0370 Short Sleep Duration Modifies the Association of Obstructive Sleep Apnea and Insomnia Symptoms with Biomarkers

Abstract Introduction Co-morbid insomnia and obstructive sleep apnea (COMISA) have been shown to be associated with higher risk of cardiovascular disease than its individual components. Insomnia with objective short sleep duration (ISSD) has been associated with adverse cardiometabolic impact i.e., hypertension or diabetes. The aim of this study is to examine whether objective short sleep duration modifies the effect on clinical (hypertension) and preclinical inflammatory and metabolic biomarkers in patients with mild-to moderate OSA (mmOSA) and insomnia symptoms. Methods A clinical sample of 164 adults (52.76±13.08 years old) with mmOSA (5 ≤ AHI 30) underwent polysomnography or home sleep testing, measures of blood pressure (BP), body mass index (BMI), fasting blood glucose, insulin, CRP and IL-6 plasma levels, and completed Epworth Sleepiness Scale (ESS) and Pittsburg Sleep Quality Index (PSQI). Presence of EDS was defined as ESS score ≥ 11. Insomnia symptoms were defined as a self-report of more than 3 nights/week over the past 4 weeks of at least one of the following symptoms in the PSQI: “Cannot get to sleep within 30 minutes” or “Wake up in the middle of the night or early morning”. Objective short sleep duration was defined as 6.8-hours sleep based on the median total sleep time. Participants were classified into 4 clinically meaningful groups: asymptomatic mmOSA (control group), mmOSA with EDS, mmOSA with insomnia symptoms and objective short sleep duration (COMISA-SSD) and mmOSA with insomnia symptoms and objective normal sleep duration (COMISA-NSD). Univariate general linear models were conducted controlling for age, gender and BMI. Results Mean average systolic and diastolic BP were elevated in COMISA-SSD group compared to COMISA-NSD group (p=.042, p=.055, respectively). Plasma lnCRP and lnIL-6 concentrations were significantly elevated in COMISA-SSD group compared to control group (p=.010, p=0.014 respectively). Also, lnHOMA and insulin resistance (lnGlucose/insulin ratio) were significantly increased in COMISA-SSD group compared to COMISA-NSD group (p=.031, p=.046, respectively). Conclusion These findings show that the additive adverse cardiometabolic effects of COMISA phenotype are primarily driven by the insomnia short sleep duration phenotype, which appears to respond better to medication than psychological interventions. Support (if any)