Hasthi U. Dissanayake

Purpose: In light of the reported association between REM-related obstructive sleep apnoea (OSA) and heightened cardiovascular risk, this study aims to compare cardiac autonomic function in patients with REM-OSA and OSA independent of sleep stage. We hypothesized that REM-OSA patients would exhibit higher sympathetic cardiac modulation based on heart rate variability (HRV) profiles. Methods: HRV was compared between the OSA group (AHI ≥ 5 events/h, n = 252) and the REM-OSA group (AHI ≥ 5 events/h, AHIREM:AHINREM ≥ 2, n = 137). Time- and frequency-domain measures of HRV were analysed during N2 and REM sleep. Results: Clinical characteristics between the two test groups differed significantly, 45% of REM-OSA patients were female, with mild OSA (median, interquartile range (IQR)) AHI of 10 (7) events/h. Only 26% of the OSA cohort were female with moderate OSA (AHI = 17 (20) events/h, p < 0.001). Compared with the OSA group, the low frequency to high frequency ratio (LF:HF) and LF power were lower and HF power was higher in the REM-OSA group during N2 (LF:HF, p = 0.012; LF; p = 0.013; HF, p = 0.007) and in REM sleep (LF:HF, p = 0.002; LF, p = 0.004; HF, p < 0.001). Patient sex and OSA severity had a significant combined effect on average N to N interval, LF power, and LF:HF ratio during N2 and REM sleep (all p < 0.001). Conclusion: Contrary to our hypothesis, REM-OSA patients demonstrated consistently higher cardiac vagal modulation, reflecting better cardiac autonomic adaptation. These results were attributed to differences in OSA severity and sex in these two groups, both independently affecting HRV. This study emphasises the need for future research into the underlying pathophysiology of REM-OSA and the potential implications of sex and OSA severity on cardiovascular risk.

Recent studies suggest that sleepy patients with obstructive sleep apnea (OSA) are at higher risk for incident cardiovascular disease. This study assessed cardiac autonomic function in sleepy versus non-sleepy patients with OSA using heart rate variability (HRV) analysis. We hypothesized that HRV profiles of sleepy patients would indicate higher cardiovascular risk. Electrocardiograms (ECG) derived from polysomnograms (PSG) collected by the Sydney Sleep Biobank were used to study HRV in groups of sleepy (ESS ≥ 10) and non-sleepy OSA patients (ESS < 10). HRV parameters were averaged across available ECG signals during N2 sleep. A total of 421 patients were evaluated, with a mean age of 54 (14) years, body mass index of 33 (9) kg/m², apnea–hypopnea index of 21 (28) events/h, and 66% male. The sleepy group consisted of 119 patients and the non-sleepy group 302 patients. Sleepy patients exhibited lower HRV values for: root mean square successive difference (RMSSD, p = 0.028), total power (TP, p = 0.031), absolute low frequency (LF, p = 0.045), and high-frequency (HF, p = 0.010) power compared to non-sleepy patients. Sleepy patients with moderate-to-severe OSA exhibited lower HRV values for: (RMSSD, p = 0.045; TP, p = 0.052), absolute LF (p = 0.051), and HF power (p = 0.025). There were no differences in other time and frequency domain HRV markers. This study shows a trend toward parasympathetic withdrawal in sleepy OSA patients, particularly in moderate-to-severe cases, lending mechanistic support to the link between the sleepy phenotype and CVD risk in OSA.

Purpose: This study aimed to evaluate the effect of mandibular advancement splint (MAS) therapy on cardiac autonomic function in patients with obstructive sleep apnoea (OSA) using heart rate variability (HRV) analysis. Methods: Electrocardiograms (ECG) derived from polysomnograms (PSG) of three prospective studies were used to study HRV of patients with OSA before and after MAS treatment. HRV parameters were averaged across the entire ECG signal during N2 sleep using 2-min epochs shifted by 30 s. Paired t-tests were used to compare PSG and HRV measures before and after treatment, and the percent change in HRV measures was regressed on the percent change in apnoea-hypopnea index (AHI). Results: In 101 patients with OSA, 72% were Caucasian, 54% men, the mean age was 56 ± 11 years, BMI 29.8 ± 5.3 kg/m², and treatment duration was 4.0 ± 3.2 months. After MAS therapy, there was a significant reduction in OSA severity (AHI, − 18 ± 16 events per hour, p < 0.001) and trends towards increased low-frequency to high-frequency ratio, low-frequency power, and reduced high-frequency power (LF:HF, − 0.4 ± 1.5, p = 0.01; LF, − 3 ± 16 nu, p = 0.02, HF, 3.5 ± 13.7 nu, p = 0.01). Change in NN intervals correlated with the change in AHI (β(SE) = − 2.21 (0.01), t = − 2.85, p = 0.005). No significant changes were observed in the time-domain HRV markers with MAS treatment. Conclusion: The study findings suggest that successful MAS treatment correlates with changes in HRV, specifically the lengthening of NN intervals, a marker for improved cardiac autonomic adaptability.

