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Circulation. 2000;101:e177-e178

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(Circulation. 2000;101:e177.)
© 2000 American Heart Association, Inc.


Circulation Electronic Pages

Psychological Factors and Ischemic Heart Disease

H. Richard Hellstrom

Department of Pathology Health Science Center at Syracuse, State University of New York, Syracuse, NY


*    Introduction
 
To the Editor:

Rozanski et al,1 in discussing the role of psychological factors in inducing ischemic heart disease (IHD), indicated that "the pathophysiological mechanisms by which behavior therapies reduce cardiac events need to be identified." I suggest that behavior therapies operate to prevent stress-induced IHD by countering mechanisms by which stress induces IHD.

The recently described altered homeostatic theory (AHT)2 asserts that mechanisms that prevent stress-induced IHD directly counter mechanisms that induce such symptoms. Importantly, the AHT is a general theory and includes multiple risk factors besides stress (such as cholesterol, smoking, and homocysteine) and multiple disorders besides IHD (such as hypertension, atherosclerosis, and stroke).

The AHT asserts that multiple risk factors for IHD and other disorders induce disease by the single action of shifting homeostasis inappropriately toward defensive fight/flight and that multiple preventative factors (such as stress reduction, vitamins, aspirin, and exercise) shift homeostasis toward health by an opposite shift of homeostasis. For IHD, chronic stress favors atherosclerosis and acute stress induces symptoms through spasm-of-resistance vessels (S-RV).

The AHT can be considered an expansion of Selye’s stress syndrome3 to other risk factors. Selye asserted that stress shifts homeostasis toward disease because of overactivity of the general adaptational or defensive fight/flight response. This defensive response is characterized by mechanisms that are generally similar to the mechanisms described by Rozanski et al1 by which psychological factors such as depression, anxiety, and social isolation favor IHD; the mechanisms described by Rozanski et al include sympathetic nervous system hyperresponsivity, expression of S-RV and . . . [Full Text of this Article]

Alan Rozanski, MD

Division of Cardiology Department of Medicine, St Luke’s/Roosevelt Hospital Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY

James A. Blumenthal, PhD

Department of Psychiatry and Behavioral Sciences Duke University Medical Center, Durham, NC

Jay Kaplan, PhD

Department of Pathology (Comparative Medicine) and Anthropology Wake Forest University School of Medicine and Wake Forest University, Winston-Salem, NC