Stress and CAD
Before discussing the link between stress and heart disease, we must operationalize stress. The reason for this is that when one does a literature search in PubMed using the search terms "stress and heart disease" one will get nearly 40,000 references. Stress contributing to cardiovascular disease has been defined as vital exhaustion, oxidative stress, psychiatric disorders, or multiple other physical stressors that impact cardiovascular functioning. This paper will discuss the effects of chronic psychological stress and its effect on cardiovascular functioning.
Psychological stress has also been difficult to define as basically because there is no objective measure of such stress. Perhaps the classic approaches are the best. Hans Seyle (1956) defined a stressful event as one in which an environmental demand surpasses the inherent regulatory capacity of the organism. Seyle also defined a psychological model of the reaction to prolonged stress, the General Adaptation Syndrome, that is still referenced today (Seyle, 1956). First the organism experiences a state of Alarm in response to a stressful event and the hypothalamic-pituitary-adrenal axis (HPA axis) is activated. If stressor persists the body attempts to adapt to the demands of the situation via hormone release and goes into the Resistance stage. This stage cannot be maintained indefinitely and eventually the organism's resources will become depleted (Exhaustion stage). Early autonomic nervous system symptoms may appear such as perspiration, increased heart rate, and others. Eventually if the stress continues etc. long-term bodily damage may occur in one or more systems including the cardiovascular system via decompensation.
Others, such as Lazurus (1966) added the notion that in order for something to be stressful it must be accompanied by a cognitive appraisal as being potentially threatening and that one does not have the resources to cope with the threat. This cognitive element of stress is extremely important because it helps explain the subjective notion of stress as well as the effects of stress on the body. Thus, we will define psychological stress as an event where the perception of the person) is that its demands exceed the person's coping abilities and is chronic (as opposed to an acute event).
The physical response to stress has been recorded in a number of body systems, but the HPA response to stress is most often discussed as it leads to a cascade of detrimental effects in other bodily systems. The HPA response to stress is organized hierarchically: Stress leads to increases in hypothalamic corticotropin-releasing factor (CRF) secretion that leads to a release from the pituitary of adrenocorticotropin hormone (ACTH) and finally leads to the adrenocortical release of cortisol. In people with chronic stress there is a hypersecretion of CRF (which is determined via levels of CRF in cerebrospinal fluid and a dulled ACTH response to CRF stimulation (Miller, Chen, & Zhou, 2007). These abnormal circadian cortisol cycles are also linked with fatigue, vulnerability to a number of health issues, and poor motivation (Miller et al., 2007). Thus, chronic stress results in hypersecretion of CRF and adrenocortical hypoactivity. This leads to persistent hyperactivity of the HPA axis and chronic over-activity of CRF-containing neurons in limbic and hypothalamic brain regions and under-activity in other brain areas. Anatomical connections between brain areas such as the hypothalamus, hippocampus, and amygdala, facilitate the activation of the HPA axis (Miller et al., 2007).
Moreover, other pathways that are affected by stress have been discovered. For example, both animal and human and studies have demonstrated that stress leads to alternations in the mechanisms involving blood flow. In these studies, psychological stress and coronary artery disease combine to reduce blood flow. This occurs mainly via coronary artery spasm or artery constriction as a result of endothelial (the inner lining of the artery) dysfunction (Smith & Ruiz, 2002). Consequently, stress can lead to major vulnerability factors via several routes that affect the cardiovascular system.
For example, Rosengren et al. (2004) investigated the relationship between chronic stressors to incidence of myocardial infarction (MI) in a sample of nearly 25,000 individuals from 262 medical centers in 52 countries. Stress was defined broadly but was assessed over four different areas. After adjusting for gender, age, smoking habits, and geographic region it was found that those who had suffered a MI reported significantly more stress over all four areas. Chronic stress at work or at home was associated with over two times the risk for developing an MI in the sample. Of course this study is correlational. One potential issue is that after having an MI the person...
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