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Research Article Free access | 10.1172/JCI116540

Myocardial electrical propagation in patients with idiopathic dilated cardiomyopathy.

K P Anderson, R Walker, P Urie, P R Ershler, R L Lux, and S V Karwandee

Cardiology Division, University of Utah Medical Center, Salt Lake City.

Find articles by Anderson, K. in: JCI | PubMed | Google Scholar

Cardiology Division, University of Utah Medical Center, Salt Lake City.

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Cardiology Division, University of Utah Medical Center, Salt Lake City.

Find articles by Urie, P. in: JCI | PubMed | Google Scholar

Cardiology Division, University of Utah Medical Center, Salt Lake City.

Find articles by Ershler, P. in: JCI | PubMed | Google Scholar

Cardiology Division, University of Utah Medical Center, Salt Lake City.

Find articles by Lux, R. in: JCI | PubMed | Google Scholar

Cardiology Division, University of Utah Medical Center, Salt Lake City.

Find articles by Karwandee, S. in: JCI | PubMed | Google Scholar

Published July 1, 1993 - More info

Published in Volume 92, Issue 1 on July 1, 1993
J Clin Invest. 1993;92(1):122–140. https://doi.org/10.1172/JCI116540.
© 1993 The American Society for Clinical Investigation
Published July 1, 1993 - Version history
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Abstract

Myocardial propagation may contribute to fatal arrhythmias in patients with idiopathic dilated cardiomyopathy (IDC). We examined this property in 15 patients with IDC undergoing cardiac transplantation and in 14 control subjects. An 8 x 8 array with electrodes 2 mm apart was used to determine the electrical activation sequence over a small region of the left ventricular surface. Tissue from the area beneath the electrode array was examined in the patients with IDC. The patients with IDC could be divided into three groups. Group I (n = 7) had activation patterns and estimates of longitudinal (theta L = 0.84 +/- 0.09 m/s) and transverse (theta T = 0.23 +/- 0.05 m/s) conduction velocities that were no different from controls (theta L = 0.80 +/- 0.08 m/s, theta T = 0.23 +/- 0.03 m/s). Group II (n = 4) had fractionated electrograms and disturbed transverse conduction with normal longitudinal activation, features characteristic of nonuniform anisotropic properties. Two of the control patients also had this pattern. Group III (n = 4) had fractionated potentials and severely disturbed transverse and longitudinal propagation. The amount of myocardial fibrosis correlated with the severity of abnormal propagation. We conclude that (a) severe contractile dysfunction is not necessarily accompanied by changes in propagation, and (b) nonuniform anisotropic propagation is present in a large proportion of patients with IDC and could underlie ventricular arrhythmias in this disorder.

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