Abstract
BackgroundObstructive sleep apnoea and the related intermittent hypoxia (IH) are widely recognised as risk factors for incident cardiovascular diseases. Numerous studies support the deleterious vascular impact of IH in rodents but an overall interpretation is challenging owing to heterogeneity in rodent species investigated and the severity and duration of IH exposure. To clarify this major issue, we conducted a systematic review and meta-analysis to quantify the impact of IH on systemic artery structure and function depending on the different IH exposure designs.
Methods我们搜索PubMed、Embase和网络科学、和included 125 articles in a meta-analysis, among them 112 using wild-type rodents and 13 using apolipoprotein E knockout (ApoE−/−) mice. We used the standardised mean difference (SMD) to compare results between studies.
ResultsIH significantly increased mean arterial pressure (+13.90 (95% CI 11.88–15.92) mmHg), and systolic and diastolic blood pressure. Meta-regressions showed that mean arterial pressure change was associated with strain and year of publication. IH altered vasodilation in males but not in females and increased endothelin-1-induced but not phenylephrine-induced vasoconstriction. Intima–media thickness significantly increased upon IH exposure (SMD 1.10 (95% CI 0.58–1.62); absolute values +5.23 (2.81–7.84) µm). This increase was observed in mice but not in rats and was negatively associated with age. Finally, IH increased atherosclerotic plaque size in ApoE−/−mice (SMD 1.08 (95% CI 0.80–1.37)).
ConclusionsOur meta-analysis established that IH, independently of other confounders, has a strong effect on vascular structure and physiology. Our findings support the interest of identifying and treating sleep apnoea in routine cardiology practice.
Abstract
This meta-analysis of rodent studies firmly establishes that intermittent hypoxia (IH), as a model of obstructive sleep apnoea, alters vascular pressure, remodelling and reactivity. Severity of IH and rodent characteristics contribute to this impact.https://bit.ly/3fm45fB
Footnotes
This article has an editorial commentary:https://doi.org/10.1183/13993003.02438-2021
Conflict of interest: O. Harki has nothing to disclose.
Conflict of interest: Q. Boete has nothing to disclose.
Conflict of interest: J-L. Pépin has nothing to disclose.
Conflict of interest: C Arnaud has nothing to disclose.
Conflict of interest: E. Belaidi has nothing to disclose.
Conflict of interest: G. Faury has nothing to disclose.
Conflict of interest: C. Khouri has nothing to disclose.
Conflict of interest: A. Briançon-Marjollet has nothing to disclose.
Support statement: This work was supported by the Fondation du Souffle/Fondation pour la Recherch en Santé Respiratoire (PhD fellowship for O. Harki), Fondation de l'Avenir, Fondation Agir Pour les Maladies Chroniques and ANR Arterylastic grant ANR-18-CE-18-0001 (PhD fellowship for Q. Boete). Funding information for this article has been deposited with theCrossref Funder Registry.
- ReceivedMarch 23, 2021.
- AcceptedJuly 25, 2021.
- Copyright ©The authors 2022. For reproduction rights and permissions contactpermissions{at}ersnet.org