Physiological Sleep and Cardiovascular Disease : When the Physiological Rhythms Are Mismatch

It is a consensus in literature that sleep is an important modulator of several physiological functions (e.g., cardiovascular, respiratory, and neurobiological function). In fact, a complex and dynamic rhythmic process involving the activation of several cortical, subcortical, and medullar neural circuits mutually interact in order to synchronize the physiological functions with sleep cycles. During physiological sleep regulation, heart rate and blood pressure lower during NREM sleep cycle, with marked increase during REM sleep cycle. In this process, autonomic nervous system has a pivotal role in the hemodynamic regulation sleepmediated. In fact, several evidences show that the vagal modulation is predominant during NREM sleep cycle while that during REM sleep cycle occur a prevalence of sympathetic modulation. Thus, due to interaction between sympathetic and parasympathetic oscillations, the hemodynamic fluctuations express the effect of the autonomic cardiovascular modulation in each sleep cycle. On the other hand, a growing body of evidences has revealed that chronic sleep deficiency promoted mainly by sleep-disordered breathing (i.e., obstructive sleep apnea) is highly prevalent in patients with cardiovascular diseases. Through a variety of factors including nocturnal hypoxemia and increased oxidative stress, production of pro-inflammatory cytokines, and autonomic and endothelial dysfunctions, a significant overlap among pathophysiology mechanisms of these two conditions has been reported. Therefore, in this chapter we will address the impact of chronic sleep deficiency promoted by obstructive sleep apnea on the cardiovascular system with focus on the autonomic nervous system.