associated with such a broad array of autoimmune and age-related diseases (Elenkov et al. 2005; Maggio et al. 2006).
In the acute stress response, the sympathetic nervous system stimulates the heart to beat faster, the heart then pumps more glucose to muscles and organs, which provides energy and increased mobility. If glucose stores are insufficient, the body relies on fatty acids from adipose tissue as a backup energy source. With the surge in heart rate comes higher blood pressure against the wall of the artery and an increase in the clotting protein fibrinogen, which protects against blood loss. Chronic stress disturbs those normal cardiovascular functions. Prospective epidemiologic studies that followed people over many years found a relationship between chronic stress and the development of hypertension and other cardiac events (Pickering 2004; Steptoe et al. 2004; Timio et al. 2001).
Alterations in cardiovascular function are integrated with pathologic changes in the immune and endocrine systems. Chronic stress induces cardiovascular abnormalities that appear to be the result of chronic inflammation; chronic inflammation might cause or contribute to early pathologic abnormalities that might progress to disease or disability. The early pathologic changes include abnormalities in heart rate and blood pressure, vascular inflammation, and atherosclerosis.
Acute stress induces immediate rises in heart rate and blood pressure that reverse once the threat disappears. Chronic forms of stress might prolong cardiac reactivity and lead to hypertension and cardiovascular disease. Cardiac reactivity is reflected in blood pressure and heart rate. Several studies have shown that couples that have normal or elevated blood pressure and experience chronic marital distress display greater cardiac reactivity when confronted with a stressful task related to marital conflict, compared to couples without chronic marital distress (Carels et al. 1998; Ewart et al. 1991). Cardiac reactivity is triggered by the sympathetic nervous system’s releasing epinephrine to the heart muscle, although other stress hormones (for example, angiotensin II, a vasoconstrictor released by the kidney on stimulation by epinephrine) are also involved (Black and Garbutt 2002).
For decades, chronic stress has been recognized as a risk factor for atherosclerosis2 and coronary artery disease (Rozanski et al. 1999). The mechanisms underlying the association include long-term immune and endocrine alterations that are associated with chronic stress. The changes include a long-term increase in cortisol, which leads to fat deposition, obesity, increased circulating fatty acids and triglycerides, insulin resistance, activation of the renin-angiotensin system, and a shift towards production of proinflammatory cytokines.
Those endocrine and immune abnormalities are integral to understanding the origins of atherosclerosis as a progressive disease caused by prolonged inflammation of the vascular walls (Greaves and Channon 2002; Libby 2002). The inflammation usually, but not always, occurs in conjunction with higher concentrations of circulating lipids. Indeed, a substantial fraction of people who have cardiovascular disease do not have the traditional risk factor, increased low-density lipoproteins (LDLs) (Libby 2002). Chronic or repeated stress may be the cause of low-
Atherosclerosis can result from fatty deposits on the inner lining of arteries, and calcification of the wall of the arteries. Arteriosclerosis includes a variety of conditions that cause thickening of artery walls and the loss of their elasticity as a result of sustained elevations in blood pressure (hypertension).