Stress, Catecholamines and Ischaemic Heart Disease

Abstract

While emotional stress has been implicated in the pathogenesis of cardiovascular disease, controversy still exists as to how exposure to stressful situations can induce such pathological changes. Emotional, environmental and sensory stress are all associated with the activation of both the sympathetic-adrenal medullary system (resulting in the release of the catecholamines, adrenaline and noradrenaline) and the pituitary-adrenal cortical system (with the release of the glucocorticoids, cortisol and/or corticosterone). There is considerable evidence linking the emotionally induced release of catecholamines with ischaemic heart disease. But it is not the catecholamines alone; the glucocorticoids also play an important role. There is a marked intensification of the cardiotoxic effects of the catecholamines by a glucocorticoid-catecholamine interaction. The interaction between the glucocorticoids and the catecholamines appears to have two phases. The first phase occurs when the circulating level of steroid is high and results in a potentiation of the cardiac stimulating action of the catecholamines. Without an adequate compensatory dilation of the coronary vessels myocardial hypoxia and necrosis will occur. The enhanced myocardial sensitivity to the catecholamines appears to be mediated by a delay in the inactivation of the catecholamines following their release, probably via an inhibition of both neuronal and extraneuronal uptake. The second phase of the interaction occurs when the circulating levels of the glucocorticoids have adapted to a lower level. Without the anti-inflammatory action of the steroids, the catecholamines initiate the release of endogenous inflammatory substances, the opening up of junctional gaps in the endothelial lining of the coronary vessels, and the aggregation of platelets. The resulting thrombosis and deposition of lipids in the coronary artery wall leads to myocardial infarction associated with coronary occlusion.