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.