What effect does psychological stress have on cardiovascular physiology? Does psychological stress contribute to cardiovascular disease? These important questions are the domain of cardiopsychology, the discipline that studies how psychosocial stressors impact the onset, course, rehabilitation and the illness processing (coping) of cardiac diseases. In this post, we look at the effects of stress on the normal heart in healthy condition, and the effects of acute or chronic stress on individuals with cardiovascular disease.
The body responds to stress primarily through the mobilization of resources initiated by the autonomic nervous system and endocrine activity. Endocrine activity consists of sympathetic adrenomedullary, pituitary-adrenocortical, and thyroid responses. The most important stress hormones released by sympathetic adrenomedullary response are epinephrine and norepinephrine. The stress hormones released in the pituitary-adrenocortical response are adrenocorticotrophic hormone (ACTH) and cortisol.
Psychological conditions shown to have an effect on cardiovascular disease include anxiety disorders, panic disorders, and depressive disorders. There is compelling evidence that acute psychological stress triggers major autonomic cardiovascular responses and cardiac events. Nonetheless, the evidence that chronic stress causes cardiovascular disease is highly controversial. Although the most prevalent opinion among cardiologists, psychiatrists, physiologists, and psychologists is that psychological stress has an effect on cardiovascular disease, these effects are not easily quantifiable or attributable with any degree of precision. What we do know is that acute stress is often accompanied by cardiovascular changes, some of which can be dangerous to certain individuals.
Data on whether chronic stress may, over time, cause cardiovascular disease are less convincing. For example, there is little validated evidence that people with anxiety-related disorders have a higher prevalence of cardiovascular disease than their less anxious counterparts. Moreover, except for postmyocardial infarction depression, there is insufficient evidence that individuals with cardiovascular disease have a higher prevalence of psychological disorders than those who have no cardiovascular disease.
Acute mental stress alters baseline parameters on the normal heart and vascular system in good health condition. Under acute stress, it is quite normal for blood pressure to rise, due to the action of neural mechanisms that regulate stress-induced blood pressure changes as a stress reaction to a dangerous situation that requires an increase in cardiac activity.
Structures of the central nervous system involved in this rapid arousal include the medulla oblongata, the medial geniculate body, the limbic system (amygdala and hypothalamus), and the brainstem. Psychological stress-induced changes in blood pressure are usually predictable and can vary depending on many variables, including duration of stress, time of measurement, expectations, psychological preparedness, and individual background.
Specific effects of psychological stress on the cardiovascular system are increased cardiac output, higher stroke volume, stronger forearm blood flow, increased left ventricular ejection fraction, higher peripheral vascular resistance, and increased cardiac microcirculation. These effects are not dangerous on the normal heart and vessels in good health condition, and they generally subside and return to normal levels after the stressor has passed.
As in the healthy heart, acute stress increases blood pressure (generally by 10–20% and sometimes to hypertensive levels) in individuals with cardiovascular disease. Acute stress also increases the heart rate of individuals with cardiovascular disease, and angina pectoris and ischemia may result from this increase in heart rate. In some cases, the stress-induced increase in heart rate also alters cardiac electrical stability and may cause life-threatening arrhythmias.
Acute stress may also cause coronary artery vasoconstriction, reduce left ventricular ejection fraction, and induce or exacerbate left ventricular wall motion abnormalities in individuals with cardiovascular disease. In this respect, studies have shown that frequent anger among individuals with cardiovascular disease may increase their vulnerability to cardiac complications.
Psychological stress produces strong limbic-hypothalamic activity, which may contribute to the yet unclear etiology of essential hypertension, i.e. high blood pressure that does not appear to have specific organic causes. Conversely, the presence of hypertension, borderline hypertension, and genetic risk for hypertension may have an impact on blood pressure reactivity to psychological stress, thus setting up an apparent circular causality between stress-hypertension-higher reactivity to stress.
Individuals with high blood pressure are characterized by a greater arterial wall-to-lumen ratios compared with healthy individuals. Thus, the same quantity of norepinephrine causes a greater increase in peripheral vascular resistance compared to healthy individuals who have a smaller arterial wall-to-lumen ratio. Also, individuals who are already suffering from angina pectoris react to stress with a greater elevation of blood pressure.
Chronic stress and prolonged bereavement have been shown to increase the risk of cardiac death. A large-scale study showed that stress due to the death of the wife caused a 40% increase in the death rate of the surviving husbands during the first 6 months of loss, with two-thirds of those deaths attributable to cardiovascular disease. A similar increases did not occur among widows following the death of their husbands.
Studies conducted on individuals who exhibit type A and type B personality patterns have tested the hypothesis that personality may affect the inset, course, and outcome of cardiovascular disease. Type A personalities are those characterized by time-urgency, high competitiveness, ambitiousness, and frequent hostility. Type B personalities are unhurried, more relaxed, and less competitive. The results of these studies show that if there is a correlation between personality patterns and cardiovascular disease, this correlation is very weak. Thus, type A or type B personalities appear to have similar outcomes in the convergence of stress and cardiovascular disease.
Anxiety is a significant factor in producing chest pain even when coronary arteriography is normal, and anxiety disorders have been confirmed as a debilitating factor. Major depressive disorder is the second significant factor, and this disorder appears to predict future cardiac events among patients with coronary artery disease. Chronic anxiety, helplessness, and depression have been specifically linked to angina pectoris and sudden death by cardiac arrest. More than 300,000 Americans experience sudden (within minutes) death each year. Excluding acute myocardial infarction-induced ventricular arrhythmias, about one in ten sudden deaths are due to cardiac arrhythmias (particularly ventricular arrhythmias).
Research by Rahe and others on the health impact of significant life changes discovered that individuals who suffer a myocardial infarction are more likely to have had a major life change during the 6 months preceding the heart attack. In another study, Rahe and Lind provided evidence that life change occurs more frequently among victims of sudden cardiac death compared with survivors of myocardial infarction.
The relationship between chronic psychological stress and hypertension remains controversial. Psychological stress-induced increases in heart rate and blood pressure reactivity do have an immediate effect on blood pressure readings. Nonetheless, this clearly demonstrable increase in blood pressure following a sudden and significant stressor does not appear to carry on to produce long-term effects on blood pressure.
In summary, the extent of coronary artery disease, the degree of left ventricular dysfunction, and the presence of arrhythmias appear to determine individual vulnerability to stress-induced sudden cardiac death. When individuals are already suffering from advanced cardiovascular disease, stress-related precipitants of sudden cardiac death are ubiquitous and may be impossible to avoid. Acute stressors often contributing to sudden cardiac death include bereavement, unemployment, financial distress, dislocation, lower education levels, individual responses to psychological stress, and social isolation. Research results are somewhat contradictory in establishing a clear association between cardiovascular disease and such factors as gender, personality patterns, anxiety, panic disorder, PTSD, bereavement, depression, and occupation.
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