Acute psychophysiologic reactivity and risk of cardiovascular disease: A review and methodologic critique.

Abstract

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

Negative emotions and acute physiological responses to stress

“…We commonly investigate these processes using acute laboratory stress models in which subjects are exposed to difficult cognitive, &ocial, or psychomotor tasks such as mental arithmetic and public speaking (4). These models are thought to be successful since these tasks consistently elicit elevations in heart rate (HR) and blood pressure (BP) and in circulating levels of epinephrine and norepinephrine (5). Although we view these tasks as psychological stressors, other aspects of the tasks may contribute to the quantity and quality of physiological response.…”

Anger and denial as predictors of cardiovascular reactivity in women

“…These effects have been observed in animals (Manuck, Kaplan, & Clarkson, 1983a;1985a) and also in acute and chronic studies of humans (Frankenhaeuser, 1983;Henry, 1983;Herd, 1981;Schneiderman, 1983), primarily using male subjects. Coronary heart disease (i.e., angina, myocardial infarction) results when arterial obstruction or atherosclerosis becomes severe enough to block blood supply to the heart (Krantz & Manuck, 1984). …”

“…Upon sacrifice, those monkeys whose psychosocial stress had resulted in high physiological reactivity showed the most advanced state of atherosclerosis. Likewise, in retrospective studies of men and women (e.g., The Framingham Heart Study, Haynes, Levine, Scotch, Feinleib, & Kannel, 1978), elevated physiological reactivity to laboratory stressors has been noted in patients with coronary heart disease or hypertension (Krantz & Manuck, 1984).A number of investigators (Folkow, Hallback, Lundgren, Silverttson, & Weill, 1973;Von Eiff, 1970) have hypothesized that such reactivity may be heritable. Studies have found that young normotensive individuals tend to manifest greater elevations in blood pressure during stressful situations when there is a family history of hypertension (Briggs & Oerting, 1937;Brod, 1960;Shapiro, 1961 testing.…”

Hostility and anger expression behavioral and cardiovascular responses to mental stress among cardiovascular disease patients

“…Everson, Goldberg, Kaplan, Julkunen, & Salonen, 1998;Porter, Stone & Schwartz, 1999;Arrighi et al, 2000). It has been presented either as a marker of pathogenic processes in atherosclerosis or as playing a role in its development (Krantz & Manuck, 1984). For example, in a recent study, Krantz et al (1999) found that among a group of cardiac patients, the patients higher in diastolic blood pressure response to stress were more likely to have cardiac events over a follow-up period of 3.5 years.…”