Abstract
The traditional mechanistic interpretation of myocardial anoxia and resulting types of heart disease, as being due exclusively to a disproportion between myocardial work or mass and coronary blood flow, is inadequate. It neglects the specific anoxiating action of an excessive influx of the sympathomimetic amines epinephrine and sympathin into the myocardium. These amines can exert their injurious and even fatal effects on the heart regardless of hemodynamic conditions and of the vol. of coronary flow.