Psychological factors in ischemic heart disease.

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 a clotting tendency (S-RV/clotting), hypercortisolemia, and neurohumoral arousal. The AHT grew mainly out of a literature review4 that provided evidence that risk and preventative factors for IHD and other disorders have opposite actions; major risk factors (such as stress, cholesterol, smoking, and homocysteine) express S-RV/ clotting, and major preventative factors (such as vitamins, aspirin, and exercise) express the opposite combination of vasodilation-of-resistance vessels (V-RV) and an anticlotting tendency (V-RV/anticlotting). The opposite actions of S-RV/clotting by risk factors and V-RV/anticlotting by preventative factors seem consistent with risk factors causing disease by shifting homeostasis inappropriately and preventative factors improving disease by correcting this adverse shift. Rozanski et al1 discussed a possible mechanism by which behavior therapies might operate, namely, improvement in coronary endothelial function. This improvement implies reduction of vasoconstrictive tendencies of resistance vessels, thus preventing S-RV. The AHT focuses on vasoconstrictive endothelial dysfunction, and the AHT is based in part on the S-RV concept,4,5 which asserts that S-RV induces symptoms in IHD.