Autonomic function is impaired in obstructive sleep apnea (OSA) and may mediate the association between OSA and cardiovascular risk. We investigated the effect of OSA therapy on autonomic function through a systematic review and meta-analysis of intervention studies. A systematic search using three databases (Medline, Embase, and Scopus) was performed up to December 9, 2020. Studies of OSA patients ≥ 18 years with autonomic function assessed before and after treatment with positive airway pressure, oral appliance, positional therapy, weight loss, or surgical intervention were included for review. Random effects meta-analysis was carried out for five groups of autonomic function indices. Risk of bias was assessed using the Cochrane Collaboration tool. Forty-three eligible studies were reviewed with 39 included in the meta-analysis. OSA treatment led to large decreases in muscle sympathetic nerve activity (Hedges’ g = −1.08; 95% CI −1.50, −0.65, n = 8) and moderate decreases in catecholamines (−0.60; −0.94, −0.27, n = 3) and radio nucleotide imaging (−0.61; −0.99, −0.24, n = 2). OSA therapy had no significant effect on baroreflex function (Hedges’ g = 0.15; 95% CI −0.09, 0.39, n = 6) or heart rate variability (0.02; −0.32, 0.36, n = 14). There was a significant risk of bias due to studies being primarily non-randomized trials. OSA therapy selectively improves autonomic function measures. The strongest evidence for the effect of OSA therapy on autonomic function was seen in reduced sympathetic activity as assessed by microneurography, but without increased improvement in parasympathetic function. OSA therapy may reduce the risk of cardiovascular disease in OSA through reduced sympathetic activity.

Physiological studies have demonstrated the importance of the autonomic nervous system in mediating acute apnoea-induced atrial fibrillation (AF). We aimed to compare Heart Rate Variability (HRV) markers of autonomic function in paroxysmal atrial fibrillation (PAF) patients with and without obstructive sleep apnoea (OSA). A secondary aim was the analysis of ectopic beats in these groups. Nocturnal ECG traces from 89 PAF patients who underwent in-laboratory polysomnography were included. After identifying ectopic beats in the ECGs, periods of arrhythmia as well as sleep apnoea events were excluded. HRV time and frequency domains were reported by sleep stage (REM vs Non-REM) for patients with and without OSA. Frequency domain analysis of HRV during non-REM sleep in PAF patients with OSA showed increased cardiac parasympathetic modulation (HF-nu: 39.13 ± 15.74 vs 47.98 ± 14.60, p = 0.008*) and reduced cardiac sympathetic modulation (LF/HF ratio: 2.05 ± 2.02 vs 1.17 ± 0.98, p = 0.007*). Results remained significant after adjusting for age, sex and BMI (adjusted p values 0.024 and 0.018 respectively). PAF patients with severe OSA (AHI ≥ 30/hr) had more AF beats and Ventricular Ectopic Beats than those without severe OSA (22.7 ± 42.8% vs 3.7 ± 17.9%, p = 0.006*, 1.7 ± 3.8 vs 0.3 ± 0.9%, p = 0.004* respectively). This is the first study of HRV in AF patients with and without OSA. It suggests a chronic increase in parasympathetic nervous modulation and relative reduction in sympathetic modulation in PAF patients with OSA.

Food production greatly contributes to greenhouse gas emissions (GHG), but there remain concerns that consuming environmentally sustainable foods can increase the likelihood of nutritional deficiencies during pregnancy. We identified commonly consumed foods of pregnant women and determined the effect of their replacement with environmentally sustainable alternatives on nutrient intake and measures of environmental sustainability. Dietary intake data from 171 pregnant women was assessed and foods that contributed the most to energy and protein intake were identified. Of these, foods producing the highest GHG emissions were matched with proposed environmentally sustainable alternatives, and their impact on nutrient provision determined. Meats, grains, and dairy products were identified as important sources of energy and protein. With the highest GHG emissions, beef was selected as the reference food. Proposed alternatives included chicken, eggs, fish, tofu, legumes, and nuts. The most pronounced reductions in CO₂ emissions were from replacing beef with tofu, legumes, and nuts. Replacing one serve per week of beef with an isocaloric serve of firm tofu during pregnancy could reduce GHG emissions by 372 kg CO₂ eq and increase folate (+28.1 µg/serve) and fiber (+3.3 g/serve) intake without compromising iron (+1.1 mg/serve) intake. Small dietary substitutions with environmentally sustainable alternatives can substantially reduce environmental impact without compromising nutrient adequacy.

Evidence from animal models indicates that maternal diet during pregnancy affects offspring cardiometabolic health. Improving carbohydrate quality during high-risk pregnancies reduces aortic intima-medial thickness; a marker for early atherosclerosis; in the infant offspring. We sought to determine whether maternal carbohydrate quantity and quality are associated with newborn aortic intima-medial thickness in healthy pregnancies. Maternal diet throughout pregnancy was evaluated in 139 mother–child dyads using a validated food frequency questionnaire. Carbohydrate intake was expressed as quantity (% total energy), quality (fibre, glycaemic index), and glycaemic burden (glycaemic load). Aortic intima-medial thickness was measured by high-frequency ultrasound of the neonatal abdominal aorta. Neither quantity nor quality of maternal carbohydrate intake during pregnancy was associated with meaningful differences in offspring maximum aortic intima-medial thickness with the exception of fibre intake in women with overweight or obesity which was inversely associated (−8 μm [95% CI −14, −1] per g fibre, p = 0.04). In healthy pregnancy, the quantity and quality of maternal carbohydrate intake is likely not a meaningful modifiable lifestyle factor for influencing offspring vascular health. The effect of carbohydrate quality may only be evident in high-risk pregnancies, consistent with previous findings. These findings may be confirmed in prospective dietary trials in pregnancy.