ABSTRACT
Clinical and electrocardiographic findings were analyzed in 100 consecutive cases of LAD. Below the age of forty years, LAD was uncommon, but its incidence increased continuously thereafter. The most frequent primary clinical diagnosis was arteriosclerotic heart disease. The functional mechanism producing LAD most often was LAHB, responsible in about 40 per cent. Approximately half the instances of LAHB were associated with old myocardial infarction of septal, anterior, or lateral regions, but half were seen in the absence of infarction or clinical coronary sclerosis and are presumed due to primary degenerative processes within these specialized conducting fibers. Approximately one-sixth of the instances of LAD were due to loss of inferior forces following inferior myocardial infarction. Typical left ventricular hypertrophy was a distinctly uncommon cause of LAD. Last, in 24 patients with LAD the mechanism or cause was not evident initially, of which two were subsequently shown to represent a very mild degree of LAHB. Also it is suggested that asymmetric myocardial hypertrophy of the anterior wall may account for some instances of LAD not otherwise explained.
