Chronic intermittent hypoxia and obstructive sleep apnea: an experimental and clinical approach

Sforza, Émilia; Roche, Frédéric

doi:10.2147/hp.s103091

Cited by 109 publications

(94 citation statements)

References 116 publications

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“…Another potential explanation for the survival benefit of OSA is “ischemic preconditioning” through chronic intermittent hypoxia, which is characteristic of OSA . This is a process by which repeated episodes of sublethal ischemia confer protection from infarction, arrhythmias, and further ischemic insults .…”

Section: Discussionmentioning

confidence: 99%

Recognized Obstructive Sleep Apnea is Associated With Improved In‐Hospital Outcomes After ST Elevation Myocardial Infarction

Mohananey

Villablanca

Gupta

et al. 2017

JAHA

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BackgroundObstructive sleep apnea (OSA) is an independent risk factor for many cardiovascular conditions such as coronary artery disease, myocardial infarction, systemic hypertension, pulmonary hypertension, and stroke. However, the association of OSA with outcomes in patients hospitalized for ST‐elevation myocardial infarction remains controversial.Methods and ResultsWe used the nation‐wide inpatient sample between 2003 and 2011 to identify patients with a primary discharge diagnosis of ST‐elevation myocardial infarction and then used the International Classification of Diseases, Clinical Modification code 327.23 to identify a group of patients with OSA. The primary outcome of interest was in‐hospital mortality, and secondary outcomes were in‐hospital cardiac arrest, length of stay and hospital charges. Our cohort included 1 850 625 patients with ST‐elevation myocardial infarction, of which 1.3% (24 623) had documented OSA. OSA patients were younger and more likely to be male, smokers, and have chronic pulmonary disease, depression, hypertension, known history of coronary artery disease, dyslipidemia, obesity, and renal failure (P<0.001 for all). Patients with OSA had significantly decreased in‐hospital mortality (adjusted odds ratio, 0.78 [95% CI, 0.73–0.84]), longer hospital stay (5.00±4.68 versus 4.85±5.96 days), and incurred greater hospital charges ($79 460.12±70 621.91 versus $62 889.91±69 124.15). There was no difference in incidence of in‐hospital cardiac arrest (adjusted odds ratio, 0.93 [95% CI, 0.84–1.03]) between these 2 groups.Conclusion ST‐elevation myocardial infarction patients with recognized OSA had significantly decreased mortality compared with patients without OSA. Although patients with OSA had longer hospital stays and incurred greater hospital charges, there was no difference in incidence of in‐hospital cardiac arrest.

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Section: Discussionmentioning

confidence: 99%

Recognized Obstructive Sleep Apnea is Associated With Improved In‐Hospital Outcomes After ST Elevation Myocardial Infarction

Mohananey

Villablanca

Gupta

et al. 2017

JAHA

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“…[16][17][18][19] OSA leads to intermittent oxygen desaturation which causes oxidative stress that further leads to cardiovascular (hypertension), metabolic (diabetes, insulin resistance, dyslipidemia, and obesity), and neurocognitive complications (impaired memory, attention, and executive dysfunction). 20 Sleep fragmentation is another possible mechanism responsible for cardiovascular, metabolic, and neurocognitive complications. 21,22 There are few studies reporting the effect of continuous positive airway pressure (CPAP) therapy on the recurrence of vascular events in stabilized patients with stroke.…”

Section: Introductionmentioning

confidence: 99%

Role of Positive Airway Pressure Therapy for Obstructive Sleep Apnea in Patients With Stroke: A Randomized Controlled Trial

