(10) STRESS PHYSIOLOGY AND IMPACT OF STRESS ON CORONARY ATHEROSCLEROTIC HEART DISEASES
Journal Title: Indian journal of applied basic medical sciences - Year 2014, Vol 16, Issue 22
Abstract
ABSTRACT: Large number of epidemiological studies including Framingham’s study have documented that stress is a important risk factor of Atherosclerotic coronary heart disease. Even and above our day to stresses related to home and job we have witnessed major acute stressful events i.e. earth quack, tsunami, flood, terrorist attacks, civil war, riots, nuclear blasts…. Historical point of view Hans Selye a father of the study of stress, established relationship between chronic stress and effects on the body. He described three stages of stress response as General Adaptation Syndrome” [GAS]. The three stages are 1] Alarm: Fight or Flight” reaction: body mobilizes resources to combat threat; activates the sympathetic nervous system 2] Resistance: Enhanced ability to fight stressor via moderate physiological arousal; ability to withstand additional stressors (e.g., infection) is reduced. 3] Exhaustion: Depletion of resources brings on diseases and disorders (e.g., chronically high heart rate and blood pressure increase chances of heart attack and stroke). Stress activates the hypothalamus-pituitary-adrenal axis, a group of structures that help the body cope with stress. The hypothalamus activities the pituitary gland, which in turn releases hormones that stimulate the adrenal glands to release the stress hormones epinephrine, nor epinephrine, and cortisol. There is release of catecholamine epinephrine (adrenaline), nor epinephrine (noradrenalin) with stimulation of Sympathetic Nervous System. Incidentally majority of studies are epidemiological .Recently there more studies explaining the pathophysiological mechanism how the stress causes CHD. Endocrinal abnormalities especially hypothalamo-pituitary-adrenal (HPA) axis, and inhibited sex steroid result an elevated waist/hip circumference ratio (WHR) and visceral obesity ,combined with insulin resistance is hall mark of metabolic basis of CV disease. Insulin resistance and other risk factors dependent on the hyperinsulinemia following insulin resistance are associated with dyslipideamia i.e. increase LDL cholesterol and triglyceride and decrease, are hallmark or culprit of atherosclerosis . Chronic stress is associated with reduced physical activity and sedentary life style further induces a state of insulin resistance. When beta cells are no longer able to compensate for insulin resistance by adequately increasing insulin production, impaired glucose tolerance appears, characterized by excessive postprandial hyperglycemia. Impaired glucose tolerance may evolve into overt diabetes another risk factor of CHD.. Because all these conditions are also accompanied by the presence of an oxidative stress, oxidative stress one of the pathogenic mechanism linking the stress insulin resistance with dysfunction of both beta cells and endothelium, eventually leading to overt diabetes and cardiovascular disease. There is evidence that chronic stress may induce a chronic inflammatory process culminating in atherosclerosis. These increased oxidative stress and inflammatory events, caused by stress, may account for the approximately 40% of atherosclerotic patients with no other known risk factors. A heightened state of cardiovascular activity, injured endothelium, and induction of adhesion molecules on endothelial cells to which recruited inflammatory cells adhere and translocate to the arterial wall. Shedding of adhesion molecules and the appearance of cytokines, and APRs in the blood are early indicators of a stress-induced APR and may be predictors of future cardiovascular disease. The most important things are 1] stress is everywhere and each and every one are exposed to stress 2]CHD is multi factorial disease and stress is one modifiable risk factor. Stress management interventions studies have further supporting the fact such successful intervention of stress management is associated with up 74% reduction in cardiac events
Authors and Affiliations
Janardan Bhatt
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