Why the study?
What are the neuroendocrine correlates of the Type A behavior pattern and their potential pathogenic role in coronary artery disease?
What are the neuroendocrine correlates of the Type A behavior pattern and their potential pathogenic role in coronary artery disease?
This review highlights that heightened sympathetic and HPA axis reactivity, along with potentially lower DHEA-S levels, may serve as neuroendocrine mediators linking Type A behavior to increased coronary artery disease risk.
Neuroendocrine reactivity may mediate Type A CAD risk; leaves open causal validation in prospective studies.
Various studies have tried to identify the possible neuroendocrine correlates of the action/emotion complex defined as Type A behavior pattern. Type A subjects have been observed quite consistently to respond to laboratory stressors with a greater sympathetic nervous system response than Type B subjects. There also seems to be a trend towards a hyperactivity of the hypothalamic-pituitary-adrenocortical axis in Type A individuals. The clinical relevance of these findings lies in the fact that there is an increasing clinical and laboratory evidence of a pathogenic role of catecholamines in coronary artery disease (CAD) and that some of these neuroendocrine correlates might actually be the mediators of the risk of CAD conferred by the Type A behavior pattern. We hypothesize that dehydroepiandrosterone-sulfate (DHEA-S), an adrenal weak androgen, is inversely correlated with the degree of Type A behavior pattern and this hypothesis seems to be confirmed by the results of a preliminary investigation that we have conducted.
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Fava et al. (1988) studied this question.
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