Going to the heart of the matter

Abstract

Objective: Negative emotions, such as anger, anxiety, and depression, have emerged as potentially important risk factors for coronary heart disease. The purpose of this article is to consider the nature and function of emotions, to review epidemiological evidence for an association between the three negative emotions and coronary heart disease (CHD), to discuss briefly the mechanisms by which emotions may be linked to CHD, and to consider this evidence in light of theoretical insights provided by mainstream psychological research on emotions. Methods: We collected articles published between 1980 and 1998 on the relationship between each negative emotion and CHD. We also collected review articles or chapters published during the same time period that considered mechanisms by which emotions may increase CHD risk. We used a qualitative approach to review the published literature. Results: Evidence that anxiety is involved in the onset of CHD is strongest, whereas evidence for an association between anger and CHD is limited but suggestive. Although depression has consistently been linked to mortality following a myocardial infarction, evidence for its role in the onset of coronary disease is quite mixed. Numerous unresolved issues leave our current understanding of the emotion–health relationship incomplete. Psychological theories of emotion are considered to help address gaps in our knowledge. Conclusion: Growing evidence indicates that negative emotions may influence the development of CHD. The focused and specific consideration of negative emotions and their possible role in the etiology of CHD gives insight into current knowledge and suggests important directions for future research.

Introduction

“A mental disturbance provoking pain, excessive joy, hope or anxiety extends to the heart, where it affects its temper, and rate, impairing general nutrition and vigor” (from Harvey [1], p. 106). Coronary heart disease (CHD) is the leading cause of death in western, industrialized countries. Traditional risk factors (such as smoking, hypertension, hypercholesterolemia, obesity, and diabetes) explain only about 40% of the occurrence of CHD 2, 3. Although links between emotions and the heart have been hypothesized for centuries, until recently, convincing evidence for such relationships was lacking. Specific emotions like anxiety, anger, and depression have emerged as potentially important risk factors for CHD. 4, 5, 6, 7, 8, 9, 10, 11, 12 Among psychological factors potentially affecting the development of CHD, emotional states (e.g., anxiety, depression) are distinct from other psychological and behavioral factors like personality or coping style [13]. Emotions may influence cardiovascular health through multiple pathways. Specific pathways may involve excessive activation of the sympathetic nervous system, or the hypothalamic–pituitary–adrenocorticol (HPA) axis 14, 15. Other pathways may involve altered autonomic regulation of the heart 14, 16 or the promotion of atherosclerosis through indirect behavioral pathways (like smoking or high-fat diets) 17, 18, 19.

Evidence exists for associations of incident CHD with three specific negative emotions: anxiety; anger; and depression. These associations have often been considered under the broader umbrella of the relationship between CHD and psychosocial factors. However, a more focused consideration of negative emotions and their possible role in the etiology of CHD may suggest important directions for future research. The purpose of this article is first to consider the nature and function of emotions, to review the epidemiological evidence for an association between CHD and each negative emotion (anger, anxiety, and depression), to discuss briefly mechanisms by which these emotions may be linked to CHD, and finally to consider this evidence in light of theoretical insights provided by mainstream psychological research on emotions. Emotions can be a consequence of ill health and affect disease prognosis; however, in this review, we are primarily interested in considering whether emotions influence the development of CHD.

For the purposes of this review, we focus on research that directly addresses the relationship between negative emotion and CHD. Causality between emotion and cardiovascular health is bidirectional and effects accumulate over a long period of time. Cross-sectional and case–control studies have been used to examine this relationship; however, because of the preservation of the temporal order of the link between emotion and disease onset, more compelling evidence is provided by prospective studies that measure emotions among initially disease-free individuals. Although emotions are usually measured at a single point in time, the measurement approaches used in these studies are designed to identify the chronic nature of the emotion experience.

We conducted a literature search using the Medline and Psychological Abstracts data bases, and collected all articles published between 1980 and 1998 on the relationship between each negative emotion and CHD. Given their methodological advantage (i.e., reporting of emotions is not subject to recall bias), we placed greater emphasis on evidence obtained from large, prospective cohort studies. We also considered evidence that acute emotion states may trigger the onset of CHD. We further searched these data bases for review articles or chapters published during the same time period, which considered mechanisms by which emotions may increase risk of CHD. Although speculation on the links between negative emotions and CHD is not new [13], the number of studies providing evidence of a prospective association with any one of the emotions (anxiety, depression, or anger) is still limited. As we are interested in the effects of specific emotions, we felt combining studies across emotions in a formal pooling procedure to be inappropriate. Even when multiple studies were available for a single emotion (e.g., anxiety), they have tended to use quite disparate methods of assessment, such as assessing phobic anxiety versus a clinical diagnosis of panic disorder. For these reasons, formal meta-analytic techniques were not warranted, and instead, we opted for a more qualitative approach to reviewing the published literature [20]. We note that systematic reviews of the literature may still be biased due to the tendency for smaller studies with null findings not to be published (publication bias); thus, as with any review of published literature, our discussion of the literature should be viewed with appropriate caution.