Abstract: | In recent years evidence has been brought forward supporting the hypothesis that myocardial infarction is not due to thrombotic occlusion of a coronary artery but to a metabolic derangement in a myocardium “conditioned” by coronary atherosclerosis. The author briefly reviews metabolic necroses experimentally induced in the animal and discusses the action of potassium in preventing their development. The basis for the clinical use of potassium and magnesium salts for the prevention of myocardial infarction is also discussed. |