The long range goal of this research is to identify specific biological mechanisms responsible for associations between indices of coronary heart disease (CHD) and such psychological characteristics as Type A behavior and high levels of hostility. The following specific aims are proposed for the period covered by this application. 1) Complete studies currently ongoing to determine whether men with more severe coronary atherosclerosis (CAD) on coronary angiography exhibit increased neuroendocrine responses to laboratory challenge than men with minimal CAD. 2) Determine the physiological mechanism responsible for the greater suppression of EKG T-wave amplitude we have observed in Type A as compared to Type B men during IV infusions of isoproterenol. 3) Continue pilot studies to evaluate the effects of high levels of hostility/cynicism on cardiovascular responses to laboratory challenges. 4) Evaluate the generalizability of responses observed in the laboratory to more naturalistic field conditions. Regarding aim #1, male patients with varying levels of angiographically documented CAD will perform mental arithmetic and vigilance tasks in the laboratory. If men with more severe CAD exhibit elevated neuroendocrine responses to the laboratory challenge in comparison to men with less severe CAD and normals, it will support the hypothesis that excessive neuroendocrine responses are involved in atherogenesis. Regarding aim #2, we shall evaluate the effects of beta and cholinergic blockade and stimulation on the T-wave suppression with isoproterenol infusion. Regarding aim #3, cardiovascular responses to harassment while performing laboratory tasks will be evaluated in men with high vs. low scores on the MMPI Hostility (Ho) scale. Excessive responses among high Ho scorers will provide important evidence regarding biological mechanisms for the increased CHD risk among hostile persons.
Aim #4 will be accomplished by having subjects in all studies under aims 1-3 collect 24 hour urine samples which will be assayed for key hormones and metabolites. If significant correlations are found with hormonal secretion in the laboratory studies, we will conclude that effects found in the laboratory do generalize to field conditions. Successful completion of these studies will help to increase our understanding of biological mechanisms responsible for the increased CHD risk among Type A persons and persons with high hostility levels. Such knowledge could lead eventually to better methods of CHD prevention.
| Muranaka, M; Lane, J D; Suarez, E C et al. (1988) Stimulus-specific patterns of cardiovascular reactivity in type A and B subjects: evidence for enhanced vagal reactivity in type B. Psychophysiology 25:330-8 |
| Williams Jr, R B (1987) Refining the type A hypothesis: emergence of the hostility complex. Am J Cardiol 60:27J-32J |
| Dembroski, T M; MacDougall, J M; Williams, R B et al. (1985) Components of Type A, hostility, and anger-in: relationship to angiographic findings. Psychosom Med 47:219-33 |
