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Stress and acute cardiovascular events

Stress and acute cardiovascular events To the Editor: The National Heart Foundation of Australia's Stress Working Party's report concluded that "the over-all body of evidence on the relationship between stress and heart disease is incomplete and inconsistent".' More importantly, the Working Party felt "that, at present, the only cardiologically-sound reason to intervene in behavioural factors is to modify the established risk factors for coronary heart disease or to assist in rehabilitation after a myocardial infarction". In short, it would seem that the Working Party believes that acute and chronic levels of stress response do not constitute a cardiovascular disease risk factor and, hence, that behaviour which provokes the stress response should not be a specific focus of intervention. The future research and public educational initiatives of the National Heart Foundation are likely to be influenced powerfully by the report's assessment of the available research evidence and the report's recommendations. We believe that were other researchers to examine the same body of evidence, most would reach conclusions that would be diametrically opposite to those that were reached by the Working Party concerning the role and the importance of stress as a causal agent in cardiovascular disease, and the importance of scientifically-based stress-management programmes. The Working Party's analysis has failed to make an elementary but fundamental distinction between the causation of long-term atherogenesis (or what might be called primary coronary heart disease) and the precipitation of acute coronary heart disease events, specifically, angina, myocardial infarction and potentially-lethal arrhythmias in individuals who already are affected by serious atherosclerosis. Current evidence does not support the thesis that stress reactivity is involved critically in the genesis of atherosclerosis (primary coronary heart disease), but overwhelming evidence exists that stress plays a major precipitative and exacerbatory role in acute coronary heart disease events. Large-scale prospective studies such as the Framingham study, which have used psychometrically-sound measures, regularly and consistently have found a relationship between acute and chronic stress reactivity and such acute coronary heart disease events.' Furthermore, the mechanisms that link causally stress reactivity and acute coronary heart disease events in humans and other mammals have been delineated scientifically. Widespread agreement exists that the sympathetic and adrenergic components of the stress response are capable of precipitating anginal episodes and arrhythmias in individuals who exhibit both severe coronary stenosis and a high level of stress reactivity. The mechanism that links stress reactivity and myocardial infarction in individuals who already are affected severely by coronary stenosis is also understood well. It is the thrombogenic component of the stress response, which has evolved to minimize blood loss in situations where the stressor is a potential or an actual physical insult. As Mason' and other colleagues of Selye" have demonstrated, psychological stressors elicit patterns of physiological reaction that are very similar, if not identical, to those that are evoked by physical stressors such as lesions. The dangers of thrombogenesis in subjects who already are at risk of infarction were confirmed amply by the recently-published data on the aspirin component of the Physicians' Health Study." It generally is agreed that aspirin has no influence on atherogenesis and that the very-impressive prophylactic effect of aspirin was mediated by its antithrombogenic properties. In view of the weight of evidence to relate acute and chronic stress reactivity to acute coronary heart disease events, it would seem eminently prudent: to research the role of stress further; and to treat stress as a variable to be targeted in behavioural interventions, particularly those that are aimed at middle-aged and older persons who reasonably can be presumed to have a substantial degree of atherosclerosis of the coronary arteries. Peter C. Birrell, PhD Senior Lecturer in Psychology Sydney H. Lovibond, PhD Professor Emeritus The University of New South Wales High Street, Kensington, NSW 2033 1. Stress Working Party. Stress and cardiovascular disease: a report from the National Heart Foundation of Australia. Mea J Aust 1988; 148: 510-514. 2. Haynes SG, Manning F, Kannel WB. The relationship of psychosocial factors to coronary heart disease in the Framingham Study Ill. Eight-year incidence of coronary heart disease. Am J Epidemiol 1980; Ill: 37-58. 3. Mason. JW. A re-evaluation of the concept of "non-specificity" in stress theory. J Psychialr Res 1971; 8: 323-333. 4. Selye H. Stress in health and disease. Sydney: Butterworths, 1976. 5. The Steering Committee of the Physicians' Health Study Research Group. Preliminary report: findings from the aspirin component of the ongoing Physicians' Health Study. N Engl J Med 1988; 318: 262-264.