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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 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.

Aim: Few studies have examined the association between objective sleep metrics and arterial and echocardiographic (left ventricular systolic/diastolic function) markers of sub-clinical cardiovascular disease (CVD). The present study examined the association of wrist actigraphy-assessed sleep metrics with arterial stiffness, endothelial dysfunction, and left ventricular systolic/diastolic function. Methods: Fifteen young, healthy adults (21-39y; 60% women) with no history of CVD, and no current sleep-disordered breathing (WatchPat200, Itamar Medical) or sleep complaints wore Actiwatch Spectrum Plus actigraphs for eight nights (Philips Respironics, Bend OR) with accompanying sleep logs. Participants underwent fasting vascular testing including central augmented aortic pressure (AP), 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%), left atrial volume index (LAVI), deceleration time (DT), and mitral valve E/e’ ratio (MVE/e’) using standardized methods. Bivariate correlations investigating the association between mean total sleep time (TST), sleep efficiency % (SE), sleep-onset latency (SOL), and wake after sleep time (WASO) with cardiovascular indices were conducted. Curvilinear regression models examining quadratic relationships between TST and the cardiovascular indices were conducted. Results: On average, participants obtained 6 hrs 44 min of TST (SD=29.1), with 86.0% SE (SD=3.1), 10.6 min SOL (SD=8.5), and 37.0 min WASO (SD=11.6). cfPWV (range: 4.8-7.5), EF% (range: 60.0-72.0), LAVI (range: 15.0-26.7 mL/m 2 ), and MVE/e’ (range: 3.2-7.8) were all within normal ranges according to age and sex normative standards. Mean FMD was 9.2% (SD=4.62, range: 4.3-19.8). Correlations indicated that greater SOL was associated with greater cfPWV (r=.63, p=0.01), and AP (r=.57, p=0.03). Lower SE (r= -.70, p=0.003) and higher WASO (r=.71, p=0.003) were associated with higher MVE/e’. WASO was associated with higher DT (r=.57, p=0.04). Curvilinear regression models revealed a quadratic relationship between TST and cfPWV (F[2,11]=9.78, p=0.004) such that shorter and longer TST were associated with greater cfPWV. No sleep metrics were associated with FMD, EF%, or LAVI. Conclusions: Among normal sleeping, apparently healthy young adults, with no history of CVD, lower levels of objective sleep quality and both shorter and longer sleep duration were associated with greater arterial stiffness, whereas only lower levels of objective sleep quality were related to worsening left ventricular diastolic dysfunction. These data may have implications for CVD risk reduction in young, healthy adults.