Heart Disease and Stress
Stress is a hard concept to define precisely, but like obscenity (to paraphrase Supreme Court Justice Potter Stewart (Jacobellis vs. Ohio. 378 U.S. 184, 197, 1964)), you (sometimes, but perhaps not always) know it when you feel it. For any given system, stress implies a load that challenges the homeostasis and integrity of the system. Stress may be intrinsic to the system, for example, the weight of a suspension bridge’s roadway platform, or extrinsic to the system, such as the effect of hurricanes, earthquakes, or traffic jams loading the bridge. Both intrinsic and extrinsic stressors pose the risk of bridge collapse. Whether a stressor is intrinsic or extrinsic, the system must have a capacity to withstand it in order to maintain structural and/or functional integrity. Thus for a suspension bridge, to continue the example, this capacity is built into the tensile strength of its suspension cables and the mass and strength under compression of the towers and buttresses supporting the cables and transmitting force to the surrounding ground. In behavioral cardiology, concern about stress and heart disease has focused on external psychological stressors, and related behaviors and affective and psychophysiological states, associated with the onset and progression of heart disease, especially coronary artery disease and sudden cardiac death.
For lack of a precise, gold-standard, quantifiable measure of stress as it relates to heart disease, stress is usually defined by subjective measures of perceived stress, by characterization and counts of common life experiences generally regarded as stressful, unwanted, or at least as disturbing homeostasis (e.g., daily hassles, hostile interactions, job strain, job loss, loss of a loved one, divorce, interpersonal conflict, moving to a new city, marriage, promotion to new work responsibilities), by experimental manipulations or ecological measurement of short-term challenges, and by exposures to epidemiologically significant events such as natural disasters, missile attacks during wartime, and terrorism. It is evident that stress is often associated with negatively valenced affective states such as anxiety, depression, and anger, but can also be associated with more positively experienced acute excitement and life experiences.
Evidence for the association of stress with heart disease is overwhelming. Numerous studies demonstrate that earthquakes are associated with a subsequent increase over background rates in myocardial infarction and sudden death. Iraqi missile attacks on Israel during the Gulf War in the 1990s, the destruction of the World Trade Center in New York in 2001, and sports events such as World Cup Soccer matches have been consistently observed to be associated with increased rates of acute coronary syndromes and lethal ventricular arrhythmias, even in individuals not physically endangered by proximity to the events. Acute episodes of anger appear to be an especially potent trigger of acute coronary events in vulnerable patients. In INTERHEART, a very large case-control study of first myocardial infarction involving over 24,000 subjects in 52 countries, chronic exposure to stress, measured by self-reports of problems with family relationships, work, or financial strain over a 1-year period, was associated with increased rate of MI, with population-attributable risk estimated at 12–33%. A dose-response relationship was observed between the number of stressful life events reported and risk of myocardial infarction, with an odds ratio for MI risk of 1.5 for individuals reporting two or more stressful life events compared to those reporting no stressful life events. Thus, epidemiological evidence supports the role of emotional stress both over the long term, in processes contributing to the development of coronary atherosclerosis, and in the short term, as a trigger of acute coronary events in vulnerable patients. Perceived stress is heightened in people with low socioeconomic status, which may also be associated with numerous other behavioral and physiological cardiac risk factors. Conversely, stress effects on cardiovascular risk are moderated by the presence of good social support. Studies comparing heart disease risk in men and women have found that for women, the relationship of stress at work to coronary heart disease risk is less clear-cut than in men, but stress at home and in interpersonal relationships is associated with increased risk of coronary disease-related events.
Stressful experiences result in derangements of autonomic nervous system regulation of the cardiovascular system, with reduced vagal tone and relatively increased sympathetic tone. Heart rate and blood pressure increase in response to acute mental stress; the extent of this increase depends in part on the nature of the stressor and also in part on individual characteristics such as trait anxiety and hostility. Interruption of sympathetic inflow to the left side of the heart by left stellate ganglionectomy reduces stress-induced ischemia and ventricular arrhythmias. Stressful experience is associated with hemoconcentration and increased blood viscosity, which may increase the risk of thrombosis, especially as clotting factors and platelet activation also increase during acute stress. Stressful experiences alter hypothalamic-pituitary axis function, with lasting consequences, such that childhood trauma is associated with elevated circulating levels of corticotrophin-releasing factor in adulthood, and stress in adulthood leads to hypercortisolemia. Endothelial dysfunction and paradoxical vasoconstriction during acute mental stress are observed in atherosclerotic coronary artery segments. During mental stress, increased heart rate and blood pressure along with coronary vasoconstriction may result in myocardial ischemia, which may be manifest as ST segment changes in the electrocardiogram, reduced left ventricular ejection fraction and regional wall motion abnormalities; stress-induced impairment of left ventricular function is associated with an increase in the risk of recurrent coronary events and survival. Yet, although mental stress-induced ischemia occurs primarily in individuals with exercise-induced ischemia, it is notable that mental stress-induced myocardial ischemia is frequently asymptomatic, and occurs at a level of increased heart rate and blood pressure less than that required to achieve ischemia during exercise. Acute mental stress also induces an inflammatory response, with elevated levels of inflammatory cytokines IL-6 and TNF-alpha, which can destabilize atherosclerotic plaque and promote plaque rupture or superimposed thrombosis. The extent to which each of these mechanisms mediates the effect of stress on heart disease risk is unknown.
Sudden emotional stress can also lead to acute cardiac events in patients who do not have coronary artery disease. Takotsubo cardiomyopathy is a rare syndrome characterized by transient left ventricular dysfunction with apical ballooning and acute heart failure in response to emotional shocks, such as surprise parties or receiving unexpected bad news. The syndrome has been attributed to rapidly increasing sympathetic tone and catecholamine levels in response to the psychological stressor.
Studies of the effects of interventions to reduce stressful experience or improve resilience in managing stress on heart disease outcomes have had decidedly mixed results. Behavioral or cognitive behavioral stress management treatment groups to reduce angry responding and time urgency reduce the incidence of recurrent MI. Inclusion of “stress management” in cardiac rehabilitation programs for post-MI patients is associated with reduced recurrent cardiac events and reduced mortality, but individualized life stress monitoring and problem-solving interventions for post-MI patients resulted in no benefit in men and increased recurrent cardiac events in women in the Montreal Heart Attack Readjustment Trial (M-HART). Cognitive behavior therapy aimed at bolstering social support also had a negative effect on recurrent cardiac events in women in the ENRICHD trial. Overall, however, exercise and stress management programs appear to reduce recurrent cardiac events, improve subjective well-being, and may reduce hemodynamic and other physiological responses to stress.
References and Further Reading
- Rozanski, A., Blumenthal, J. A., Davidson, K. W., Saab, P. G., & Kubzansky, L. (2005). The epidemiology, pathophysiology, and management of psychosocial risk factors in cardiac practice. The emerging field of behavioral cardiology. Journal of the American College of Cardiology, 45, 637–651.CrossRefGoogle Scholar
- Shapiro, P. A. (2011). Heart disease. In J. L. Levenson (Ed.), Textbook of psychosomatic medicine (2nd ed., pp. 407–440). Washington, DC: APPI.Google Scholar