Abstract
The atherogenetic uptake of low density lipoprotein (LDL) is accelerated by the catecholamines adrenaline and noradrenaline at their pathophysical blood concentrations in rabbits and rats. A similar effect in man could account for the coronary risk factor status of cigarette smoking, hypertension, stress, etc. when associated with elevated circulating catecholamines. In human atheromatous lesions, the concentration of macrophages is greater in plaques which have fissured or ulcerated than in those which have not. This is compatible with the proposition that macrophages contribute to plaque fissure, the commonest immediate cause of coronary thrombosis.
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