A morphologic study of the cardiac conduction system in ungulates, dog, and man

Glomset, Daniel J.; Glomset, Anna T.A.

doi:10.1016/s0002-8703(40)90530-0

Cited by 98 publications

(21 citation statements)

References 13 publications

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“…in nguate.Tis iffrene hsbeen stressed by An experiment with the object of studying the in ungulates. This difference has effects of thiamin deficiency on cardiac conduction Glomset and Glomset (1940). is described.…”

Section: Discussionmentioning

confidence: 90%

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Cardiac Lesions in Thiamin Deficiency

Jf¹

1948

Heart

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Experience of beriberi occurring among British and Australian prisoners of war indicated that heart block was not infrequent.There is no general agreement about the effect of thiamin deficiency on the heart, and in particular on cardiac conduction. The only electrocardiographic abnormality noted by Aalsmeer and Wenckebach (1929) was a shortening of the P-R interval. Keefer (1930) in 29 cases of beriberi noted no characteristic cardiographic change, though cardiac conduction was sometimes slightly altered: 15 of the 29 cases had evidence of cardiac insufficiency; these showed enlargement of the right auricle, right ventricle, pulmonary conus, and pulmonary artery. Jolliffe '(1939) in experimental thiamin deficiency found cardiographic changes in 2 of 5 human volunteers: in one, sinus arrhythmia, sinus arrest, and inversion of T III appeared after 11 days of deficiency, and in a second inversion of T III appeared after 8 days of deficiency. The changes reported by Weiss and Wilkins (1937) and by Dustin et al. (1939) included tachycardia, prolongation of electric systole, low voltage complexes, and flattening or inversion of T waves. Dock (1940) recorded 5 cases of idiopathic cardiac hypertrophy with mural thrombi thought to result from thiamin deficiency, in 4 of whom there was disturbance of conduction-right bundle branch block in 3 and latent A-V block in 1 case. Casanova (1946) observed flat bifid P waves, prolongation of the P-R interval, and auricular fibrillation (once) in beriberi.Most accounts of the pathology of the heart in beriberi have been limited to a description of the macroscopic abnormalities. It is uncertain whether the enlargement of the right side of the heart is due to dilatation alone or to dilatation combined with hypertrophy.Weiss and Wilkins (1937) found that the weight of the heart was generally normal and that there was a moderate dilatation of the right ventricle. Wenckebach (1934) and Weiss and Wilkins (1937) observed a " hydropic" degeneration of the muscle fibres.Disturbances of A-V conduction are not mentioned in most clinical accounts qf beriberi and lesions affecting the specialized muscle of the conducting system have not been noted on histological examination. Thus Blankenhorn (1945) gave as the first of the criteria for the diagnosis of beriberi heart disease " an enlarged heart with normal sino-auricular rhythm."As there is no general recognition of the appearance of conduction defects in human thiamin deficiency it was thought advisable to record the clinical impression of its not infrequent occurrence. In the light of our clinical experience it was considered that analysis of the effects upon cardiac conduction of prolonged severe thiamin deficiency in animals would be of value and should determine whether the changes present had a functional or organic basis. EXPERIMENTAL METHODSPigs were used since they are known to be the animals most susceptible to thiamin deficiency. The animals were obtained when five weeks old. The dietetic method was largely that of Wintrobe (19...

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Section: Discussionmentioning

confidence: 90%

“…Glomset and Glomset (1940) have shown that in man Purkinje cells do not exist in the main bundle nor in the upper part of the right branch. The cells that are described as Purkinje elements in the left branch and lower part of the right branch differ markedly from those found in ungulates.…”

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confidence: 98%

Cardiac Lesions in Thiamin Deficiency

Jf¹

1948

Heart

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“…These were described as 'granules' ('K6rner') by Purkinje (1845) and are to-day known as 'Purkinje cells'. Histologists describe them as short, thick cylinders with peripheral myofibrils, two to five of them in cross-section making up a fibre (Wahlin, 1935;Glomset & Glomset, 1940;Truex & Copenhaver, 1947). It may be asked whether the boundaries of these cells are comparable to ordinary cell membranes in the sense that they represent effective barriers to the movement 23-2 SILVIO WEIDMANN of ions.…”

Section: Discussionmentioning

confidence: 99%

The electrical constants of Purkinje fibres

Weidmann¹

1952

The Journal of Physiology

606

266

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“…Isolated collections of Purkinje fibres have been described in different parts of the atria by a few observers in various mammals, and Todd & van der Stricht (1919) claimed that Purkinje fibres are present in all parts of both atria in the adult human heart; this latter claim is not substantiated by other workers. Recently, Glomset & Glomset (1940) claimed to have found muscle fibres identical in size and structure with those usually associated with the SPA. node in many places in both atria and ventricles in a number of mammalian hearts.…”

Section: Homoiothermal Vertebratesmentioning

confidence: 99%