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M any targets for cardiovascular disease interventions- eg, smoking, high serum cholesterol level, and high blood pressure-are more clear-cut and easily defined than stress. Rather than being a unitary construct that can be indexed by a single number or condition, stress results from personal and environmental factors and the interactions between those factors. Despite this complexity, recent research has shown that it is possible to define and measure specific sources of personal and environmental stress that appear to increase risk of cardiovascular disease. In this section we review (1) state-of-the-art research on the impact of these sources of stress on risk of cardiovascular disease, the mechanisms of impact, and the effects on risk of interventions to reduce stress; (2) gaps in research on stress and risk of cardiovascular disease; and (3) recommendations for public policies, educational programs, and research relevant to stress and cardiovascular disease risk.
Williams et al. (Wed,) studied this question.