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Stress, inflammation and cardiovascular disease
1epartment of Microbiology, Boston University School of Medicine, Room L-504, 715 Albany Street, Boston, MA 02118, USA. pblack@bu.edu
Insights
Psychological stress can trigger chronic inflammation, leading to atherosclerosis, even in individuals without traditional risk factors. This stress response involves hormonal changes and inflammatory markers that promote cardiovascular disease development.
Area of Science:
- Cardiovascular Science
- Psychoneuroimmunology
- Inflammation Biology
Background:
- Atherosclerosis is increasingly understood as a chronic inflammatory disease.
- Psychosocial factors are implicated in cardiovascular disease etiology.
- A significant portion of atherosclerosis patients lack identifiable conventional risk factors.
Purpose of the Study:
- To review evidence linking psychological stress to chronic inflammation and atherosclerosis.
- To explore the mechanisms by which stress promotes inflammatory cardiovascular processes.
- To identify stress-induced inflammatory markers as potential early predictors of cardiovascular disease.
Main Methods:
- Review of existing scientific literature on stress, inflammation, and cardiovascular disease.
- Analysis of physiological pathways activated by psychological stress.
- Examination of inflammatory mediators and their role in atherogenesis.
Main Results:
- Psychological stress activates the sympathetic nervous system, HPA axis, and renin-angiotensin system, releasing hormones and homocysteine.
- Stress induces endothelial injury, adhesion molecule expression, and inflammatory cell recruitment to the arterial wall.
- Stress triggers an acute phase response with macrophage activation, cytokine production, and mast cell activation, promoting inflammation and an atherosclerotic lipid profile.
Conclusions:
- Repetitive or chronic psychological stress can induce a chronic inflammatory process culminating in atherosclerosis.
- Stress-induced inflammatory events may explain atherosclerosis in patients without other known risk factors.
- Blood levels of adhesion molecules, cytokines, and acute phase proteins are early indicators of stress-induced inflammation and potential predictors of future cardiovascular disease.
Abstract:
Various psychosocial factors have been implicated in the etiology and pathogenesis of certain cardiovascular diseases such as atherosclerosis, now considered to be the result of a chronic inflammatory process. In this article, we review the evidence that repeated episodes of acute psychological stress, or chronic psychologic stress, may induce a chronic inflammatory process culminating in atherosclerosis. These inflammatory events, caused by stress, may account for the approximately 40% of atherosclerotic patients with no other known risk factors. Stress, by activating the sympathetic nervous system, the hypothalamic-pituitary axis, and the renin-angiotensin system, causes the release of various stress hormones such as catecholamines, corticosteroids, glucagon, growth hormone, and renin, and elevated levels of homocysteine, which induce 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. An acute phase response (APR), similar to that associated with inflammation, is also engendered, which is characterized by macrophage activation, the production of cytokines, other inflammatory mediators, acute phase proteins (APPs), and mast cell activation, all of which promote the inflammatory process. Stress also induces an atherosclerotic lipid profile with oxidation of lipids and, if chronic, a hypercoagulable state that may result in arterial thromboses. Shedding of adhesion molecules and the appearance of cytokines, and APPs in the blood are early indicators of a stress-induced APR, may appear in the blood of asymptomatic people, and be predictors of future cardiovascular disease. The inflammatory response is contained within the stress response, which evolved later and is adaptive in that an animal may be better able to react to an organism introduced during combat. The argument is made that humans reacting to stressors, which are not life-threatening but are "perceived" as such, mount similar stress/inflammatory responses in the arteries, and which, if repetitive or chronic, may culminate in atherosclerosis.