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Review Article Open Access
The exposure to psychological stress can increase the risk of cardiovascular disease due to impaired endothelial function. Mediators such as glucocorticoids, catecholamines, angiotensin II and/or pro-inflammatory cytokines, induced by stress, can contribute to endothelial dysfunction due to increased levels of oxidative stress. The endothelial dysfunction induces reduced expression and/or endothelial nitric oxide synthase enzyme functionality, as well as the impairment of the actions triggered by its metabolite, nitric oxide. Chronic psychological stress leads to atherosclerosis development, which has an endothelial dysfunction at early stages. The oxidative damage and inflammatory mediators, induced by chronic psychological stress, play a key role in this process. Furthermore, chronic psychological stress can contribute to the formation of unstable atherosclerotic lesions as a result of immune system cells accumulation and molecules adhesion, leading to thrombosis and cardiac complications. According to what was stated above, we aim to discuss about the endothelial function impairment mediated by psychological stress, and the involvement of mediators such as glucocorticoids, catecholamines, angiotensin II and pro-inflammatory cytokines in this response. This review covers current advancements to understand how chronic psychological stress could lead to atherosclerosis development.
Congestive Heart Failure,Coronary Heart Disease