Background: Individuals with obstructive sleep apnoea (OSA) are at increased risk of cognitive impairment. However, the physiological mechanisms that link OSA to this impairment are unclear. We assessed the association between novel physiological biomarkers (i.e. respiratory event-related electroencephalography (EEG) activity and autonomic responses) and the risk of cognitive impairment.
Methods: Participants with OSA (apnoea-hypopnoea index ≥5 events·h-1) from the Canadian Sleep and Circadian Network observational cohort were studied. Brain Response to Event (BReTE) was derived from EEG power (defined as mean (median post-event power/median pre-event power) (frequency range: 0.5-50 Hz)) for each individual. Event-related autonomic responses were measured by heart rate response to events (ΔHR: the difference between maximum post-event heart rate and minimum heart rate during event) and photoplethysmography (PPG)-derived vasoconstriction activity (event-related area and depth of PPG decline). Cognitive performance was assessed using the Montreal Cognitive Assessment (MoCA), Wechsler Digit Symbol Coding (DSC) and Rey Auditory Verbal Learning Test-Delayed Recall (RAVLT-DR). Multiple logistic regression examined the independent associations between biomarkers and outcomes.
Results: We studied 537 individuals (42% female) with a median age of 55 years. In fully adjusted models, each 1sd decrease in BReTE was associated with higher odds of poor cognitive performance indicated by MoCA <26 (OR 1.42, 95% CI 1.13-1.79; p=0.003), DSC <25th percentile (OR 1.35, 95% CI 1.02-1.84; p=0.04) and RAVLT-DR <25th percentile (OR 1.50, 95% CI 1.13-2.02; p=0.007). Additionally, those with low ΔHR compared to the mid-range group were at increased risk of poor cognitive performance. Vasoconstriction indices were not associated with cognitive performance.
Conclusion: Blunted EEG and heart rate responses to respiratory events are linked to poorer cognitive performance in OSA, highlighting the value of EEG in identifying individuals at risk for cognitive impairment.
Background: Interstitial lung abnormalities (ILA) share common risk factors with coronary heart disease (CHD), including increased age and cigarette smoking; however, the relationship between ILA and CHD has not been well described.
Methods: Participants from the Genetic Epidemiology of Chronic Obstructive Pulmonary Disease study (COPDGene) and Age Gene/Environment Susceptibility (AGES)-Reykjavik studies with ILA assessment, clinical CHD and coronary artery calcium (CAC) data were included. In both cohorts, CHD was defined by clinical history and additionally by CAC >100. Multivariable logistic regression assessed the relationship between ILA and CHD; Cox proportional hazards models were used to assess mortality associated with ILA and CHD.
Results: 9% of participants with CHD had ILA in both COPDGene and AGES-Reykjavik. Participants with ILA had increased odds of CHD defined by clinical history in COPDGene (OR 1.6, 95% CI 1.2-2.0; p<0.001) and AGES-Reykjavik (OR 1.6, 95% CI 1.2-2.0; p<0.001); similar results were seen with CAC >100. In both COPDGene and AGES-Reykjavik, participants with both CHD and ILA had a greater risk of death compared to those with CHD but without ILA (HR 2.0, 95% CI 1.4-2.7; p<0.001; and HR 1.3, 95% CI 1.1-1.4; p<0.001, respectively). In AGES-Reykjavik, ILA was associated with an over 9-fold increase in the odds of a respiratory death (OR 9.6, 95% CI 3.2-29.0; p<0.0001) among participants with CHD.
Conclusion: ILA are a common co-occurrence with CHD and associated with worse mortality, suggesting that ILA are a clinically important comorbidity in patients with CHD.
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：