Recent behavioral and biomedical research has suggested that psychophysiologic responsiveness (reactivity) to emotional stress may be a marker of processes involved in the development of cardiovascular disorders. The assessment of reactivity focuses on acute changes in functioning as opposed to the sole assessment of resting levels of variables. This article reviews evidence linking behaviorally induced cardiovascular and endocrine changes to coronary heart disease and essential hypertension. Particular attention is given to methodologic issues involving measurement. It is concluded that reactivity to stress is a construct with multiple dimensions: Different tasks and situations appear to elicit different patterns of physiologic responses. Further, an evaluation of evidence reveals that reactivity per se should currently not be regarded as a proven risk factor. Promising evidence does, however, justify continued laboratory and naturalistic, hypothesis-testing research. Recommended are methodologic studies to identify (a) the psychologic dimensions of stimuli that elicit reactivity in different subject groups, and (b) the patterns of physiologic responses produced. Such research would set the stage for epidemiologic studies to further examine relations between behavior and disease processes.Research on cardiovascular disorders has become one of the most developed areas in study of behavioral influences on health. As more evidence has focused on mechanisms linking psychological and behavioral factors to disease, it has been suggested that physiologic responsiveness to emotional stress might be a marker of pathogenic processes involved in the etiology of coronary heart disease (CHD) or essential hypertension (EH; see

Atherosclerosis disturbs the normal vasomotor response (no change or dilation) of large coronary arteries to mental stress; in patients with atherosclerosis paradoxical constriction occurs during mental stress, particularly at points of stenosis. This vasomotor response correlates with the extent of atherosclerosis in the artery and with the endothelium-dependent response to an infusion of acetylcholine. These data suggest that in atherosclerosis unopposed constriction caused by a local failure of endothelium-dependent dilation causes the coronary arteries to respond abnormally to mental stress.

An extensive research literature in the behavioral sciences and medicine suggests that psychological and social factors may play a direct role in organic coronary artery disease (CAD) pathology. However, many in the medical and scientific community regard this evidence with skepticism. This chapter critically examines research on the impact of psychological and psychosocial factors on the development and outcome of coronary heart disease, with particular emphasis on studies employing verifiable outcomes of CAD morbidity or mortality. Five key variables identified as possible psychosocial risk factors for CAD are addressed: acute and chronic stress, hostility, depression, social support, and socioeconomic status. Evidence regarding the efficacy of psychosocial interventions is also presented. It is suggested that, taken as a whole, evidence for a psychological and social impact on CAD morbidity and mortality is convincing. However, continued progress in this area requires multidisciplinary research integrating expertise in cardiology and the behavioral sciences, and more effective efforts to communicate research findings to a biomedical audience.

To assess the causal relation between acute mental stress and myocardial ischemia, we evaluated cardiac function in selected patients during a series of mental tasks (arithmetic, the Stroop color--word task, simulated public speaking, and reading) and compared the responses with those induced by exercise. Thirty-nine patients with coronary artery disease and 12 controls were studied by radionuclide ventriculography. Of the patients with coronary artery disease, 23 (59 percent) had wall-motion abnormalities during periods of mental stress and 14 (36 percent) had a fall in ejection fraction of more than 5 percentage points. Ischemia induced by mental stress was symptomatically "silent" in 19 of the 23 patients with wall-motion abnormalities (83 percent) and occurred at lower heart rates than exercise-induced ischemia (P less than 0.05). In contrast, we observed comparable elevations in arterial pressure during ischemia induced by mental stress and ischemia induced by exercise. A personally relevant, emotionally arousing speaking task induced more frequent and greater regional wall-motion abnormalities than did less specific cognitive tasks causing mental stress (P less than 0.05). The magnitude of cardiac dysfunction induced by the speaking task was similar to that induced by exercise. Personally relevant mental stress may be an important precipitant of myocardial ischemia--often silent--in patients with coronary artery disease. Further examination of the pathophysiologic mechanisms responsible for myocardial ischemia induced by mental stress could have important implications for the treatment of transient myocardial ischemia.