Title : Impact of rising stress and deteriorating Working conditions on Cardiovascular Risk of Medical professionals
Abstract:
The relationship between work-related stress and healthcare professionals' risk of developing Coronary
Heart Disease (CHD) is examined in this presentation. Numerous mechanisms, including persistent
overstimulation and dysregulation of the autonomic nervous system and the hypothalamic-pituitaryadrenal
(HPA) axis, are thought to play a role in how chronic work stress contributes to the development
of CHD. Such much stimulation may harm the body, causing CHD, infections, and an accelerated ageing
process. Additionally, by encouraging unhealthy behaviours, reduced likelihood to seek help and poor
adherence to medical treatments, work stress may indirectly increase the risk of CHD. Workplace strain,
which is characterised by high job demands and limited control, is known to play a substantial role in
stress-related disorders. An expanded version of the job strain model adds social support as a third
component, with Iso-strain jobs—those with high demands, little control, and little social support, like
that of healthcare professionals—being associated with the highest risk of sickness. Despite the fact that
the American Heart Association acknowledges a person's stress response as a potential risk factor for
CHD, work stress is not on their list of recognised risk factors. The INTERHEART study found a connection
between psychological stressors and an increased risk of acute myocardial infarction. Significant global
stress was found to have a lesser effect than smoking but was comparable to hypertension and abdominal
obesity. Additionally, the study discovered that cases had more stress at home than controls, proving
that stress from both the work and home environments raises the risk of CHD. Additional investigations
have shown, with comparable findings across many trials utilising different designs and methodology that
self-reported continuing stress is associated with a greater risk of incidents of CHD. In previously healthy
people, depression has also been linked to the development of CHD, with clinical depression serving as a
more reliable indicator than sad mood. Worsened coronary atherosclerosis and endothelial dysfunction
have been seen in experimental investigations as a result of social disruption. Psychosocial factors have
been linked to vascular function, inflammation, increased blood clotting, and decreased fibrinolysis. The
sequence of events as well as the particular pathophysiological nature of psychosocial variables' influence
on CHD are yet unknown. It is crucial to address work-induced stress as a potential CHD risk factor
for healthcare professionals given the important findings of the INTERHEART study and the consistency
across other investigations. Prioritising job stress reduction, boosting social support, and promoting stress
management and coping mechanisms are important steps in the fight against the negative impacts of
stress on health. To better understand the pathways connecting stress and CHD, and to develop tailored
therapies for healthcare professionals dealing with work-related stress, more study is required.
