Significance of marked left axis deviation

Left axis deviation: a reassessment.

“…32 If these observations are correct, then any leftward shift in the QRS axis with normal adult aging, including left anterior hemiblock, would represent part of a spectrum of unifascicular conduction delay.32 In the study of 8000 Japanese-American men referred to In discussing the sequence or coincidence of atherosclerotic coronary artery disease and left axis deviation, electrocardiographic-pathologic correlative studies have identified frequent myocardial fibrosis and infarction attributed to coronary artery disease. 14, 16,27,28,30 It is rational to infer, in this setting, that ischemic heart disease in its own right causes fibrosis that partially or completely interrupts conduction in one or more fascicles. This mechanism presupposes a decrease in flow via the coronary circulation to or relatively near specialized atrioventricular conduction pathways, especially the infranodal system.…”

“…Experimental laceration of the left anterior aspect of the primate (baboon) ventricular septum was then shown to produce marked left axis deviation ascribed to interruption of the anterior rami of the left bundle branch.26 Neither thickness of the left ventricular wall per se, nor electrical position of the heart, were considered important in the development of left axis deviation.26 An electrocardiographic-necropsy study of 96 adults reaffirmed that left ventricular hypertrophy in itself was not responsible for left axis deviation, and implicated instead a conduction defect in the anterior division of the left bundle branch. 27 In 1966, a comprehensive study by Pryor et al of the clinical significance of left axis deviation dealt with the roles of both acquired and congenital heart disease, emphasizing that the left axis shift occurred in endocardial cushion defect, congenitally corrected transposition of the great arteries, type B preexcitation, tricuspid atresia and single ventricle.28 These authors not only suggested hyperkalemia as a newly recognized reversible cause of left axis deviation, but also commented on "pseudo-left axis deviation" in pulmonary emphysema, and observed that surgical injury to the superior division of the left bundle could cause left axis deviation after operation for congenital discrete aortic stenosis or idiopathic hypertrophic subaortic stenosis.28 There was conflicting opinion as to whether two anatomically distinct left branches existed, but the authors argued compellingly that it was conceptually important to consider the fibers of the left bundle as if they were arranged in superior and inferior divisions in order to approach rationally the diseases that alter the sequence of depolarization of myocardium supplied by these proposed radiations. 28 Other investigators soon considered the gradual leftward migration of the frontal QRS axis, concluding that this electrocardiographic trend was a common sequel of aging, independent of the population prevalence of coronary atherosclerosis.29 Soon thereafter, a study of 353 necropsy patients ages 19-94 years indicated that the lesion causing left axis deviation in most cases involved the anterior-superior division of the left bundle branch.…”

On the Significance of the Negative T Wave Pattern in Lead AVL in Horizontal Heart

“…Regarding this point one must remember that there are some other electrocardiographic patterns which are caused by a parti cular rotation of the electrical axis and by an abnormal divergence between the QRS axis and T vectors in some leads on the horizon tal plane: T, < Ts [5,6,13]; TVj > TVe [8,9,It,14]; marked left axis deviation beyond -30°C [1,3,4,7,12]. Like the syn drome 'T negative in aVL', these tracings also appear normal in all other respects, except for the above-mentioned electrocardiographic patterns.…”

“…Some authors have described these patterns as an early electrocardiographic sign of left ventricular strain or as a damage of the lateral wall of the left ventricle. Such statement cannot be accepted unreservedly: clinical investigations [8,9] and necroscopic observations [3,4,7,14] have shown that, although a significant number of these subjects who manifest these patterns have myo cardial disease, in certain number of cases these syndromes re presented a normal variant of the electrocardiogram.…”