“…Several studies have found relationships of short sleep duration, low sleep quality, and autonomic dysfunction with carotid intima-media thickness (IMT) and brachial-ankle pulse wave velocity (baPWV), which are major surrogate markers of atherosclerosis and established predictors of cardiovascular events [14,15]. We recently reported associations among sleep quality, autonomic nervous function, carotid IMT, baPWV, and nocturnal hypertension in subjects with risk factors for atherosclerosis who participated in the Hyogo Sleep Cardio-Autonomic Atherosclerosis (HSCAA) study [11,16,17,18]. The aim of this review was to summarize findings regarding the impact of sleep and autonomic nervous function on atherosclerosis, and elucidate their underlying mechanisms related to the progression of atherosclerosis.…”
Behavioral and psychosocial factors related to development of cardiovascular disease have been gaining increased attention. Notably, sleep is considered to be one of the most important behavioral factors involved in progression of atherosclerosis and cardiovascular events, with autonomic nervous function a potential mechanism. Several studies have shown associations of sleep and autonomic dysfunction with major surrogate markers of atherosclerosis, such as carotid intima-media thickness and arterial stiffness. Endocrinological, immunological, oxidative, inflammatory, and metabolic responses, as well as endothelial dysfunction may mediate the effects of the autonomic nervous system. For this review, we examined recent findings related to sleep, autonomic nervous dysfunction, and atherosclerosis, with the aim of understanding the involved pathophysiological mechanisms.
“…Several studies have found relationships of short sleep duration, low sleep quality, and autonomic dysfunction with carotid intima-media thickness (IMT) and brachial-ankle pulse wave velocity (baPWV), which are major surrogate markers of atherosclerosis and established predictors of cardiovascular events [14,15]. We recently reported associations among sleep quality, autonomic nervous function, carotid IMT, baPWV, and nocturnal hypertension in subjects with risk factors for atherosclerosis who participated in the Hyogo Sleep Cardio-Autonomic Atherosclerosis (HSCAA) study [11,16,17,18]. The aim of this review was to summarize findings regarding the impact of sleep and autonomic nervous function on atherosclerosis, and elucidate their underlying mechanisms related to the progression of atherosclerosis.…”
Behavioral and psychosocial factors related to development of cardiovascular disease have been gaining increased attention. Notably, sleep is considered to be one of the most important behavioral factors involved in progression of atherosclerosis and cardiovascular events, with autonomic nervous function a potential mechanism. Several studies have shown associations of sleep and autonomic dysfunction with major surrogate markers of atherosclerosis, such as carotid intima-media thickness and arterial stiffness. Endocrinological, immunological, oxidative, inflammatory, and metabolic responses, as well as endothelial dysfunction may mediate the effects of the autonomic nervous system. For this review, we examined recent findings related to sleep, autonomic nervous dysfunction, and atherosclerosis, with the aim of understanding the involved pathophysiological mechanisms.
“…However, only 73 subjects with poor sleep quality were included in the study; therefore, the power to identify the association was poor. Recently, the HSCAA cohort study [8], including 306 patients with cardiovascular risks, found that low sleep quality was associated with the progression of arterial stiffness over a 3-year follow-up period, the OR of which was (3.62; 95% CI: 1.04-12.55). However, no specific scientific discussions were available regarding this association among hypertensive patients in these findings.…”
Section: Discussionmentioning
confidence: 99%
“…Thus, there may be a link between sleep disturbances and arterial stiffness. In fact, several previous studies have investigated the association between abnormal sleep conditions and arterial stiffness, but they have reported inconsistent findings [5][6][7][8][9]. Therefore, the relationship between sleep conditions and arterial stiffness remains inconclusive.…”
The association between sleep conditions and arterial stiffness remains inconclusive. We aimed to investigate the relationship of sleep duration and quality with brachial-ankle pulse-wave velocity (baPWV) in hypertensive patients. A total of 14,485 hypertensive adults were included in this cross-sectional analysis. Information about sleep duration and quality was obtained via questionnaire. A baPWV level ≥1800 cm/s was defined as indicative of arterial stiffness. Compared with participants with a sleep duration <8 h per day, participants with a sleep duration ≥8 h per day had a significantly higher baPWV level (β = 13.7 cm/s; 95% CI: 3.9, 23.5) and a nonsignificantly higher prevalence of arterial stiffness (39.7% vs. 33.0%; OR, 1.08; 95% CI: 0.99-1.19). Similarly, compared with participants with good or medium sleep quality, participants with poor sleep quality had a significantly higher baPWV level (β = 16.3 cm/s; 95% CI: 0.1, 32.6) and a nonsignificantly greater prevalence of arterial stiffness (36.6% vs. 35.3%; OR, 1.13; 95% CI: 0.97-1.32). When sleep duration and quality were examined jointly, participants with a sleep duration ≥8 h and/or poor sleep quality had a significantly higher baPWV level (β = 14.4 cm/s; 95% CI: 5.3, 23.4) and a greater prevalence of arterial stiffness (38.8% vs. 32.7%; OR, 1.10; 95% CI: 1.01-1.20) than those with a sleep duration <8 h and good/medium sleep quality. In summary, among hypertensive patients, a longer sleep duration (≥8 h per day) and poor sleep quality were associated with higher baPWV levels and a higher prevalence of arterial stiffness.
“…Activity index as a parameter of sleep quality was calculated as total body motion during sleep time, with a higher activity index value considered to be related to lower sleep quality. Poor sleep quality (PSQ) was defined as an activity index value equal to or greater than 50, as previously described [ 37 , 38 ]. Physical activity (mean activity counts per minute of body motion during awake and sleep time), sleep/awake physical activity ratio (parameter for diurnal rhythm), total sleep time (total minutes as sleep), %sleep (percentage of sleeping time of total time lying in bed), sleep efficiency (percentage of time scored as sleep), and time awake after sleep onset (number of minutes noted as awake during sleep time) were also analyzed.…”
Rationale and purpose
Although sleep disorders are shown to be involved in occurrence of diabetes, impacts of several quantitative parameters related to sleep on insulin secretion and sensitivity is yet to be elucidated. We cross-sectionally examined relationships among quantitative sleep quality, sleep apnea, and autonomic function with insulin secretion and sensitivity in 399 patients without previous diagnosed diabetes who underwent 75-g oral glucose tolerance test (75gOGTT).
Method
Poor sleep quality (PSQ) was defined as an activity index ≥50 by actigraphy. Sleep apnea was measured by apnomonitor, while standard deviation of all normal-to-normal R-R intervals (SDNN) was measured by active tracer. Parameters of insulin secretion and sensitivity were measured by 75gOGTT.
Results
Patients with PSQ exhibited significantly lower insulinogenic index (r = 0.155, p < 0.01), a parameter of insulin secretion, with the association independent of other clinical factors including apnea and SDNN (β = −0.156, p < 0.01). In contrast, presence of sleep apnea (r = −0.143, p < 0.05) and the lower SDNN (r = −0.150, p < 0.01) were significantly and inversely associated with BIGTT-S, an insulin sensitivity parameter, with the association of SDNN with BIGTT-S remaining significant even after adjustments for PSQ and sleep apnea (β = −0.111, p < 0.05).
Conclusion
Poor sleep quality is an independent predictor of pancreatic β-cell function, which could be involved in occurrence of type 2 diabetes.
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