Abstract P198: Short Sleep Duration, Greater Cognitive Arousal, And Eveningness Are Associated With Reduced Left Ventricular Function In Insomnia Disorder

Abstract

Aim: Insomnia is associated with cardiovascular disease (CVD), particularly the phenotype with objective short sleep duration and associated physiological arousal. However, what objective sleep and arousal characteristics among patients with insomnia are related to markers of cardiovascular structure and function remains unknown. The present study examined the association of objective sleep metrics and self-reported arousability with arterial stiffness, endothelial function, and left ventricular function among patients with insomnia disorder. Methods: Sixteen young, healthy adults (age: M [ SD ]=30[7]; 56.3% women) meeting diagnostic criteria for insomnia disorder and reporting no history of CVD, underwent fasting vascular testing including carotid-femoral pulse wave velocity (cfPWV) to assess arterial stiffness (SphymocorXCEL TM ), brachial-artery flow mediated dilation (FMD) to assess endothelial function, and 2D echocardiography to assess left ventricular function (Terason uSmart 3300 TM ). Left ventricular function was assessed by ejection fraction (EF), global longitudinal strain (GLS), mitral valve E/e’ (MVE/e’), and lateral e’ using standardized methods. Ten participants wore a portable sleep monitor for 1 night (WatchPat200, Itamar Medical) and an actigraph for 8 nights (Actiwatch Spectrum Plus, Philips Respironics). All participants completed the Pre Sleep Arousal Scale (PSAS; somatic & cognitive subscales), and the Arousal Predisposition Scale (APS). Bivariate correlations and curvilinear regressions (total sleep time [TST] only) were conducted for the associations between actigraphy-assessed TST and WatchPat (WP) TST, actigraphy-assessed mean bedtime, and PSAS and APS scores with cardiovascular markers. Each set of one sleep metric with all six cardiovascular markers were Bonferroni corrected (α level: p <0.007). Results: On average, participants obtained 7h,9min of TST (range: 6h,26min - 8h,41min) and went to bed at 23:40 (range:21:47-2:13) via actigraphy, and slept 6h,51min via WP. Mean PSAS Somatic, PSAS Cognitive, and APS scores were 13.7(SD=4.5), 24.5(SD=7.5), and 27.9(SD=7.6), respectively. cfPWV (range:4.6-8.0), EF% (range:55.0-70.9), GLS% (range:-25- -19), and MVE/e’ (range:3.6-13.3) were all within age and sex normative ranges. Mean FMD was 7.8% (SD=2.6, range:4.4-14.6), and lateral e’ was 15 cm/s (SD=4.5, range:9-22). Correlations indicated that greater PSAS cognitive scores were related to worsening (less negative) GLS% ( r =0.77, p =0.001), later bedtimes were associated with lower lateral e’ ( r =-0.84, p =0.004), and shorter WPTST was associated with lower EF% (r=0.84, p=0 . 002). Conclusion: Among young adults with insomnia disorder, greater cognitive arousal, later bedtimes, and shorter objective total sleep time were associated with subclinical worsening of left ventricular strain, diastolic and systolic function.