Gupta

Shukla

Mohammed

et al. 2018

Journal of Clinical Sleep Medicine

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Study Objectives: Obstructive sleep apnea (OSA) is an independent risk factor for stroke. The objective of this study was to assess the effect of continuous positive airway pressure (CPAP) treatment on prevention of new vascular events among patients with stroke and OSA. Methods: Consecutive conscious patients presenting with first imaging-confirmed arterial stroke were included, 6 weeks or more after ictus. All patients underwent clinical and polysomnography (PSG) testing. Patients with an apnea-hypopnea index (AHI) of > 15 events/h were randomized to posttitration nightly CPAP treatment and non-CPAP (received best medical treatment) groups. On follow-up at 3, 6, and 12 months from randomization, evaluation was carried out for any new vascular events as the primary outcome measure, and for clinical stroke outcomes (using the Barthel Index and modified Rankin scale) and neuropsychological parameters as the secondary outcome measures. Results: Among the 679 patients with stroke who were screened, 116 reported for PSG, 83 had AHI > 15 events/h, and 70 (34 in CPAP and 36 in non-CPAP) were randomized. Thirteen patients could not be randomized because of a lack of CPAP devices. Four patients crossed over from the CPAP to the non-CPAP group. Age (mean age 53.41 ± 9.85 in CPAP versus 52.69 ± 13.23 years in non-CPAP, P = .81) and sex distribution (24 males in CPAP versus 33 males in non-CPAP, P = .79) were similar in both groups. At 12-month follow-up, there was 1 vascular event (3.33%) in the CPAP group and 6 events (15%) in the non-CPAP group (P = .23). Modified Rankin scale score improvement by ≥ 1 at 12-month follow-up was found in significantly more patients in the CPAP group than in the non-CPAP group (53% versus 27%). I NTRO DUCTI O NStroke is common, the second leading cause of death and disability, and is the cause of high health care costs.1,2 Important risk factors for stroke are hypertension, atrial fibrillation, diabetes, and smoking. These are well-established intervention targets for stroke's primary and secondary prevention. that leads to oxygen desaturation and sleep fragmentation. This further leads to an increased risk of cardiovascular disease, stroke, and death. [4][5][6] It has been established that OSA is an independent risk factor for stroke 1,7 and also aggravates other risk factors (hypertension, coronary artery disease, diabetes, and atrial fibrillation).1 The prevalence of OSA among patients with stroke is around 50% to 80%. Even with neurological improvement in patients with stroke, their OSA does not remit or improve. [8][9][10] The high prevalence of OSA among patients with stroke is associated with an unfavorable clinical course in terms of early neurological worsening, delirium, BRIEF SUMMARY Current Knowledge/Study Rationale: Stroke is a common cause of death and disability and obstructive sleep apnea (OSA) is an independent risk factor for stroke. The objective of this study was to assess the effect of continuous positive airway pressure (CPAP) treatment in prevention of new vascular ...

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“…The most commonly used experimental IH protocol is the introduction of low O 2 by rapid delivery of a hypoxic mixture to an airtight chamber followed by flushing with normoxic RA. Reducing the ambient chamber oxygen to 5-10% results in an SaO 2 of 60-80%(23). IH exposure is given during daytime when rodents generally sleep.…”

mentioning

confidence: 99%

Intermittent Hypoxia and Hypercapnia Accelerate Atherosclerosis, Partially via Trimethylamine-Oxide

Xue¹,

Zhou²,

Poulsen³

et al. 2017

Am J Respir Cell Mol Biol

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Obstructive sleep apnea (OSA) is a common disorder characterized by intermittent hypoxia and hypercapnia (IHC) during sleep. OSA has been shown to be a risk factor for atherosclerosis, but the relation of IHC to the induction or progression of atherosclerosis is not well understood. To dissect the mechanisms involved, we compared atherosclerotic lesion formation in two mouse models, i.e., apolipoprotein E (ApoE) and low density lipoprotein receptor (Ldlr)-deficient mice, with or without IHC exposure. Ten-week-old ApoE or Ldlr mice were fed a high-fat diet for 4 or 8 weeks while being exposed to IHC for 10 hours/day or room air (RA) for 24 hours/day. En face lesions of the aorta, aortic arch, and pulmonary artery (PA) were examined. Moreover, 3,3-dimethyl-1-butanol (DMB), an inhibitor of microbial trimethylamine (TMA) production, was used to determine the contribution of TMA-oxide (TMAO) to IHC-induced atherosclerosis. Eight weeks of IHC exposure expedited the formation of atherosclerosis in both the PA and aortic arch of ApoE mice, but only in the PA of Ldlr mice (ApoE PA 8 wk, IHC 35.4 ± 1.9% versus RA 8.0 ± 2.8%, P < 0.01). The atherosclerotic lesions evolved faster and to a more severe extent in ApoE mice as compared with Ldlr mice (PA IHC 8 wk, ApoE 35.4 ± 1.9% versus Ldlr 8.2 ± 1.5%, P < 0.01). DMB significantly attenuated but did not totally eliminate IHC-induced PA atherosclerosis. Our findings suggest that IHC, a hallmark of OSA, accelerates the progression of atherosclerosis in the aorta and especially in the PA. This process is partly inhibited by DMB, demonstrating that microbial metabolites may serve as therapeutic targets for OSA-induced atherosclerosis.

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Chronic intermittent hypoxia and obstructive sleep apnea: an experimental and clinical approach

Cited by 109 publications

References 116 publications

Recognized Obstructive Sleep Apnea is Associated With Improved In‐Hospital Outcomes After ST Elevation Myocardial Infarction

Recognized Obstructive Sleep Apnea is Associated With Improved In‐Hospital Outcomes After ST Elevation Myocardial Infarction

Role of Positive Airway Pressure Therapy for Obstructive Sleep Apnea in Patients With Stroke: A Randomized Controlled Trial

Intermittent Hypoxia and Hypercapnia Accelerate Atherosclerosis, Partially via Trimethylamine-Oxide

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