Abstract
Spatial vectorcardiograms were obtained in five patients with clinical, enzymatic and electrocardiographic evidence of inferior wall myocardial infarction in which the scalar recordings were suggestive of left posterior hemiblock associated with complete right bundle branch block. The frontal plane vectorcardiogram showed abnormal rightward deviation of the maximal QRS vector which could not be attributed to right ventricular hypertrophy, pulmonary disease, extensive lateral myocardial infarct or an extremely vertical heart. Symptomatic A-V block occurred in all cases. The initial 10, 20 and 30 msec were superiorly oriented in two of the four patients with inferior wall myocardial infarction. Wide Q waves in lead aVF were also present. When inferior wall myocardial infarction coexisted with LPH the presence of normal, or small, q waves suggested that the infarction was not transmural, or that an incomplete left bundle branch block or an anteroseptal infarction were present. A-V conduction disturbances appearing in patients with inferior wall myocardial infarction and bifascicular block were of the Wenckebach or Mobitz type. In the former instance the block was in the A-V node; in the latter case it was below the His bundle. The incidence of left posterior hemiblock can be higher than frequently assumed considering that the current criteria, although highly specific, are not sensitive enough. Spatial vectorcardiograms were obtained in five patients with clinical, enzymatic and electrocardiographic evidence of inferior wall myocardial infarction in which the scalar recordings were suggestive of left posterior hemiblock associated with complete right bundle branch block. The frontal plane vectorcardiogram showed abnormal rightward deviation of the maximal QRS vector which could not be attributed to right ventricular hypertrophy, pulmonary disease, extensive lateral myocardial infarct or an extremely vertical heart. Symptomatic A-V block occurred in all cases. The initial 10, 20 and 30 msec were superiorly oriented in two of the four patients with inferior wall myocardial infarction. Wide Q waves in lead aVF were also present. When inferior wall myocardial infarction coexisted with LPH the presence of normal, or small, q waves suggested that the infarction was not transmural, or that an incomplete left bundle branch block or an anteroseptal infarction were present. A-V conduction disturbances appearing in patients with inferior wall myocardial infarction and bifascicular block were of the Wenckebach or Mobitz type. In the former instance the block was in the A-V node; in the latter case it was below the His bundle. The incidence of left posterior hemiblock can be higher than frequently assumed considering that the current criteria, although highly specific, are not sensitive enough.
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