believed to be mediated by adverse physiological responses to recurrent periods of pharyngeal occlusion and consequent oxyhemoglobin desaturation-resaturation. These responses result in free radical generation, release of proinflammatory and prothrombotic mediators, and surges in sympathetic nervous system activity and blood pressure. Th...

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Section: Discussionmentioning

confidence: 65%

Obstructive Sleep Apnea–Hypopnea and Incident Stroke

Redline¹,

Yenokyan

Gottlieb³

et al. 2010

Am J Respir Crit Care Med

1,119

494

View full text Add to dashboard Cite

show abstract

“…Sleep fragmentation, sleep deprivation, and so-called intermittent hypoxia (IH),which is defined as repetitive short cycles of desaturation followed by rapid reoxygenation, have been proposed to play a significant role in the initiation of the inflammatory process in OSAS [21,25,26]. There is also strong evidence that OSAS has some association with the development of atherosclerosis, coronary heart disease, and other cardiovascular diseases via the promotion of inflammation [4,27,28].…”

Section: Discussionmentioning

confidence: 99%

Red Cell Distribution Width in Patients with Obstructive Sleep Apnea Syndrome

Özsu

Abul

Gülsoy

et al. 2012

Lung

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“…There is evidence that SA may even have a negative effect on the early course of vascular diseases and also on the functional outcome several months after brain infarction [6,7,8]. It was shown before that SA is an independent risk factor for atherosclerotic artery disease [9,10]. The exact pathophysiological link between SA and stroke remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Biomarkers of Inflammation and Endothelial Dysfunction in Stroke with and without Sleep Apnea

et al. 2012

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Objective: Although sleep apnea (SA) is a risk factor for ischemic stroke and an important prognostic factor in affected patients, the exact pathophysiological link between SA and stroke is unknown. We investigated whether the plasma concentration of biomarkers of inflammation and endothelial dysfunction, including soluble tumor necrosis factor receptor-1 and -2 (sTNF-R1 and sTNF-R2), tumor necrosis factor-β (TNF-β), soluble intercellular cell adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) are increased in patients with acute stroke and SA compared with stroke patients without SA. Design/Methods: In total, 76 patients with ischemic stroke admitted to the stroke unit were included in this study. Plasma concentrations of biomarkers were determined after CT scans on admission. All patients received cardiorespiratory polygraphy within the first 72 h after admission. In all patients, demographic data, National Institutes of Health Stroke Scale scores and cerebrovascular risk factors were assessed. Results: An apnea-hypopnea index (AHI) ≥10/h was found in 37 of our patients (48.7%). In these patients with SA, sTNF-R1 and sTNF-R2 levels were significantly higher than in patients with an AHI lower than 10/h. TNF-β, however, showed no significant difference between both groups, just like the soluble intercellular and vascular cell adhesion molecules sICAM-1 and sVCAM-1. Conclusions/Relevance: SA is associated with raised levels of sTNF-R1 and sTNF-R2 in patients with acute ischemic stroke. Taking into account the established impact of these two markers on the causation and course of cerebrovascular disease, these proteins may be part of the pathophysiological pathway linking SA to stroke.

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Atherosclerosis and Obstructive Sleep Apnea in Patients with Ischemic Stroke

Cited by 43 publications

References 49 publications

Obstructive Sleep Apnea–Hypopnea and Incident Stroke

Obstructive Sleep Apnea–Hypopnea and Incident Stroke

Red Cell Distribution Width in Patients with Obstructive Sleep Apnea Syndrome

Biomarkers of Inflammation and Endothelial Dysfunction in Stroke with and without Sleep Apnea

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