[Frontiers in Bioscience E4, 2007-2021, January 1, 2012]

Sleep deprivation, sleep apnea and cardiovascular diseases

Levy Patrick1,2,3, Tamisier Renaud1,2,3, Arnaud Claire1,2, Monneret Denis1,2,4, Baguet Jean-Philippe3, Stanke-Labesque Francoise 1,2,4, Dematteis Maurice1,2, Godin-Ribuot Diane1,2, Ribuot Christophe1,2, Pepin Jean-Louis1,2,3

1Hypoxia PathoPhysiology (HP2) Laboratory, Joseph Fourier University, Grenoble, France, 2Inserm unit 1042, Grenoble, France,3EFCR, Locomotion, Rehabilitation and Physiology Department, Grenoble University Hospital, France, 4Cardiology Department, Grenoble University Hospital, France, Biology and Pathology Institute (IBP), Grenoble University Hospital, France

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. Sleep deprivation and cardiovascular outcomes
3.1. Scientific evidence
3.2. What are the mechanisms linking sleep duration and cardiovascular outcomes?
3.3. Sleep deprivation and metabolic dysregulation
4. Pathophysiology of Obstructive Sleep Apnea(OSA) and associated cardiovascular and metabolic consequences
4.1. Overall mechanisms
4.2. Oxidative stress and inflammation
5. OSA is a major cause of cardiovascular and metabolic morbidity
5.1. Overall mechanisms
5.2. Clinical data.
5.2.1. Hypertension
5.2.2. Atherosclerosis
5.2.3. Arrhythmias and stroke
5.2.4. Heart Failure, systolic and diastolic dysfunction
5.2.5. Cardiovascular mortality
5.2.6. Metabolic changes
6. Conclusions
7. References

1. ABSTRACT

Sleep dramatically influences cardiovascular regulation. Changes in sleep duration or quality as seen in sleep disorders may prevent blood pressure to fall during sleep as expected in human physiology. This supports the increased prevalence of hypertension and drug-resistant hypertension in those with sleep loss. Other cardiovascular outcomes i.e. coronary lesions seem to be associated with sleep duration. Systemic inflammation, oxidative stress and endothelial dysfunction seem to be associated with both sleep loss and sleep disorders. The most critical example is Obstructive Sleep Apnea (OSA). Sympathetic activation, oxidative stress and systemic inflammation are the main intermediary mechanisms associated with sleep apnea and intermittent hypoxia. There are now convincing data regarding the associations between hypertension, arrhythmias, stroke, coronary heart disease, increased cardiovascular mortality and OSA. There are also data in OSA and in animal models supporting the link between sleep apnea and atherosclerosis and dysmetabolism. Whether treating sleep apnea enables the reversal of chronic cardiovascular and metabolic consequences of OSA, remains to be studied in adequately designed studies, particularly in comparison with usual treatment strategies.