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Publications [#277196] of Redford B. Williams

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Journal Articles

  1. Jr, RBW (1987). Psychological factors in coronary artery disease: Epidemiologic evidence. Circulation, 76(1 II SUPPL.), I-117-I-123.
    (last updated on 2019/04/19)

    This article reviews the epidemiologic evidence linking psychological factors and various indexes of coronary heart disease (CHD) that has been gathered since the Amelia Island Conference in 1978. In general, studies of populations not selected according to CHD risk support the conclusion that the global type A construct is predictive of increased risk of coronary events. In high-risk groups, including patients undergoing coronary angiography, the evidence with respect to global type A is much less clear. This stems from the fact that most of these studies, although generally failing to find statistically significant relationships between coronary events and type A behavior, are flawed in a number of ways, including inadequate statistical power of results, use of less than adequate instruments, and failure to take an apparent interaction between type A behavior and age into account. Nevertheless, taken together, these findings suggest that it may be possible to identify measures of coronary-prone behavior that are more powerful than the global type A measure. Extensive evidence suggests that such measures may be found in the domain of hostility and anger. Measures of hostility and anger coping styles have been found to be associated with coronary atherosclerosis in populations in which global type A was not related to disease, and measures of hostility have predicted increased coronary events and total mortality in prospective population samples followed for from 20 to 25 years. Preliminary evidence suggests that hostility/anger characteristics may account for the increased coronary risk associated with global type A behavior. Important goals for future research include identification of better measures of hostility/anger and related constructs and characterization of the biological mechanisms linking such characteristics to disease end points.

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