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(Circulation. 1961;24:41.)
© 1961 American Heart Association, Inc.

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A Histopathologic Study of the Atrioventricular Communications in Two Hearts with the Wolff-Parkinson-White Syndrome

MAURICE LEV M.D.¹; REXFORD KENNAMER M.D.¹; MYRON PRINZMETAL M.D.¹; QUINTILIANO H. DE MESQUITA M.D.¹

¹ From the Congenital Heart Disease Research and Training Center, Hektoen Institute for Medical Research, the Departments of Pathology of North-western University Medical School, and The University of Chicago School of Medicine, Chicago, Illinois, the Institute for Medical Research, Cedars of Lebanon Hospital, Los Angeles, California, and the Cardiovascular Institute of the Matarazzo Hospital, São Paulo, Brazil.

The atrioventricular communications and the AV node, bundle, and bundle branches of two cases with the WPW syndrome were studied histologically. One case was that of chronic Chagas' myocarditis and the other possible chronic Chagas' myocarditis.

Accessory muscular communications in the right atrioventricular junction were found in one heart, and no communications outside the conduction system in the other.

Inflammatory changes were found in the conduction system of both hearts.

The literature of the anatomic changes in hearts with the WPW syndrome, and that with the presence of accessory atrioventricular muscular communications without the WPW syndrome are reviewed.

From the study of the literature and of our two cases, it appears that some cases of the WPW syndrome are associated with accessory communications and others are not, and accessory communications may be present without this syndrome. Of the four cases with this syndrome, however, in which a thorough study has been made of all possible conduction pathways, three showed accessory communications. On the other hand, inflamatory changes in the pre-atrioventricular nodal area, AV node, bundle and bundle branches have been found in many cases of the WPW syndrome.

It is thus clear that an anatomic base has as yet not been established for the WPW syndrome. It is possible that a different mechanism may be responsible in different cases. The high incidence of inflammation of the conduction system in the studied cases makes accelerated conduction an attractive hypothesis, where no accessory bundles have been found. More correlative histologic and clinical work needs to be performed in this field.

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