Abstract
Introduction: Poor sleep is a risk factor for cardiovascular disease and all-cause mortality; however, the mechanisms underlying this relationship remain poorly understood. Since sleep health is a complex construct extending beyond mere sleep duration, we aimed to examine the relationship between granular sleep health indicators and arterial stiffness. Methods: We analyzed Framingham Offspring cohort (Exam 9) and OMNI cohort 1 (Exam 4) participants with sleep study and applanation tonometry data (n= 847, 56.6% females). Participants wore an M1 device to obtain ECG-derived sleep spectrograms to assess sleep quality and the Nonin WristOx device for oximetry data over two consecutive nights. Sleep variables of interest included total sleep time, duration of stable and unstable NREM, duration of elevated low-frequency coupling (e-LFC), and duration and number of nocturnal hypoxia events. Measures of aortic stiffness and pressure pulsatility included carotid-femoral pulse wave velocity (PWV), and central pulse pressure (CPP). Results: Characteristics of the sample are presented in Table 1. Several sleep measures were associated with PWV in univariable analysis, but significance attenuated after age/sex adjustment (Table 2). After adjusting for cardiovascular risk factors and sociodemographics, duration of e-LFCnb remained associated with CPP (β = 0.036, p = 0.02) Conclusion: Sleep measures associated with aortic stiffness are closely tied to age and sex. Longer duration of e-LFCnb, a hallmark of carotid body-driven elevated sympathetic tone and periodic breathing, is associated with greater pressure pulsatility. Longitudinal studies are needed to fully elucidate the role of e-LFCnb in vascular health
Published Version
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