Usefulness of home sleep apnea tests in heart failure patients

Obstructive sleep-disordered breathing and cancer: mechanism of association

Utility of home sleep apnea testing devices in patients with cardiac conditions—critical manual interpretation of the raw data is important

Does coffee consumption impact sleep-disordered breathing?

Finding a needle in the haystack—narcolepsy and obstructive sleep apnea

Pharmaceuticals are back in the Game for OSA Treatment

In memoriam Christian Guilleminault (1938–2019)

The reduction of apnea–hypopnea duration ameliorates endothelial dysfunction, vascular inflammation, and systemic hypertension in a rat model of obstructive sleep apnea Abstract Purpose We aimed to investigate the effect of obstructive sleep apnea (OSA) and apnea–hypopnea duration on endothelial, ventricular function, blood pressure, and inflammation in a rat model. Methods We established a novel rat model of OSA. Wistar rats were randomized to six groups according to 4-week different treatments: (1) OSA (apnea for 60 s in a 90-s window of breathing [60 s/90 s] with anesthesia), (2) OSA 30 s/90 s with anesthesia, (3) partial recovery (60 s/90 s for 2 weeks, followed by 15 s/90 s for 2 weeks with anesthesia), (4) complete recovery (60 s/90 s for 2 weeks with anesthesia, and then normal breathing for 2 weeks), (5) sham (normal breathing in the device with anesthesia), and (6) control group (normal breathing, normal cage, no anesthesia). We recorded blood pressure, endothelial function, left ventricular function, and inflammation at different time points. Results Vascular inflammation and endothelial dysfunction occurred in OSA models. More systemic inflammatory and endothelial dysfunction were observed in longer apnea–hypopnea duration group and they were reversed in both partial and complete recovery groups. Left ventricular weight/body weight ratio was significantly higher in the OSA (60s/90s) group than complete recovery, sham, and control groups, which remained unchanged in partial recovery group (p < 0.05). Conclusions Longer apnea–hypopnea duration is related to more systemic inflammatory and endothelial dysfunction, and hypertension and cardiac remodeling. These can be reversed after a period of recovery, which indicates that time parameters for assessing OSA, such as apnea–hypopnea duration, should be considered instead of apnea–hypopnea index only.

Maternal chronic intermittent hypoxia in rats causes early atherosclerosis with increased expression of Caveolin-1 in offspring Abstract Objective The objective of our research was to explore the effects of maternal and postpartum chronic intermittent hypoxia (CIH) exposure on atherosclerosis in adulthood offspring of rats, and the role of Caveolin-1 in the course. Methods Sixteen rats were assigned to two groups (n = 8), maternal normoxia and CIH group. After delivery, two male pups per litter were selected and breastfed for 1 month, which then randomly received postpartum normoxia or CIH. Thus, 4 groups were created as follows (n = 8): (1) maternal normoxia and postpartum normoxia group, (2) maternal CIH and postpartum normoxia group, (3) maternal CIH and postpartum CIH group, and (4) maternal normoxia and postpartum CIH group. The offspring were weighed at birth and weaning. After the duration of 12-week experiment, morphological changes, the expression of Caveolin-1 and NF-κB p65 in the aorta were detected. Results Maternal CIH resulted in significantly lower body weight and thicker intima (P < 0.001). CIH upregulated the expression of Caveolin-1 and NF-κB p65 significantly (P < 0.01). There was a synergistic effect of maternal and postpartum CIH on the thickening of intima (P < 0.05), also on the expression of Caveolin-1 and NF-κB p65 (P < 0.01). Conclusions The results demonstrate that maternal CIH exposure causes a postpartum catch-up growth and early atherosclerotic changes followed by upregulating Caveolin-1 expression. Besides, maternal CIH enhances the atherosclerotic changes caused by postpartum CIH. Oxidative stress probably implicates in above effects.

Polysomnographic features of low arousal threshold in overlap syndrome involving obstructive sleep apnea and chronic obstructive pulmonary disease Abstract Purpose In patients with overlap syndrome (OVS), the pathophysiologies of obstructive sleep apnea (OSA) and chronic obstructive pulmonary disease can interact with one another. Focusing on low arousal threshold, the authors evaluated polysomnographic features of OVS patients. Methods This retrospective, multicenter study was conducted at three hospitals in Japan. Patients aged ≥ 60 years who underwent polysomnography and pulmonary function testing were reviewed. Severity of airflow limitation (AFL) was classified according to the Global Initiative for Chronic Obstructive Lung Disease criteria. Low arousal threshold was predicted based on the following polysomnography features: lower apnea-hypopnea index (AHI); higher nadir oxygen saturation, and larger hypopnea fraction of total respiratory events. These features were compared among patients with only OSA (n = 126), OVS with mild AFL (n = 16), and OVS with moderate/severe AFL (n = 22). Results A low arousal threshold was more frequently exhibited by OVS patients with moderate/severe AFL than by those with OSA only (p = 0.016) and OVS with mild AFL (p = 0.026). As forced expiratory volume in 1 s/forced vital capacity (FEV1/FVC) decreased in OVS patients, the mean length of apnea decreased (r = 0.388, p = 0.016), hypopnea fractions increased (r = − 0.337, p = 0.039), and AHI decreased (r = 0.424, p = 0.008). FEV1/FVC contributed to low arousal threshold independent of age, sex, smoking history, hospital, or body mass index in all subjects (OR 0.946 [95% CI 0.909–0.984]) and in OVS patients (OR 0.799 [95% CI 0.679–0.940]). Conclusions This study first described peculiar polysomnographic features in OVS patients with moderate/severe AFL, suggesting a high prevalence of low arousal threshold.