Pre-existing Obstructive Sleep Apnoea Research Articles

Gestational intermittent hypoxia induces endothelial dysfunction, reduces perivascular adiponectin and causes epigenetic changes in adult male offspring.

Obstructive sleep apnoea (OSA) is characterized by intermittent hypoxia, which causes oxidative stress and inflammation and increases the risk of cardiovascular disease. OSA during pregnancy causes adverse maternal and fetal outcomes. The effects of pre-existing OSA in pregnant women on cardiometabolic outcomes in the offspring are unknown. We evaluated basic metabolic parameters, as well as aortic vascular and perivascular adipose tissue (PVAT) function in response to adiponectin, and examined DNA methylation of adiponectin gene promoter in PVAT in 16-week-old adult offspring exposed to gestational intermittent hypoxia (GIH). GIH decreased body weights at week 1 in both male and female offspring, and caused subsequent increases in body weight and food consumption in male offspring only. Adult female offspring had normal levels of lipids, glucose and insulin, with no endothelial dysfunction. Adult male offspring exhibited dyslipidaemia, insulin resistance and hyperleptinaemia. Decreased endothelial-dependent vasodilatation, loss of anti-contractile activity of PVAT and low circulating PVAT adiponectin levels, as well as increased pro-inflammatory gene expression and DNA methylation of adiponectin gene promoter, occurred in adult male offspring. Our results suggest that male offspring of women with OSA could be at risk of developing cardiometabolic disease during adulthood. Perturbations during pregnancy can program the offspring to develop cardiometabolic diseases later in life. Obstructive sleep apnoea (OSA) is a chronic condition that frequently affects pregnancies and leads to adverse fetal outcomes. We assessed the offspring of female mice experiencing gestational intermittent hypoxia (GIH), a hallmark of OSA, for changes in metabolic profiles, aortic nitric oxide (NO)-dependent relaxations, perivascular adipose tissue (PVAT) anti-contractile activities and the responses to adiponectin, and DNA methylation of the adiponectin gene promoter in PVAT tissue. Pregnant mouse dams were exposed to intermittent hypoxic cycles ( 21-12%) for 18 days. GIH resulted in lower body weights of pups at week 1, followed by significant weight gain by week 16 of age in male but not female offspring. Plasma lipids, leptin and insulin resistance were higher in GIH male adult offspring. Endothelium-dependent relaxation in response to ACh and the anti-contractile activity of PVAT in the abdominal aorta was reduced in GIH adult male offspring. Incubation of arteries from GIH adult male offspring with adiponectin restored the anti-contractile activity of PVAT. Both circulating and PVAT tissue homogenate levels of adiponectin, as well as gene expression of adiponectin in PVAT, were lower in GIH male offspring, along with an increased gene expression of inflammatory cytokines. Pyrosequencing of adiponectin gene promoter in PVAT showed increased DNA methylation in GIH male offspring. Our results indicate that GIH leads to vascular disease in adult male offspring through PVAT dysfunction, which was associated with low adiponectin levels and epigenetic modifications on the adiponectin gene promoter.

Proportion of Surgical Patients With Undiagnosed Obstructive Sleep Apnoea

Editor's key points † Obstructive sleep apnoea (OSA) is associated with perioperative morbidity but is under-diagnosed in the community. † In this study of Canadian surgical patients, both anaesthetists and surgeons often failed to diagnose OSA. † Preoperative diagnosis Background. Obstructive sleep apnoea (OSA) affects � 9-24% of the general population, and 90% remain undiagnosed. Those patients with undiagnosed moderate-to-severe OSA may be associated with an increased risk of perioperative complications. Our objective was to evaluate the proportion of surgical patients with undiagnosed moderate-to-severe OSA. Methods. After research ethics board approval, patients visiting preoperative clinics were recruited over 4 yr and screened with the STOP-BANG questionnaire. The 1085 patients, who consented, subsequently underwent polysomnography (PSG) (laboratory or portable) before operation. Chart review was conducted in this historical cohort to ascertain the clinical diagnosis of OSA by surgeons and anaesthetists, blinded to the PSG results. The PSG study-identified OSA patients were further classified based on severity using the apnoea- hypopnoea index (AHI) cut-offs. Results. Of 819 patients, 111 patients had pre-existing OSA and 58% (64/111) were not diagnosed by the surgeons and 15% (17/111) were not diagnosed by the anaesthetists. Among the 708 study patients, PSG showed that 233 (31%) had no OSA, 218 (31%) patients had mild OSA (AHI: 5- 15); 148 (21%) had moderate OSA (AHI: 15 -30), and 119 (17%) had severe OSA (AHI.30). Before operation, of the 267 patients with moderate- to-severe OSA, 92% (n¼245) and 60% (n¼159) were not diagnosed by the surgeons and the anaesthetists, respectively. Conclusions. We found that anaesthetists and surgeons failed to identify a significant number of patients with pre-existing OSA and symptomatic undiagnosed OSA, before operation. This study may provide an impetus for more diligent case finding of OSA before operation.

