Left axis deviation induced experimentally in a primate heart

Watt, Thomas B.; Murao, Satoru; Pruitt, Raymond D.

doi:10.1016/0002-8703(65)90186-9

Cited by 78 publications

(14 citation statements)

References 4 publications

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“…Watt and Pruitt (17), using intact dog hearts, were able to produce some epicardial delay with rather large septal lacerations in the distribution of the major divisions but could not produce significant frontal axis shifts. Watt et al were able to produce axis shifts in a primate heart (35), and attributed their results to species differences in the conducting system.…”

Section: Myerburg Nillson Gelbandmentioning

confidence: 99%

Physiology of Canine Intraventricular Conduction and Endocardial Excitation

Myerburg

Nilsson

Gelband

1972

Circulation Research

181

111

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The sequence of conduction through the intraventricular conducting system and endocardial muscle was studied by microelectrode mapping of large areas of isolated canine ventricular tissue. We found that most of the endocardium of the right ventricular free wall is activated simultaneously whereas the left endocardial muscle is activated in an apex-to-base sequence. Right septal activation is from apex to base, and the left septum is activated first at the junction of the middle and lower thirds of the septum and then as a bidirectional wave front toward the apex and the base. These right-left differences occur because the sites of impulse input into muscle on the right encompass the entire free wall, base of the papillary muscle, and the lowermost septum, and on the left are primarily limited to the lower ventricular cavity, lower septum, and bases of the papillary muscles. These patterns of left ventricular excitation relate to the presence of a functionally continuous ring of conducting tissue formed by a merger of the major divisions of the left bundle branch on the upper left ventricular free wall. The "ring" itself is electrophysiologically isolated from muscle, but connects to a network of subendocardial conducting tissue extending to the apex and having input to muscle only in its lower portions. KEY WORDSAV conduction papillary muscles bundle branches conducting system Purkinje fibers cardiac electrophysiology septal activation myocardial activation ventricular muscle• The relationship between the anatomy of the intraventricular portion of the AV conducting system and the physiology of AV conduction and ventricular excitation is pertinent to our understanding of major areas of cardiac electrophysiology. The nature and location of impulse input from the intraventricular conducting system into the ventricular myocardium, the physiological interactions between conducting tissue and ordinary muscle cells, and the sequence of activation of the endocar-Downloaded from curred, but the apex-to-base muscle activation persisted. White numbers on black background = conducting cells; black numbers on white background = muscle cells.

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Section: Myerburg Nillson Gelbandmentioning

confidence: 99%

Physiology of Canine Intraventricular Conduction and Endocardial Excitation

Myerburg

Nilsson

Gelband

1972

Circulation Research

181

111

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“…The explanation for this in IMI is probably contained in the classic concept of unopposed and enhanced anterior and superior forces due to the loss of muscle posteroinferiorly. Because the early transseptal forces may be maintained intact, the departure from normal does not begin in this group until well within or after the normal Q time zone.12 Experimentally produced LAFB in animals has been found to shift the mean QRS axis superiorly23 24 and to delay the activation time of the epicardium of the lateral basal surface of the left ventricle.25 The normal net direction of spread of depolarization, therefore, is presumably altered in LAFB, permitting abnormal spread of depolarization anteriorly and superiorly from the region already activated through the left posterior fascicle. Thus, this abnormal, superiorly directed positivity in LAFB arises from slight initial delay, sustained dysynchrony, and abnormality of direction of activation of the territory supplied by the left anterior fascicle.…”

Section: Discussionmentioning

confidence: 95%

Distinguising features of left anterior fascicular block and inferior myocardial infarction as presented by body surface potential mapping.

Sohi¹,

Flowers²

1979

Circulation

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Total body surface maps obtained from 19 patients with previous inferior myocardial infarction (IMI) were compared with maps obtained from 19 patients with left anterior fascicular block (LAFB) and six more patients in whom electrocardiographic changes were indistinguishable between IMI and LAFB. Three distinguishing features were detected: 1) abnormal high anterior positivity developed both in IMI and LAFB, but its onset was earlier in LAFB; 2) a broad rim of abnormal right lower negativity was seen in both groups, but in IMI it was within the first 40 msec, whereas in LAFB it was found in the middle and later parts of depolarization; 3) abnormal left lower negativity was seen in all the patients with LAFB, but was absent in IMI. Thus, despite similarities in the abnormalities detected, we found definite temporal and topographical differences that should aid in differentiating between IMI and LAFB in ambiguous cases.

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“…These pathophysiological considerations suggest, therefore, that a selective histological investigation of the conducting system would be indicated rather than a search for pathological 'foci' somewhere in the heart. Indeed, lesions of the conducting system are not only credited with enhancing cardiac desynchronization in general, but the lesions of the bundle-branches, the left in particular, are held to have a precise bearing on shifts of QRS axis (Watt, Murao, and Pruitt, 1965;Rosenbaum, 1970).…”

Section: Discussionmentioning

confidence: 99%