Effect of Shift Work and Sleep Disorders

Multiple experts have advised that working in shift prompted circadian disruption by proceeding the body to work adversely to the physiological cycle, later affecting to cardiovascular events [21, 22]. A meta-analysis pointed that irregular sleep duration of fewer than seven hours or longer than eight hours was responsible to adult mortality. Decreased sleep duration is particularly correlated with congenital heart diseases and cardiovascular diseases [1]. Working in shift exhibits an individual to the light at an abnormal periods. Additionally, sleep disorders like obstructive sleep apnea, insomnia, and altered pattern or reduced sleep duration induces failure of synchronization among the body’s physiological circadian rhythm and functions. In turn, the condition heightens the risk of cardiovascular diseases [23, 24]. This circadian disruption induces floods of unnecessary hormones when they are not needed in that much concentration, and decreased concentration when they are most needed. The condition will further change stress response flexibility; eventually leading to excess glucocorticoid and incites its cognitive and metabolic consequences. These consequences raise the risk of cardiovascular diseases.
Moris et al. in 2016 condcuted an RCT which pointed that the circadian disruption evoke increased blood pressure and biomarkers for inflammatory states, such as interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrotic factor (TNF), having each as an independent cardiovascular diseases’ risk factor. These outcomes were enhanced along with prolonged duration of circadian disruption [6]. Rising blood pressure in circadian disruption occur in systolic and diastolic blood pressure [6]. A different multicenter study called SOLID-TIMI 52 trial, implemented long-term followups of 13,026 subject. The study reveals the connection within the causes of circadian disruption, such as various sleep disorders and working in shift, heightened the chance for cardiovascular disorders. Individually, each cause is an independent risk factor. Moreover, the consequence is magnified if an individual holds more than one risk factor [7]. In 2018, Jarrin et al. carried a study to re-evaluate the data from two earlier trials. They investigated the connection of two insomnia phenotypes, one with normal, conventional sleep duration and one with insufficient sleep duration, with outcomes affecting cardiovascular system. They discovered that insomnia with insufficient sleep duration decreased the activation of parasympathetic nervous system, eventually prompting sympathovagal imbalance [8]. The heart rate and its variation varied among individuals with normal sleep duration and individuals with less than six hours of sleep. The result was observed across shorter duration but not in longer period [8]. The outcomes are produced by weakened parasympathetic activity, leading to increased blood pressure and tachycardia; it further reduces insulin secretion and increases markers for inflammation, such as cytokines, having the definite alterations to portray circadian disruption. Weakened parasympathetic activity adds to the development of cardiovascular morbidity [25, 26]. Suppose shift work is blended with stressful circumstances. In that case, as was confirmed by Dutheil et al., the condition commences to more persistent and frequent tachycardia. They observed emergency physicians throughout a 14-hours shift and a 24-hours shift. The emergency physicians displayed recurrent tachycardia occurrences, reaching up to 180 beats per minute. The cardiac stress was experienced doubly on the shift day as opposed to the non-shift days [9].
Changes in body physiological functions tax an additional stress and worsen the disease prognosis in patients with previous history of cardiovascular events. A Japanese study by Kanno et al. investigated the impacts of insomnia on heart failure patients and exhibited that insomnia has the ability to worsen heart failure’s prognosis [10]. Insomniac patients expressed markedly elevated aldosterone (p=0.047) and renin concentrations (p=0.042) [10]. Likewise, insomniac and ST-elevation myocardial infarction (STEMI) patients found that melatonin decreased their anxiety and increased the quality of sleep compared to oxazepam, and also perceived to have a beneficial effect on cardiovascular health [12]. However, SLEPT trial confirmed that, despite increasing psychosocial health, sleep intervention did not improve the reading of systolic blood pressure in a short period (24 hours) [11]. Intervention therapies for sleep, such as Tai Chi Chih (TCC) or cognitive behavioral therapy (CBT), recorded improvement in cardiovascular hazard in a year, as confirmed in a research which assessed the impacts of sleep on markers, such as insulin, inflammatory markers, and lipid profile [13].

CONCLUSIONS

The circadian rhythm is accountable for a coordinated and well-ordered purposes of numerous functions in cardiovascular, immunological, and metabolic systems. Cyclical peaks and fluctuations control these functions, as well as numerous other hormonal and biological system. Working in shift and several sleep disorders, such as obstructive sleep apnea, insomnia, and reduced sleep contribute to the disposition of circadian disruption, which later raises the risk cardiovascular diseases. The effect can be immediately associated to melatonin or cortisol concentrations, or indirectly by its impacts on metabolic and immunological systems. If supplemented by stressful work circumstances as experienced by healthcare professionals, shift work can further increase the risk of cardiovascular diseases. Therefore, it is inferred that the cardiovascular disorders’ risk can be lessened by managing and treating the disorders which cause circadian disruption. While assessing the risk of cardiovascular diseases in patients, the possibility of treating the root cause for circadian disruption should perpetually be regarded.