Psychosocial Aspects of Atherosclerosis

Mental or emotional stress has long been considered among the risk factors for heart attack. To begin to understand why, a brief explanation of what causes a heart attack seems in order.

The underlying cause of cardiovascular disease that most often leads to heart attack is atherosclerosis. Atherosclerosis develops as a response to endothelial dysfunction, a. malfunction of the inside lining of the arteries supplying the heart muscle with blood. As early as the first decade of life, fatty streaks appear in the large arteries of the body. These fatty streaks are composed of intracellular lipid (fat) accumulation just beneath the inside layer of the artery wall. Beginning in the third decade, the fatty streaks change, developing pools of extracellular fat inside the lining of the artery wall. These pools of fat eventually form a fatty core, which becomes fibrous and, in time, may contain calcium deposits. Under the right conditions, this core in the inside surface of the vessel wall ruptures, and when it does, it bleeds, forming a clot, or thrombus. If big enough, the thrombus occludes the flow of blood through the artery, starving the part of the heart muscle it feeds of oxygen, resulting in the death of that portion of the heart muscle. This death of heart muscle is a myocardial infarction, the lay term for which is heart attack.

What causes the endothelial dysfunction in the first place? Certainly age, gender, and genetics play a roll, but equally important are other risk factors that we now know speed its development. These include mental stress, lack of exercise, high blood pressure (hypertension), high blood cholesterol (specifically high levels of low-density lipoprotein, or LDL), a low level of high-density lipoprotein in the blood (HDL), diabetes, smoking, and, the most recent additions to the list, elevated C-reactive protein (a highly sensitive version of an old test to measure inflammation in the blood vessels) and high levels of homocysteine in the blood. The more risk factors, the more likely it is a person will develop atherosclerosis. Of these, mental stress is probably the most difficult to define, qualify, and quantify, but adds power to the other risk factors.

Mental or emotional stress has been known to trigger various heart problems, but the mechanisms are complicated and somewhat elusive, details of which are beyond the scope of this writing. We know that over time, mental stress can result in hypertension, arterial inflammation, elevated cholesterol, elevated homocysteine levels, elevated glucose, and obesity (one of the hormones that is released during stress, cortisol, is an appetite stimulant). Acutely, mental stress causes the blood vessels to narrow and the blood to clot more readily. When the sympathetic nervous system is stimulated, as it is during mental stress, plasma norepinephrine increases, resulting in rapid, but short-lived (i.e., less than 10 min) vasoconstriction and can precipitate ventricular arrhythmias that, under the right circumstances, can cause sudden death. However, mental stress also causes endothelial dysfunction by preventing the vessel wall from relaxing, resulting in decreased blood flow through the arteries lasting nearly 1 hr. Frequent stressful stimuli thereby result in lengthy states of endothelial dysfunction and vasoconstriction. In addition, Cortisol, one of the “stress” hormones produced by the adrenal glands, is elevated in the blood after mental stress, resulting in high blood pressure and high blood glucose, effects that last up to hours.

Other psychosocial stressors include social isolation, anger, and hostility (likely among the toxic components of the Type A behavior pattern) and depression, all of which have been implicated in the development of cardiovascular disease. An abbreviated discussion of each follows.

Atherosclerosis and Social Isolation

Several epidemiologic studies and scientific investigations have demonstrated correlations between social isolation and increased cardiovascular morbidity and mortality. Socially isolated individuals may face a poorer prognosis because of reduced availability of, or reluctance to seek, rapid medical assistance or an adverse response to decreased human contact, or it may be that socially isolated people may be less likely to take actions to prevent cardiovascular disease onset or progression.

Anger, Hostility, and Atherosclerosis

An episode of anger more than doubles the risk for acute myocardial infarction for 2 hr. Even recalling the anger associated with a particular situation results in cardiac patients’ hearts pumping less blood, an effect not found in normal subjects.

Patients who have high levels of hostility do not do as well as those who do not following procedures to open occluded coronary arteries. Indeed, they are nearly three times more likely to experience a reocclusion of the vessel.

Depression and Atherosclerosis

Several studies have linked depression with cardiovascular morbidity and mortality. In people 65 years of age and older, depressive symptoms independently predict the development of heart disease and total mortality. Depressed patients who have suffered acute myocardial infarction are three to five times more likely to die during the first year than patients who are not depressed. Up to half the time, symptoms of depression precede acute myocardial infarction and are present in those undergoing coronary artery bypass graft surgery. Milani and associates (1996) found that 97 percent of depressed patients who had had a myocardial infarction remained depressed at 6 months if they did not participate in a cardiovascular rehabilitation program, yet only 33 percent of the patients in a cardiovascular rehabilitation program remained depressed at 3 months, suggesting social isolation may also be a factor.

Thus, mental stress, in the form of emotional stress, social isolation, anger and hostility, or depression, is a significant factor in those with or at risk for cardiovascular disease. Comprehensive stress management is an integral element in the management of this population and is necessarily a vital component of cardiovascular rehabilitation programs.

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