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ARTICLE

Psychosocial Factors and Coronary Calcium in Adults without Clinical Cardiovascular Disease

right arrow Ana V. Diez Roux, MD, PhD; Nalini Ranjit, PhD; Lynda Powell, PhD; Sharon Jackson, PhD; Tené T. Lewis, PhD; Steven Shea, MD; and Colin Wu, PhD

6 June 2006 | Volume 144 Issue 11 | Pages 822-831

Background: Psychosocial factors have been linked to coronary events, but the mechanisms underlying these associations have not been established. Evidence is mixed regarding associations of psychosocial factors with subclinical coronary atherosclerosis.

Objective: To examine associations of 4 psychosocial factors (depressive symptoms, anger, anxiety, and chronic stress) with the presence of subclinical coronary atherosclerosis.

Design: Cross-sectional study.

Setting: The Multiethnic Study of Atherosclerosis, a population-based study of subclinical atherosclerosis.

Patients: A multiethnic sample of 6789 adults, 45 to 84 years of age, with no history of clinical cardiovascular disease.

Measurements: Coronary calcium was assessed by using chest computed tomography, and psychosocial factors were assessed by using questionnaires with validated scales.

Results: There was no evidence that higher levels of the psychosocial measures were associated with greater prevalence of calcification or with greater amounts of calcium among persons with calcium. Age- and risk factor–adjusted relative prevalences of coronary calcification in men for the top fourth category versus the bottom fourth category of anger, anxiety, and depressive symptoms were 0.94 (95% CI, 0.88 to 1.01), 0.97 (CI, 0.90 to 1.04), and 0.97 (CI, 0.90 to 1.05), respectively; these values for women were 1.01 (CI, 0.90 to 1.15), 0.93 (CI, 0.83 to 1.05), and 0.92 (CI, 0.82 to 1.04), respectively. Relative prevalences for the top versus the bottom category of chronic stress burden were 1.02 (CI, 0.94 to 1.11) for men and 0.88 (CI, 0.79 to 0.99) for women.

Limitations: Current measures of psychosocial factors may be a poor proxy for cumulative exposure during development of atherosclerosis.

Conclusion: Depressive symptoms, anger, anxiety, and chronic stress burden were not associated with coronary calcification in a multiethnic sample of asymptomatic adults.


Editors' Notes
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Context

  • The role of psychosocial risk factors in the pathogenesis of coronary heart disease (CHD) is difficult to ascertain after patients develop CHD symptoms.

Contribution

  • The authors administered standardized questionnaires about psychosocial factors and did electron-beam chest computed tomography in a community-based sample of 6814 adults without CHD symptoms. The prevalence of coronary calcium varied from approximately 35% to approximately 70% by race and ethnicity and sex. Psychosocial factors were not associated with coronary artery calcium scores.

Cautions

  • The study used 1-time measurement of psychosocial factors, whose effects are probably cumulative.

Implications

  • The results make it less likely that psychosocial factors are a contributing cause of CHD.

—The Editors

 

Author and Article Information
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From University of Michigan, Ann Arbor, Michigan; Rush University Medical Center, Chicago, Illinois; Wake Forest University School of Medicine, Winston-Salem, North Carolina; Columbia University, New York, New York; and National Institutes of Health, Bethesda, Maryland.

Note: Drs. Diez Roux and Ranjit had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. A full list of participating MESA investigators and institutions can be found at http://www.mesa-nhlbi.org.

Acknowledgments: The authors thank the other investigators, the staff, and the participants of MESA for their valuable contributions, and Sarah Burgard for assistance with initial data analyses.

Grant Support: By the National Heart, Lung, and Blood Institute (contracts N01-HC-95159 through N01-HC-95165 and N01-HC-95169) (Multiethnic Study of Atherosclerosis) and in part by R01 HL076831 (Dr. Diez Roux).

Potential Financial Conflicts of Interest: None disclosed.

Requests for Single Reprints: Ana V. Diez Roux, MD, PhD, Department of Epidemiology, School of Public Health, University of Michigan, 1214 South University, 2nd Floor, Ann Arbor, MI 48103; e-mail, adiezrou{at}umich.edu.

Current Author Addresses: Drs. Diez Roux and Ranjit: Department of Epidemiology, School of Public Health, University of Michigan, 1214 South University, 2nd Floor, Ann Arbor, MI 48103.

Dr. Powell: Department of Preventive Medicine and Department of Behavioral Sciences, Rush University Medical Center, Suite 470, 1700 West Van Buren, Chicago, IL 60612.

Dr. Jackson: Department of Public Health Sciences, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157.

Dr. Lewis: Department of Preventive Medicine, Rush University Medical Center, Suite 470, 1700 West Van Buren, Chicago, IL 60612.

Dr. Shea: Departments of Medicine and Epidemiology, Columbia University, 630 West 168th Street, New York, NY 10032.

Dr. Wu: National Heart, Lung, and Blood Institute, National Institutes of Health, 2 Rockledge Center, Room 8218, 6701 Rockledge Drive, Bethesda, MD 20892-7938.

Author Contributions: Conception and design: A.V. Diez Roux, N. Ranjit, L. Powell, S. Jackson, S. Shea.

Analysis and interpretation of the data: A.V. Diez Roux, N. Ranjit, L. Powell, S. Jackson, C. Wu.

Drafting of the article: A.V. Diez Roux, N. Ranjit.

Critical revision of the article for important intellectual content: A.V. Diez Roux, N. Ranjit, L. Powell, S. Jackson, T.T. Lewis, S. Shea, C. Wu.

Final approval of the article: A.V. Diez Roux, N. Ranjit, L. Powell, S. Jackson, T.T. Lewis, S. Shea, C. Wu.

Provision of study materials or patients: A.V. Diez Roux, S. Shea, S. Jackson.

Statistical expertise: A.V. Diez Roux, N. Ranjit, C. Wu.

Obtaining of funding: A.V. Diez Roux, S. Shea.

Collection and assembly of data: A.V. Diez Roux, S. Jackson, S. Shea.


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