Cognitive stress and cardiovascular reactivity. II. Relationship to atherosclerosis, arrhythmias, and cognitive control

Abstract

This is the second of a two-part series on the effects of cognitive stress on cardiovascular disease. This paper reviews the relationship between cognitive stress and cardiovascular reactivity as it relates to the development of atherosclerosis and arrhythmias. In addition, the moderation of cardiovascular reactivity by the opportunity to exercise control over the stressor is discussed. The findings may be summarized as follows. First, recent animal work has suggested that the magnitude of heart rate change in the presence of a conditioned aversive stimulus is positively correlated with the extent of coronary atherosclerosis under diets high and low in atherogenic potential. Second, cardiovascular reactivity in humans may be related to several factors that could have an influence on the pathogensis of atherosclerosis. These factors include: increased beta-adrenergic driving, increased shearing force on the intimal lining of the vessels, changes in pulsatile flow and the subsequent smooth muscle reparatory process. Cognitive (psychological) stress has also been related to ST segment depression, rate-pressure product changes, and changes in cardiac contractility. Animal studies have shown that the susceptibility to ventricular fibrillation may be enhanced by the presence of a conditioned aversive stimulus and may be reduced through adaptation to the aversive environment. The balance between sympathetic and parasympathetic influences on the myocardium may also play a critical role in the susceptibility of an already diseased heart to succumb to fatal arrhythmias during a behavioral stressor. Finally, studies in which subjects may exercise some control over an aversive stimulus suggest that cardiovascular reactivity may be pronounced and sustained in situations requiring frequent adjustment to changes in the criteria for successful performance, and/or the presence of positive incentives.