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(Circulation. 1999;99:2192-2217.)
© 1999 American Heart Association, Inc.

Clinical Cardiology: New Frontiers

Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

Alan Rozanski, MD; James A. Blumenthal, PhD; Jay Kaplan, PhD

From the Division of Cardiology, Department of Medicine, St Luke's/Roosevelt Hospital Center, and the Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY (A.R.); the Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC (J.A.B.); and the Department of Pathology (Comparative Medicine) and Anthropology, Wake Forest University School of Medicine and Wake Forest University, Winston-Salem, NC (J.K.).

Correspondence to Alan Rozanski, MD, Division of Cardiology, St Luke's/Roosevelt Hospital Center, 114th Street and Amsterdam Avenue, New York, NY 10025. E-mail ar77{at}columbia.edu

Abstract

Abstract—Recent studies provide clear and convincing evidence that psychosocial factors contribute significantly to the pathogenesis and expression of coronary artery disease (CAD). This evidence is composed largely of data relating CAD risk to 5 specific psychosocial domains: (1) depression, (2) anxiety, (3) personality factors and character traits, (4) social isolation, and (5) chronic life stress. Pathophysiological mechanisms underlying the relationship between these entities and CAD can be divided into behavioral mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviors, such as poor diet and smoking, and direct pathophysiological mechanisms, such as neuroendocrine and platelet activation. An extensive body of evidence from animal models (especially the cynomolgus monkey, Macaca fascicularis) reveals that chronic psychosocial stress can lead, probably via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis. Evidence from monkeys also indicates that psychosocial stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation in premenopausal females, leading to accelerated atherosclerosis. Also reviewed are data relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research from animal models demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. In the presence of underlying atherosclerosis (eg, in CAD patients), acute stress also causes coronary vasoconstriction. Recent data indicate that the foregoing effects result, at least in part, from the endothelial dysfunction and injury induced by acute stress. Hyperresponsivity of the sympathetic nervous system, manifested by exaggerated heart rate and blood pressure responses to psychological stimuli, is an intrinsic characteristic among some individuals. Current data link sympathetic nervous system hyperresponsivity to accelerated development of carotid atherosclerosis in human subjects and to exacerbated coronary and carotid atherosclerosis in monkeys. Thus far, intervention trials designed to reduce psychosocial stress have been limited in size and number. Specific suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change. The importance of maximizing the efficacy of behavioral interventions is underscored by the recognition that psychosocial stresses tend to cluster together. When they do so, the resultant risk for cardiac events is often substantially elevated, equaling that associated with previously established risk factors for CAD, such as hypertension and hypercholesterolemia.

Key Words: coronary disease • stress • psychology

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				K. Matthews, J. Schwartz, S. Cohen, and T. Seeman Diurnal Cortisol Decline is Related to Coronary Calcification: CARDIA Study. Psychosom Med, September 1, 2006; 68(5): 657 - 661. [Abstract] [Full Text] [PDF]

				J. Giese-Davis, F. H. Wilhelm, A. Conrad, H. C. Abercrombie, S. Sephton, M. Yutsis, E. Neri, C. B. Taylor, H. C. Kraemer, and D. Spiegel Depression and stress reactivity in metastatic breast cancer. Psychosom Med, September 1, 2006; 68(5): 675 - 683. [Abstract] [Full Text] [PDF]

				J. Zhang, R. Niaura, J. R. Dyer, B.-J. Shen, J. F. Todaro, J. M. McCaffery, A. Spiro III, and K. D. Ward Hostility and Urine Norepinephrine Interact to Predict Insulin Resistance: The VA Normative Aging Study. Psychosom Med, September 1, 2006; 68(5): 718 - 726. [Abstract] [Full Text] [PDF]

				Writing Committee Members, D. P. Zipes, A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society Europace, September 1, 2006; 8(9): 746 - 837. [Full Text] [PDF]

				T. Rutledge, S. E. Reis, M. B. Olson, J. Owens, S. F. Kelsey, C. J. Pepine, S. Mankad, W. J. Rogers, C. N. B. Merz, G. Sopko, et al. Depression Symptom Severity and Reported Treatment History in the Prediction of Cardiac Risk in Women With Suspected Myocardial Ischemia: The NHLBI-Sponsored WISE Study. Arch Gen Psychiatry, August 1, 2006; 63(8): 874 - 880. [Abstract] [Full Text] [PDF]

				A. Caspi, H. Harrington, T. E. Moffitt, B. J. Milne, and R. Poulton Socially Isolated Children 20 Years Later: Risk of Cardiovascular Disease Arch Pediatr Adolesc Med, August 1, 2006; 160(8): 805 - 811. [Abstract] [Full Text] [PDF]

				S. A. Thomas, E. Friedmann, C.-W. Kao, P. Inguito, M. Metcalf, F. J. Kelley, and S. S. Gottlieb Quality of life and psychological status of patients with implantable cardioverter defibrillators. Am. J. Crit. Care., July 1, 2006; 15(4): 389 - 398. [Abstract] [Full Text] [PDF]

				W. T. Gallo, E. H. Bradley, J. A. Dubin, R. N. Jones, T. A. Falba, H.-M. Teng, and S. V. Kasl The persistence of depressive symptoms in older workers who experience involuntary job loss: results from the health and retirement survey. J. Gerontol. B. Psychol. Sci. Soc. Sci., July 1, 2006; 61(4): S221 - S228. [Abstract] [Full Text] [PDF]

				L. Keltikangas-Jarvinen, L. Pulkki-Raback, S. Puttonen, J. Viikari, and O. T. Raitakari Childhood Hyperactivity as a Predictor of Carotid Artery Intima Media Thickness Over a Period of 21 Years: The Cardiovascular Risk in Young Finns Study Psychosom Med, July 1, 2006; 68(4): 509 - 516. [Abstract] [Full Text] [PDF]

				W. Raasch, C. Wittmershaus, A. Dendorfer, I. Voges, F. Pahlke, C. Dodt, P. Dominiak, and O. Johren Angiotensin II Inhibition Reduces Stress Sensitivity of Hypothalamo-Pituitary-Adrenal Axis in Spontaneously Hypertensive Rats Endocrinology, July 1, 2006; 147(7): 3539 - 3546. [Abstract] [Full Text] [PDF]

				A. V. Diez Roux, N. Ranjit, L. Powell, S. Jackson, T. T. Lewis, S. Shea, and C. Wu Psychosocial factors and coronary calcium in adults without clinical cardiovascular disease. Ann Intern Med, June 6, 2006; 144(11): 822 - 831. [Abstract] [Full Text] [PDF]