Hostility and Cardiovascular Disease⁎

Hostility and Cardiovascular Disease⁎

Journal of the American College of Cardiology © 2011 by the American College of Cardiology Foundation Published by Elsevier Inc. EDITORIAL COMMENT H...

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Journal of the American College of Cardiology © 2011 by the American College of Cardiology Foundation Published by Elsevier Inc.

EDITORIAL COMMENT

Hostility and Cardiovascular Disease* Mary A. Whooley, MD,† Jonathan Wong, BA‡ San Francisco and Irvine, California

An association between hostility and coronary heart disease (CHD) was initially described one-half century ago. Two cardiologists, Friedman and Rosenman (1,2), identified a “coronary prone behavior pattern” that they called “type A,” which was primarily composed of competitiveness, excessive drive, and an enhanced sense of time urgency. They found that patients with “Type A behavior pattern” had both an increased prevalence of CHD risk factors and an increased incidence of CHD events (3). In an effort to reduce the excess risk of CHD associated with Type A behavior, Friedman et al. (4,5) conducted a randomized trial of 862 post-myocardial infarction patients in the Recurrent Coronary Prevention Project. During 4.5 years of follow-up, subjects randomly assigned to both cardiac counseling and Type A behavioral counseling had fewer recurrent events than those assigned to cardiac counseling alone (4,5). See page 1222

Although the association between Type A behavior and CHD was subsequently called into question (6,7), these important findings put psychological factors on the map as potential risk factors for CHD. Soon thereafter, Williams et al. (8), Shekelle et al. (9), and others identified hostility and anger as the key components of Type A behavior that were responsible for its connection with CHD. During the past 25 years, numerous studies have evaluated the links between hostility, anger, and CHD. In a comprehensive metaanalysis published in 2009, Chida and Steptoe (10) found that anger and hostility were associated with a 19% increased risk of incident CHD events among otherwise healthy subjects (25 studies) and a 24% increased risk of recurrent events among patients with existing CHD (19 studies). The association with recurrent events persisted after adjustment for baseline disease status and treatment. *Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. From the †Department of Medicine, VA Medical Center and University of California, San Francisco, California; and the ‡University of California Irvine School of Medicine, Irvine, California. Dr. Whooley and Mr. Wong have reported that they have no relationships relevant to the contents of this paper to disclose.

Vol. 58, No. 12, 2011 ISSN 0735-1097/$36.00 doi:10.1016/j.jacc.2011.06.018

In this issue of the Journal, Newman et al. (11) extend this body of published reports with their analysis of data from the 1995 Nova Scotia Health Survey. In a prospective study of 1,749 adults who were initially free of CHD, they measured observed hostility with the Expanded Structured Interview and evaluated self-reported hostility using subscales of the Cook-Medley hostility scale. During 10 years of follow-up, 8.9% (140 of 1,572) of patients with any observed hostility and 5.1% (9 of 177) of patients without any observed hostility developed CHD. After adjustment for age, sex, Framingham risk score, and other psychosocial variables, observed hostility was associated with a 2-fold greater risk of incident CHD (p ⫽ 0.04). In contrast, self-reported hostility was not predictive of incident CHD. Notable strengths of this study include its relatively large sample size, long-term follow-up, adjustment for other psychosocial risk factors, particularly depressive symptoms (12), and use of a standardized interview to characterize hostility. Hostility, typically defined as a negative mistrustful attitude that includes aggressive behavior and frequent angry feelings toward others (13), is a multidimensional construct that presents a significant challenge for investigators to accurately define and quantify. Patient-reported scales require self-awareness of hostility and tend to be influenced by reporting bias (14), whereas interview-based methods provide a more objective measure of hostility through observed interpersonal interactions (15). In the current study, the structured observed hostility interview was recorded and reviewed to ensure standardization. Although other studies have used interview-based measures of hostility to study its association with CHD (16,17), no prior study has directly compared the predictive value of patientreported versus interview-based hostility measures on CHD outcomes. It is important to note that the absolute difference in risk of CHD between subjects with and without hostility was small (3.8% during 10 years of follow-up). Likewise, the limited number of patients without hostility made the results somewhat challenging to interpret. The authors initially divided participants into 5 categories (ranging from no to frequent hostile statements) and reported a significant test for trend between hostility category and incident CHD (p ⫽ 0.01). However, because there were no significant differences in CHD across categories 2 through 5, all subsequent analyses evaluated incident CHD in patients with any observed hostility (n ⫽ 1,572) versus no observed hostility (n ⫽ 177). Given that 90% of study participants had some observed hostility, it is difficult to consider hostility as a risk factor. A more valuable message might be that the absence of hostility was protective against CHD. Another issue is that the mechanisms linking hostility (or lack of hostility) with CHD were not explored. Hostility is known to be associated with poor health behaviors such as physical inactivity, dietary indiscretion, higher body mass index, and smoking (18 –20). In the meta-analysis by Chida

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Whooley and Wong Hostility and Cardiovascular Disease

and Steptoe (10), there were no significant associations between anger or hostility and CHD among the subset of studies that controlled for possible behavioral covariates. Thus, although the current study adjusted for smoking, it remains possible that the observed association was explained by physical inactivity or other health behaviors. An alternative potential mechanism linking hostility and CHD involves the sympathetic nervous system. Exaggerated adrenergic responses to stressful psychological stimuli can increase blood pressure (21); induce coronary vasoconstriction (22); increase inflammation (23); and activate platelets (24). A triggering event, such as an outburst of anger, might increase the risk of nonfatal myocardial infarction or CHD death (25). However, Sloan et al. (26) recently conducted a trial in which 158 hostile volunteers were randomly assigned to a 12-week cognitive behavior therapy program for hostility or to a wait-list control. The intervention reduced hostility and anger as expected, but surprisingly, this was not accompanied by improvements in cardiac autonomic modulation. These findings raised questions about autonomic nervous system dysregulation as a pathophysiological mechanism underlying the hostility–CHD relationship. In summary, Newman et al. (11) have demonstrated that observed hostility is superior to patient-reported hostility for the prediction of incident CHD, independent of baseline Framingham risk score and other psychosocial variables. However, 90% of the participants were classified as having observed hostility, and thus it might be more useful to consider the absence of hostility as protective. Whether reducing hostility can improve cardiovascular outcomes is unknown. The next step is to better understand the exact mechanisms of this association and, in particular, to evaluate whether health behaviors might explain the effects of hostility on CHD. Reprint requests and correspondence: Dr. Mary A. Whooley, University of California-San Francisco, VA Medical Center, 4150 Clement Street (111A1), San Francisco, California 94121. E-mail: [email protected].

JACC Vol. 58, No. 12, 2011 September 13, 2011:1229–30

5. 6. 7. 8. 9. 10. 11.

12. 13. 14. 15. 16.

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18. 19.

20. 21. 22. 23.

REFERENCES

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Key Words: hostility y ischemic heart disease y observational study.