Stress Mechanism in Coronary Heart Disease

Although the direct role of stress in disease is still not known, a number of important factors have linked stress to the emergence of various diseases.

The stress response known as the ‘fight or flight’ mechanism is integral in helping an individual to deal with everyday activities. When a person faces a stressor which is the internal or external demands on the body, the A1/A2 noadrenergic neurons in the medulla oblongata of the brain is activated (Pezzone

et al 1993). These two neurons act as intermediates for stress signals in the central nervous system (Gaillet S 1993) Noradrenaline (NA) and PRL-releasing peptide (PrRP) that are produced by these neurons (Morales et al 2000) will stimulate the release of ACTH from the anterior pituitari through the CRH hypothalamic neurons (Maruyama et al., 2001). ACTH will control the release of corticosteroids from the medulla adrenal through endocrinal action (Owens & Nemeroff, 1991). The ACTH and CRH hormones are linked to the first stage of HPA-axis activation while cortisol is the final product.

When the response is repeatedly activated, the usual homeostatic equilibrium is disturbed and a cumulative effect ensures that ultimately leads to various stress related disorders (Marmot & Brunner, 2001). This is directly linked to the various physiological reactions that resulted from the stress response, namely an increase in the sympathetic nervous system, increase in the body’s metabolism, increase in heart rate, increase in blood pressure and an increase in the breathing rate. The “fight or flight” response is adaptive to acute stress but maladaptive to chronic stress (Salposky & Mott, 1987).

Although, coronary heart disease are caused by multifactors similar to other chronic degenerative conditions, stress has been clearly implicated (Cossette et al 2001). Stress causes over- or underactivity of physiological systems which produces allostatic load. A study done on older Americans identified five established cardiovascular risk factors related to allostatic load (Seeman et al 1997). These include systolic and diastolic blood pressure, waist-hip ratio, ratio of total cholesterol to high density lipoprotein (HDL) cholesterol and HDL cholesterol level as well as raised concentrations of glycated hemoglobin, urinary epinephrine (adrenaline), norepinephrine (noradrenaline), cortisol and dehydroepiandrosterone sulphate. Studies found that altering of the HPA axis have linked these factors with long term exposure to adverse psychosocial circumstances (McEwen, 1998).

Many cardiovascular patients with high levels of stress continues to show decline in morbidity as stress affects mechanisms related to cardiac events especially clustering of traditional cardiovascular risk factors, endothelial dysfunction, myocardial ischemia, plaque rupture, thrombosis and malignant arrhythmias (Merz et al 2002).

References

Pezzone MA, Lee WS, Hoffman GE, Pezzone KM, Rabins BS. 1993. Activation of brainstem cathecholaminergic neurons by conditioned and unconditioned aversive stimuli as revealed by c-Fos immunoreactivity. Brain Res., 608:301

Gaillet S. 1993. Effects of discrete lesions in the ventral noradrenergic ascending bundle on the corticotropic stress response depending on the site of the lesion and on the plasma levels of adrenal steroids. Neuroendocrinology, 58:408-419

Morales T, Hinuma S, Sawchenko PE. 2000. Prolactin-releasing peptide is expressed in afferents to the endocrine hypothalamus, but not in neurosecretory neurons. J Neuroendocrinology, 12:131-140

Maruyama M, Matsumoto H, Fujiwara K, Noguchi J, Kitada C, Fujino M, Inoue K. 2001. Prolactin-Releasing Peptide as a Novel Stress Mediator in the Central Nervous System. Endocrinology, 142(5):2932-2038

Owens MJ, Nemeroff CB. 1991. Physiology and pharmacology of corticotropin-releasing factor. Pharmacol Rev., 43:425-473.

Marmot M, Brunner. 2001. Epidemiological applications of Long-term stess in daily life. . In Theorell T (ed.): Everyday Biological Stress Mechanisms.Adv Psychosom Med. Basel, Karger; 22:80-89

Salposky RM, Mott GE. 1987. Social subordinance in wild baboons is associated with suppressed high density lipoprotein-cholesterol concentrations: the possible role of chronic social stress. Endocrinology, 121:1605-1610

Cossette S, Frasure-Smith N, Lesperance F. 2001. Clinical Implications of a Reduction in Psychological Distress on Cardiac Prognosis in Patients Participating in a Psychosocial Intervention Program. Psychosomatic Med., 63:257–266

Seeman TE, Singer BH, Rowe JW, Horwitz RI, McEwen BS. 1997. Price of Adaptation-Allostatic Load and its health consequences. Arch Intern Med, 157:2259-2268

McEwen BS. 1998. Protective and damaging effects of stress mediators. N Eng J Med., 338:171-179

Merz C, Bairey N, Dwyer J, Nordstrom CK, Walton KG, Salerno JW & Scheider RH. 2002. Psychosocial stress and cardiovascular disease:Pathophysiological links. Behav. Med., 27(4):141-147

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