relevant situations being sampled, we could determine cognitive appraisal and emotional response differences between high and low hostile subjects. Already results from one study ( Suarez & Blumenthal, 1991) suggest that among coronary patients with high Ho scores, higher SBP levels are significantly positively associated with self-reported ratings of emotional stress.
Second, our findings of a divergent relationship between lipids and reactivity in Type A and B persons as well as in hostile and nonhostile persons suggest a new avenue of research, that of biologically synergistic relationships between traditional CHD risk factors and hostility in determining reactivity. Thus, we can begin to ask the question: How do traditional risk factors alter the physiological responses patterns of high and low hostile subjects? Our preliminary data already suggest that lipids can moderate the response pattern associated with hostility, but other factors may also have a similar impact on hostility-related reactivity. For example, smoking has been associated with increased reactivity to stressful stimuli ( MacDougall, Dembroski, Slaats, Herd, & Eliot, 1983). It would seem likely that hostile persons who smoke may be at greatest risk of CHD, and thus exhibit the greatest magnitude of reactivity to socially relevant stressors. Equally as important, nonhostile persons who smoke may obviate the "protective" quality afforded by being nonhostile, and thereby exhibit exaggerated physiological responses to behavioral stressors.
Third, it will be important to obtain measures of vagal tone in future studies of the generalizability of hostility effects and of the impact of lipids on reactivity. This will permit us to determine whether reactivity to interpersonal conflicts and the effects of lipids on this reactivity are mediated in any way by the weak parasympathetic function we are observing in coronary-prone person.
The aim of this chapter was to present new approaches that may prove useful in understanding the complexity of not only behaviorally induced reactivity but also the potential CHD risk associated with coronary-prone behaviors. At the very least we have made an attempt to develop new models that are based on empirical evidence while reflecting our conceptual and theoretical framework of the behavioral and biological links to CHD. What is clear from our approach is that future studies should aim at investigating the interactive effects of psychological, biological, and environmental factors on physiological reactivity and CHD risk.
Airaksinen K., Ikaheimo M. J., Linnaluoto M. K., Niemela M., & Takkunen J. T. ( 1987). "Impaired vagal heart rate control in coronary artery disease". British Heart Journal, 58, 92-597.