Key result
Stress-induced atherosclerosis may be driven by inflammation and neuroendocrine pathway activation.
Highlights the potential role of inflammation and neuroendocrine pathways in the pathogenesis of stress-induced atherosclerosis.
Hypothesis-generating for stress-related CVD mechanisms; prospective trials needed before any clinical application.
There is increasing recognition in medical fields of the importance of behavioral and psychosocial factors in the development of cardiovascular disease. Although the pathogenesis underlying stress-induced atherosclerosis is not well known, inflammation may play a key role. Activation of stress-induced neuroendocrine pathways, such as the hypothalamo-pituitary-adrenal axis, and the sympathetic nervous and renin angiotensin systems, direct neurogenic inflammation may also contribute to the development of stress-induced atherosclerosis. (Korean Circulation J 2005;35:101-105)
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Ick Mo Chung (2005) conducted a review in Stress-induced atherosclerosis. Stress was evaluated. Stress-induced atherosclerosis may be driven by inflammation and the activation of neuroendocrine pathways, including the hypothalamo-pituitary-adrenal axis and sympathetic nervous systems.
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