{'fraction_non_alphanumeric': 0.01096319498825372, 'fraction_numerical': 0.0, 'mean_word_length': 5.726315789473684, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
On the mechanism of sustained ventricular arrhythmias associated with acute myocardial infarction.

The effects of rapid ventricular epicardial stimulation on the cardiac rhythm were studied in eight dogs, five days after coronary artery ligation, and in eight controls. Various degrees of ventricular arrhythmias were noted upon cessation of stimulation in the coronary ligated animals only. These post stimulation rhythm disorders were directly related to the frequency of stimulation. The QRS complexes of the post stimulation arrhythmias were of multiform configuration and were entirely different from the ones recorded during stimulation. Also, similar configuration of post stimulation arrhythmias could be observed following stimulation at widely separated sites. Both the mode of initiation and of termination of the post stimulation arrhythmias support the presence of circus movement around and in the infarction as the basis of sustained ventricular arrhythmias in acute myocardial infarction. The present study suggests also that the acutely damaged myocardial tissue becomes both a source for ectopic activity and an obstacle, around which re-entry circuits may be produced by these ectopic ventricular beats, and prolonged ventricular arrhythmias thus sustained.