Proportion of surgical patients with undiagnosed obstructive sleep apnoea

Obstructive sleep apnoea (OSA) affects ~9-24% of the general population, and 90% remain undiagnosed. Those patients with undiagnosed moderate-to-severe OSA may be associated with an increased risk of perioperative complications. Our objective was to evaluate the proportion of surgical patients with undiagnosed moderate-to-severe OSA. After research ethics board approval, patients visiting preoperative clinics were recruited over 4 yr and screened with the STOP-BANG questionnaire. The 1085 patients, who consented, subsequently underwent polysomnography (PSG) (laboratory or portable) before operation. Chart review was conducted in this historical cohort to ascertain the clinical diagnosis of OSA by surgeons and anaesthetists, blinded to the PSG results. The PSG study-identified OSA patients were further classified based on severity using the apnoea-hypopnoea index (AHI) cut-offs. Of 819 patients, 111 patients had pre-existing OSA and 58% (64/111) were not diagnosed by the surgeons and 15% (17/111) were not diagnosed by the anaesthetists. Among the 708 study patients, PSG showed that 233 (31%) had no OSA, 218 (31%) patients had mild OSA (AHI: 5-15); 148 (21%) had moderate OSA (AHI: 15-30), and 119 (17%) had severe OSA (AHI>30). Before operation, of the 267 patients with moderate-to-severe OSA, 92% (n=245) and 60% (n=159) were not diagnosed by the surgeons and the anaesthetists, respectively. We found that anaesthetists and surgeons failed to identify a significant number of patients with pre-existing OSA and symptomatic undiagnosed OSA, before operation. This study may provide an impetus for more diligent case finding of OSA before operation.

Can obstructive sleep apnoea be a complication of uvulopalatopharyngoplasty?

Polysomnography is currently used for diagnosis, evaluation and selection of therapy in patients with obstructive sleep apnoea (OSA), but clinically successful uvulopalatopharyngoplasty (UPPP) is not necessarily reflected by post-operative improvement of polysomnographic recordings. Post-operative polysomnography may suggest deterioration of pre-existing OSA or, in snorers, de-novo precipitation of OSA. Thus, if polysomnography is a reliable indicator of OSA, then OSA may be a post-operative risk of UPPP. (i) to assess the possible deleterious effect of UPPP on sleep patterns; (ii) to further define the role of cardioisotope scanning in the evaluation of OSA; (iii) to assess the reliability of polysomnography given the clinical and cardiosotope scan findings. Symptoms, polysomnography and radionuclide ventriculography were prospectively compared pre- and post-operatively in 41 patients undergoing UPPP. In 12 patients (29 per cent), there were disparate results between pre- or post-operative polysomnography and the clinical and/or radionuclide ventriculography, as follows: In four of 16 patients with abnormal pre-operative ventricular performance, there was pre-operative symptomatology of severe OSA and a bedmate's reports of apnoeic episodes. This was in contrast to normal or near normal sleep apnoea recordings. In eight patients, post-operative improvement of symptoms was reported, despite deterioration of post-operative polysomnographic recordings. In these patients the post-operative improvement of symptoms was also reflected by improved ventricular performance. Worsening of ventricular performance was not demonstrated in any patient. In conclusion, UPPP does not induce OSA. Polysomnography may underestimate or even misdiagnose cases of OSA.(ABSTRACT TRUNCATED AT 250 WORDS)