Abstract
Within a few minutes after its onset, intense pain of acute myocardial infarction was abolished by briefly spraying the precordium with ethyl chloride. Prompt relief of pain did not prevent tissue necrosis, but may have ameliorated the clinical course. We infer that the stimulus for pain in acute infarction is of extremely short duration but gives rise to a secondary, self-sustaining pain cycle which may be terminated by altering the flow of nerve impulses from the skin. The case also illustrates the increased susceptibility to digitalis which develops some days after myocardial infarction.