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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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				B. D. Johnson, L. J. Shaw, C. J. Pepine, S. E. Reis, S. F. Kelsey, G. Sopko, W. J. Rogers, S. Mankad, B. L. Sharaf, V. Bittner, et al. Persistent chest pain predicts cardiovascular events in women without obstructive coronary artery disease: results from the NIH-NHLBI-sponsored Women's Ischaemia Syndrome Evaluation (WISE) study Eur. Heart J., June 2, 2006; 27(12): 1408 - 1415. [Abstract] [Full Text] [PDF]

				P. E. Falcoz, S. Chocron, F. Laluc, M. Puyraveau, D. Kaili, M. Mercier, and J. P. Etievent Gender analysis after elective open heart surgery: a two-year comparative study of quality of life. Ann. Thorac. Surg., May 1, 2006; 81(5): 1637 - 1643. [Abstract] [Full Text] [PDF]

				I. Rebollo and D. I. Boomsma Genetic and Environmental Influences on Type A Behavior Pattern: Evidence From Twins and Their Parents in The Netherlands Twin Register Psychosom Med, May 1, 2006; 68(3): 437 - 442. [Abstract] [Full Text] [PDF]

				S. M. O'BRIEN, L. V. SCOTT, and T. G. DINAN Antidepressant therapy and C-reactive protein levels The British Journal of Psychiatry, May 1, 2006; 188(5): 449 - 452. [Abstract] [Full Text] [PDF]

				S. Ramachandruni, R. B. Fillingim, S. P. McGorray, C. M. Schmalfuss, G. R. Cooper, R. S. Schofield, and D. S. Sheps Mental Stress Provokes Ischemia in Coronary Artery Disease Subjects Without Exercise- or Adenosine-Induced Ischemia J. Am. Coll. Cardiol., March 7, 2006; 47(5): 987 - 991. [Abstract] [Full Text] [PDF]

				T. Rutledge, S. E. Reis, M. Olson, J. Owens, S. F. Kelsey, C. J. Pepine, S. Mankad, W. J. Rogers, G. Sopko, C. E. Cornell, et al. Depression is associated with cardiac symptoms, mortality risk, and hospitalization among women with suspected coronary disease: the NHLBI-sponsored WISE study. Psychosom Med, March 1, 2006; 68(2): 217 - 223. [Abstract] [Full Text] [PDF]

				C. Vlachopoulos, F. Kosmopoulou, N. Alexopoulos, N. Ioakeimidis, G. Siasos, and C. Stefanadis Acute mental stress has a prolonged unfavorable effect on arterial stiffness and wave reflections. Psychosom Med, March 1, 2006; 68(2): 231 - 237. [Abstract] [Full Text] [PDF]

				J. Denollet, S. S. Pedersen, A. T.L. Ong, R. A.M. Erdman, P. W. Serruys, and R. T. van Domburg Social inhibition modulates the effect of negative emotions on cardiac prognosis following percutaneous coronary intervention in the drug-eluting stent era Eur. Heart J., January 2, 2006; 27(2): 171 - 177. [Abstract] [Full Text] [PDF]

				C. Dickens, L. McGowan, C. Percival, J. Douglas, B. Tomenson, L. Cotter, A. Heagerty, and F. Creed Association Between Depressive Episode Before First Myocardial Infarction and Worse Cardiac Failure Following Infarction Psychosomatics, December 1, 2005; 46(6): 523 - 528. [Abstract] [Full Text] [PDF]

				Y. J. Akashi, H. Musha, K. Kida, K. Itoh, K. Inoue, K. Kawasaki, N. Hashimoto, and F. Miyake Reversible ventricular dysfunction takotsubo cardiomyopathy Eur J Heart Fail, December 1, 2005; 7(7): 1171 - 1176. [Abstract] [Full Text] [PDF]

				M. M. J. De Jong, S. M. Burns, M. L. Campbell, M. Chulay, M. J. Grap, L. N.B. Pierce, and T. Simpson Development of the American Association of Critical-Care Nurses' Sedation Assessment Scale for Critically Ill Patients Am. J. Crit. Care., November 1, 2005; 14(6): 531 - 544. [Abstract] [Full Text] [PDF]

				K. E. Innes, C. Bourguignon, and A. G. Taylor Risk Indices Associated with the Insulin Resistance Syndrome, Cardiovascular Disease, and Possible Protection with Yoga: A Systematic Review J Am Board Fam Med, November 1, 2005; 18(6): 491 - 519. [Abstract] [Full Text] [PDF]

				H. S. Lett, J. A. Blumenthal, M. A. Babyak, T. J. Strauman, C. Robins, and A. Sherwood Social Support and Coronary Heart Disease: Epidemiologic Evidence and Implications for Treatment Psychosom Med, November 1, 2005; 67(6): 869 - 878. [Abstract] [Full Text] [PDF]