Sleep and cardiovascular disease

Abstract

This review centres around the recent evidence in examining the intersection of sleep and cardiovascular disease (CVD). Sleep in this review will be further subdivided to consider both sleep quantity and quality along and will also consider some of the more common sleep disorders, such as insomnia and obstructive sleep apnoea, in the context of CVD. Sleep disorders have been further explored in several specific populations which are both at risk of sleep disorders and CVD. Secondly, the review will present some of the risk factors for CVD that are affected by sleep and sleep disorders which include hypertension, diabetes, and obesity. It will also examine the potential underlying mechanisms including inflammation, appetite control, endocrine, and genetic processes that are affected by sleep and sleep disorders leading to increased risk of CVD development. In addition, we will consider the observed bi-directional relationships between sleep and cardiovascular risk factors. For example, obesity, a risk factor for CVD can be affected by sleep, but in turn can increase the risk of certain sleep disorder development which disrupts sleep, leading to further risk of obesity development and increased CVD risk. Finally, the review will explore emerging evidence around lifestyle interventions that have included a sleep component and how it impacts the management of CVD risk factor. The need for increased awareness of the health effects of poor sleep and sleep disorders will be discussed alongside the need for policy intervention to improve sleep to facilitate better health and well-being.

The Role of Sleep in Cardiovascular Disease

“…Proper sleep, defined as 4–5 sleep cycles of light, deep, and rapid eye movement (REM) sleep, is essential to maintaining cardiometabolic homeostasis [ 6 ]. Disruptions in both sleep duration and quality have been implicated as risk factors for CVD [ 7 – 9 ]. This may be due to immune dysregulation, increased sympathetic tone, chronic endocrine stress response, and endothelial dysfunction [ 10 ].…”