Complete heart block (CHB) was observed in 24 of 350 patients with myocardial infarction who were studied under conditions of continuous electrocardiographic monitoring. CHB occurred predominantly in posterior and anteroseptal infarctions. In posterior infarction CHB was observed in patients who also developed first degree (10) and types I and II second degree (2°-I and 2°-II) atrioventricular (A-V) block but not bundle-branch block (BBB). In anteroseptal infarction CHB was found in patients with BBB, occasionally in patients with 2°-II A-V block, but not in patients with 1°a nd 2°-I A-V block. Right BBB with a Q wave in lead V1 was the usual form of BBB observed in patients with CHB and anteroseptal infarction. One mechanism for sudden death in anteroseptal infarction is the abrupt development of CHB following the onset of BBB. Evidence is presented attributing CHB to a lesion in the A-V node in posterior infarction and to bilateral BBB in anteroseptal infarction.
Additional Indexing Words: Bilateral bundle-branch blockWenckebach's phenomenon Complete heart block Type II second degree A-V block Stokes-Adams attacks IN RECENT YEARS there has been considerable interest in continuous electrocardiographic monitoring of patients with acute myocardial infarction during the early stages of their disease.1 One purpose of this surveillance has been to detect disturbances of atrioventricular (A-V) conduction that lead to complete heart block (CHB) with critical slowing of the ventricular rate or the complete absence of ventricular depolarization. As yet, none of the reports2-8 on electrocardiographic monitoring have specifically dealt with abnormalities signaling impending CHB, although Lown and associates7 have stated that in general advanced degrees of block develop slowly, allowing time for lifesaving interventions such as electrical pacing.9-12Our interest arose from the observation that some patients developed CHB abruptly from one atrial beat to the next without antecedent dropped ventricular beats or prior abnormality of the P-R interval. In this group the rapidity of the course did not allow time for the initiation of pacing once CHB occurred. Clearly, death could be avoided only if it were possible to recognize in advance those patients prone to this arrhythmia. To this end we reviewed electrocardiograms obtained by continuous monitoring in 350 patients with a diagnosis of acute myocardial infarction (table 1). From this total, 24 patients with CHB were identified. When the data were examined, certain patterns emerged which might allow more accurate prediction of CHB.
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