Dataset Information

Intermittent hypoxia by obstructive sleep apnea is significantly associated with electro-anatomical remodeling of the left atrium preceding structural remodeling in patients with atrial fibrillation.

ABSTRACT:

Background

Obstructive sleep apnea (OSA) is one of the risk factors for atrial fibrillation (AF). However, the mechanism underlying the atrial structural and electro-anatomical remodeling by OSA has not yet been clearly elucidated.

Methods

This study was conducted in 83 patients who had undergone catheter ablation for AF (49 with OSA and 34 Controls without OSA). The left atrial (LA) maps were created in all the patients using a three-dimensional electro-anatomical mapping system. The LA with a bipolar voltage of <0.5 mV was defined as the low voltage area (LVA); %LVA was defined as the ratio of the LVA to the total surface area of the LA.

Results

The LVA and %LVA were significantly greater in the OSA group as compared with the Control group, however, there was no difference in the LA area. The 3 % oxygen desaturation index (ODI) was significantly correlated with the %LVA (r = 0.268, P = 0.014), but not with the LA area. Multiple regression analysis with adjustments identified 3 %ODI ≥30 (3.088, 1.078-8.851, P = 0.036) as being significantly associated with the %LVA.

Conclusions

In patients with AF complicated by OSA, significant increase of the LVA, but not of the LA area, was observed. The intermittent hypoxia severity was significantly associated with the LVA. These results suggest that intermittent hypoxia by OSA might be one of the mechanisms of electro-anatomical remodeling of the LA, possibly preceding structural remodeling represented by LA enlargement, in patients with AF.

SUBMITTER: Takada Y

PROVIDER: S-EPMC11372619 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature

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Publications

Intermittent hypoxia by obstructive sleep apnea is significantly associated with electro-anatomical remodeling of the left atrium preceding structural remodeling in patients with atrial fibrillation.

Takada Yasuyuki Y Shiina Kazuki K Orihara Shunichiro S Takata Yoshifumi Y Takahashi Takamichi T Kani Junya J Kusume Takahiro T Terasawa Muryo M Nakano Hiroki H Saitoh Yukio Y Yazaki Yoshinao Y Tomiyama Hirofumi H Chikamori Taishiro T Satomi Kazuhiro K

International journal of cardiology. Heart & vasculature 20240813

<h4>Background</h4>Obstructive sleep apnea (OSA) is one of the risk factors for atrial fibrillation (AF). However, the mechanism underlying the atrial structural and electro-anatomical remodeling by OSA has not yet been clearly elucidated.<h4>Methods</h4>This study was conducted in 83 patients who had undergone catheter ablation for AF (49 with OSA and 34 Controls without OSA). The left atrial (LA) maps were created in all the patients using a three-dimensional electro-anatomical mapping system. ...[more]

PMID: 39234287

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Project description:Obstructive sleep apnea syndrome (OSAS) is a significant risk factor for left atrial (LA) remodeling. Intermittent hypoxemia occurs during the sleep cycle in patients with OSAS and plays a crucial role in cardiovascular pathologies such as stroke, arrhythmia, and coronary artery disease. However, there is very little information about the role of intermittent hypoxemia in LA remodeling in patients with OSAS. In total, 154 patients with sleep-related breathing disorders (SRBD) were prospectively recruited for this study. All enrolled SRBD patients underwent polysomnography and echocardiography. Significant OSAS was defined as an oxygen desaturation index (ODI) of ≥10 per hour. Intermittent hypoxia/reoxygenation (IHR) stimulation was used to test the effect of hypoxia on the viability, reactive oxygen species, apoptosis, and inflammation-associated cytokine expression in the HL-1 cell line. To investigate the effect of patients' exosomes on HIF-1 and inflammation-associated cytokine expression, as well as the relationship between ODI and their expression, exosomes were purified from the plasma of 95 patients with SRBD and incubated in HL-1 cells. The LA size was larger in patients with significant OSAS than in those without. There was a significant association between ODI, lowest SpO2, mean SpO2, and LA size (all p < 0.05) but not between the apnea-hypopnea index and LA size. IHR condition caused increased LDH activity, reactive oxygen species (ROS) levels, and apoptosis in HL-1 cells and decreased cellular viability (all p < 0.05). The expression of HIF-1α, TNF-α, IL-6, and TGF-β increased in the IHR condition compared with the control (all p < 0.05). The expression of HIF-1α, IL-1β, and IL-6 increased in the HL-1 cells incubated with exosomes from those patients with significant OSAS than those without (all p < 0.05). There was a significantly positive correlation between ODI and the expression of HIF-1α, TNF-α, IL-1β, IL-6, and TGF-β; a significantly negative correlation between mean SpO2 and IL-6 and TGF-β; and a significantly negative correlation between the lowest SpO2 and HIF-1α (all p < 0.05). In conclusion, intermittent hypoxemia was strongly associated with LA remodeling, which might be through increased ROS levels, LDH activity, apoptosis, and the expression of HIF-1α and inflammation-associated cytokines.

Project description:Obstructive sleep apnea (OSA) is a common disorder characterized by episodic obstruction to breathing due to upper airway collapse during sleep. Because of the episodic airway obstruction, intermittently low O2 (hypoxia) and high CO2 (hypercapnia) ensue. OSA has been associated with adverse cardiovascular and metabolic outcomes, although data regarding potential causal pathways are still evolving. As changes in inspired O2 and CO2 can affect the ecology of the gut microbiota and the microbiota has been shown to contribute to various cardiometabolic disorders, we hypothesized that OSA alters the gut ecosystem, which, in turn, exacerbates the downstream physiological consequences. Here, we model human OSA and its cardiovascular consequence using Ldlr-/- mice fed a high-fat diet and exposed to intermittent hypoxia and hypercapnia (IHH). The gut microbiome and metabolome were characterized longitudinally (using 16S rRNA amplicon sequencing and untargeted liquid chromatography-tandem mass spectrometry [LC-MS/MS]) and seen to covary during IHH. Joint analysis of microbiome and metabolome data revealed marked compositional changes in both microbial (>10%, most remarkably in Clostridia) and molecular (>22%) species in the gut. Moreover, molecules that altered in abundance included microbe-dependent bile acids, enterolignans, and fatty acids, highlighting the impact of IHH on host-commensal organism cometabolism in the gut. Thus, we present the first evidence that IHH perturbs the gut microbiome functionally, setting the stage for understanding its involvement in cardiometabolic disorders. IMPORTANCE Intestinal dysbiosis mediates various cardiovascular diseases comorbid with OSA. To understand the role of dysbiosis in cardiovascular and metabolic disease caused by OSA, we systematically study the effect of intermittent hypoxic/hypercapnic stress (IHH, mimicking OSA) on gut microbes in an animal model. We take advantage of a longitudinal study design and paired omics to investigate the microbial and molecular dynamics in the gut to ascertain the contribution of microbes on intestinal metabolism in IHH. We observe microbe-dependent changes in the gut metabolome that will guide future research on unrecognized mechanistic links between gut microbes and comorbidities of OSA. Additionally, we highlight novel and noninvasive biomarkers for OSA-linked cardiovascular and metabolic disorders.

Dataset Information

Intermittent hypoxia by obstructive sleep apnea is significantly associated with electro-anatomical remodeling of the left atrium preceding structural remodeling in patients with atrial fibrillation.

Background

Methods

Results

Conclusions

Publications

Intermittent hypoxia by obstructive sleep apnea is significantly associated with electro-anatomical remodeling of the left atrium preceding structural remodeling in patients with atrial fibrillation.

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