ABSTRACT
BACKGROUND: No therapy has been shown to reduce the risk of major adverse cardiovascular events (MACE) and death in patients with obstructive sleep apnea (OSA). OBJECTIVES: To investigate the long-term relationship between metabolic surgery and incident MACE in patients with OSA and obesity. METHODS: Adult patients with BMI 35-70 kg/m2 and moderate-to-severe OSA at a US health system (2004-2018) were identified. Baseline characteristics of patients who underwent metabolic surgery were balanced with a nonsurgical control group using overlap weighting methods. Multivariable Cox regression analysis estimated time-to-incident MACE. Follow-up ended in September 2022. RESULTS: 13,657 patients (7496 [54.9%] men; mean age, 52.0 years [SD 12.4]; median BMI, 41.0 [IQR, 37.6-46.2]), including 970 patients in the metabolic surgery group and 12,687 patients in the nonsurgical group, with a median follow-up of 5.3 years (IQR, 3.1-8.4 years) were analyzed. The mean between-group difference in body weight at 10 years was 26.6 kg (95% CI, 25.6-27.6) or 19.3% (95% CI, 18.6%-19.9%). The 10-year cumulative incidence of MACE was 27.0% (95% CI, 21.6%-32.0%) in the metabolic surgery group and 35.6% (95% CI, 33.8%-37.4%) in the nonsurgical group (adjusted HR, 0.58 [95% CI, 0.48-0.71], P < .001). The 10-year cumulative incidence of all-cause mortality was 9.1% (95% CI, 5.7%-12.4%) in the metabolic surgery group and 12.5% (95% CI, 11.2%-13.8%) in the nonsurgical group (adjusted HR, 0.63 [95% CI, 0.45-0.89], P = .009). CONCLUSIONS: Among patients with moderate-to-severe OSA and obesity, metabolic surgery, compared with nonsurgical management, was associated with a significantly lower risk of incident MACE and death.
ABSTRACT
Background We leverage a large clinical cohort to elucidate sleep-disordered breathing and sleep-related hypoxia in incident atrial fibrillation (AF) development given the yet unclear contributions of sleep-related hypoxia and pulmonary physiology in sleep-disordered breathing and AF. Methods and Results Patients who underwent sleep studies at Cleveland Clinic January 2, 2000, to December 30, 2015, comprised this retrospective cohort. Cox proportional hazards models were used to examine apnea hypopnea index, percentage time oxygen saturation <90%, minimum and mean oxygen saturation, and maximum end-tidal carbon dioxide on incident AF adjusted for age, sex, race, body mass index, cardiopulmonary disease and risk factors, antiarrhythmic medications, and positive airway pressure. Those with spirometry were additionally adjusted for forced expiratory volume in 1 second, forced vital capacity, and forced expiratory volume in 1 second/forced vital capacity. This cohort (n=42 057) was 50.7±14.1 years, 51.3% men, 74.1% White individuals, had median body mass index 33.2 kg/m2, and 1947 (4.6%) developed AF over 5 years. A 10-unit apnea hypopnea index increase was associated with 2% higher AF risk (hazard ratio [HR], 1.02 [95% CI, 1.00-1.03]). A 10-unit increase in percentage time oxygen saturation <90% and 10-unit decreases in mean and minimum oxygen saturation were associated with 6% (HR, 1.06 [95% CI, 1.04-1.08]), 30% (HR, 1.30 [95% CI, 1.18-1.42]), and 9% (HR, 1.09 [95% CI, 1.03-1.15]) higher AF risk, respectively. After adjustment for spirometry (n=9683 with available data), only hypoxia remained significantly associated with incident AF, although all coefficients were stable. Conclusions Sleep-related hypoxia was associated with incident AF in this clinical cohort, consistent across 3 measures of hypoxia, persistent after adjustment for pulmonary physiologic impairment. Findings identify a strong role for sleep-related hypoxia in AF development without pulmonary physiologic interdependence.
ABSTRACT
Sleep dysfunction has been identified in the pathophysiology of Alzheimer's disease (AD); however, the role and mechanism of circadian rhythm dysfunction is less well understood. In a well-characterized cohort of patients with AD at the mild cognitive impairment stage (MCI-AD), we identify that circadian rhythm irregularities were accompanied by altered humoral immune responses detected in both the cerebrospinal fluid and plasma as well as alterations of cerebrospinal fluid biomarkers of neurodegeneration. On the other hand, sleep disruption was more so associated with abnormalities in circulating markers of immunity and inflammation and decrements in cognition.
