Objective To investigate the effect of angiopoietin-like protein 3 (ANGPTL3) on lipid metabolism in patients with obstructive sleep apnea (OSA). Methods A total of 59 OSA patients and 20 healthy controls from the First Affiliated Hospital of Zhengzhou University between May 2023 and February 2024 were included in the study. All participants underwent overnight polysomnography (PSG). Based on the apnea-hypopnea index (AHI), the OSA patients were divided into a mild group and a moderate-to-severe group. Morning blood samples were collected after an 8-hour fast to measure lipid profiles and ANGPTL3 levels. Statistical analyses were performed using SPSS 25.0 software. Results The levels of total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and ANGPTL3 were significantly higher, while high-density lipoprotein cholesterol (HDL-C) was significantly lower in the OSA group compared with the control group (P<0.05). ANGPTL3 level was higher in the moderate-to-severe OSA group than that in the mild OSA group and the control group, and higher in the mild OSA group than that in the control group (P<0.05). In the severe hypoxemia group, ANGPTL3 level was significantly higher than that in the mild-to-moderate hypoxemia group (P<0.05). The ANGPTL3 level was also significantly higher in the hyperlipidemia group compared wiht the non-hyperlipidemia group (P<0.05). In the OSA group, ANGPTL3 was positively correlated with TC, TG, percentage of cumulative time with oxygen saturation below 90% in total sleep time (T90) and oxygen desaturation index (ODI), and negatively correlated with lowest arterial oxygen saturation (LSaO2) and mean arterial oxygen saturation (MSaO2). After adjusting for relevant confounding factors, logistic regression analysis indicated that ANGPTL3 might be a potential independent risk factor for OSA, with an odds ratio of 1.021 (95%CI 1.002 - 1.040). Conclusions The level of ANGPTL3 is elevated in OSA patients. The elevation of blood lipid levels in OSA patients may be associated with chronic intermittent hypoxia-induced regulation of ANGPTL3 levels.
Objective To study the correlation between smoking and obstructive sleep apnea (OSA). Methods A total of 454 patients from October 2015 to July 2021 were retrospectively collected for nocturnal polysomnography monitoring (no less than 7 hours). The patients were divided into an OSA group (n=405) and a control group (n=49, patients with primary snoring) according to the results of polysomnography monitoring. According to the apnea hypopnea index (AHI) and the lowest oxygen saturation during sleep, the severity of OSA was classified into a mild to moderate group (5 times/h ≤ AHI<30 times/h) and a severe group (AHI ≥30 times/h). The patients were inquired about their smoking history, then the patients diagnosed with OSA were further divided into a smoking group, a smoking cessation group, and a non-smoking group based on their smoking history. Results The smoking rate of the patients in the OSA group was higher than that in the control group (50.9% vs. 32.7%, P<0.05), while the smoking rate in the severe OSA group was higher than that in the mild to moderate group (55.7% vs. 39.8%, P<0.05). Smoking was positively correlated with AHI, cumulative percentages of time spent at oxygen saturation below 90% (Ts90%), and total apnea time (r value was 0.196, 0.197, 0.163, P<0.05), while negatively correlated with the lowest and average SpO2 during sleep (r value was –0.202, –0.214, P<0.05). The logistic regression analysis with severe OSA as the outcome variable showed that smoking (OR=1.781) and obesity (OR=1.930) were independent risk factors of severe OSA (P<0.05). The comparison between groups of the OSA patients with different smoking states showed that the proportion of severe OSA, AHI, Ts90%, and total apnea time (77.8%, 53.55 times/h, 18.35%, and 111.70 minutes, respectively) of the smoking group were higher than those of the non-smoking group (62.8%, 40.20 times/h, 8.40%, and 76.20 minutes, respectively, P<0.05). The lowest SpO2 and average SpO2 during sleep (69.50%, 93.00%, respectively) of the smoking group were lower than those of the non-smoking group (75.00%, 94.00%, respectively, both P<0.05). The average SpO2 of the smoking cessation group was higher than that of the smoking group (94.00% vs. 93.00%, P<0.05), and the Ts90% of the smoking cessation group was lower than that of the smoking group (6.75% vs. 18.35%, P<0.05). Conclusions Smoking significantly affects the degree of sleep-disordered breathing and may be an independent risk factor for severe OSA. Smoking can exacerbate the severity of OSA and the degree of hypoxia, while smoking cessation can improve the degree of hypoxia in OSA patients.