Sleep, Autonomic Nervous Function and Atherosclerosis

Abstract

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.

Sleep and brain health

“…26 There is also some evidence linking sleep duration with cardiac arrhythmias. 32 Oxidative stress, systemic inflammation, and autonomic and endothelial dysfunction can play role. 27 It may be reasonable to hypothesize that habitual long sleep can reset the circadian pacemaker into a chrono-biological state, and neuro-cardio-electrophysiological excitability can alter conduction of cardiac impulses and predispose to alterations in hearth rhythm.…”

“…In the Physicians' Health Study, prolonged sleep time exceeding 8 hours was related to atrial fibrillation (AF). 32 In animal models, chronic sleep fragmentation was found to determine morphological changes of vessels, characterized by derangement of elastic fibers and recruitment of inflammatory cells. 28 Other studies provided indirect evidence of the potential relationship between sleep and AF: prolonged P-wave duration and P-wave dispersion and higher risk of atrial electro-mechanical delay have been reported in sleep deprived adults.…”

“…[29][30][31] Several studies demonstrated the nexus between short and long sleep with carotid intima-media thickness and brachial-ankle pulse wave velocity, which are surrogate indices of atherosclerosis and arterial stiffness and reliable markers of cardiovascular risk. 32,35 Notably, sleep loss and fragmentation result into blunted vasomotor reactivity of cerebral vessels and impaired cerebral hemodynamics that, in turn, predispose brain to damage. Short sleep and low sleep quality increases the levels of several cytokines like IL-1β, IL-6, and TNF-α and promotes a pro-inflammatory state.…”

“…Short sleep and low sleep quality increases the levels of several cytokines like IL-1β, IL-6, and TNF-α and promotes a pro-inflammatory state. 32 In animal models, chronic sleep fragmentation was found to determine morphological changes of vessels, characterized by derangement of elastic fibers and recruitment of inflammatory cells. 33 Platelet aggregation can contribute to mediate the effects of nervous dysautonomia on progression of atherosclerotic changes.…”

“…34 Autonomic dysfunction can also affect the release of neurotransmitters as norepinephrine, acetylcholine, and neuropeptide Y, which become diffusely distributed to smooth muscle and endothelial cells and take part in regulation of arterial tone. 32,35 Notably, sleep loss and fragmentation result into blunted vasomotor reactivity of cerebral vessels and impaired cerebral hemodynamics that, in turn, predispose brain to damage. [36][37][38]…”