Cellular electrophysiological changes in "round heart disease" of turkeys: A potential basis for dysrhythmias in myopathic ventricles

Stanly Einzig, Barry Lee S. Detloff, Barbara K. Borgwardt, Nancy A. Staley, George R. Noren, David G. Benditt

Research output: Contribution to journalReview articlepeer-review

18 Scopus citations


Summary: Arrhythmias are commonly recorded in "round heart disease", a presumed viral, congestive cardiomyopathy of turkeys. To assess whether cellular electrophysiological changes may be associated with arrhythmia susceptibility, we compared transmembrane action potential characteristics in left and right ventricular endocardial muscle fibres from 19 inbred myopathic turkeys with findings in 13 normal control turkeys (age 1 to 74 days). In left ventricular tissue, as a group, action potential duration at 50% repolarisation (APD50) was reduced in myopathic hearts (201 ± 6(SEM) vs 228 ± 9 ms in controls, P <0.01), while the maximum rate of phase 0 (dV/dtmax) action potential amplitude, diastolic resting membrane potential and action potential duration at 90% repolarisation (APD90) did not differ from control turkeys. By contrast, in myopathic right ventricular tissue, as a group, both APD50 (186 ± 5 vs 206 ± 4 ms in controls) and APD90 (208 ± 4 vs 228 ± 3 ms in controls) were shorter (P <0.01). The plateau potential in both right and left ventricular tissue was significantly higher in inbred turkeys.Since a spectrum of cardiac dilatation and hypertrophy is present in myopathic turkeys, we examined the effect of hypertrophy on action potential characteristics. In "round heart disease" turkeys, left ventricular hypertrophy was characterised by reduced dV/dtmax (98 ± vs 274 ± 26 V s-1, P <0.01) and right ventricular hypertrophy by further shortening of both APD50 (174 ± 7 vs 202 ± 6 ms, P <0.01) and APD90 (193 ± vs 224 ± 5 ms, P <0.01), but no change in dV/dtmax (105 ± 13 vs 120 ± 9 V s-1, P = NS). These results indicate that certain electrophysiological differences (eg reduced action potential duration), may, in part, contribute to dysrhythmia susceptibility in this presumed viral cardiomyopathy model.

Original languageEnglish (US)
Pages (from-to)643-651
Number of pages9
JournalCardiovascular Research
Issue number11
StatePublished - Nov 1981

Bibliographical note

Funding Information:
This work was supported in part by grant HL18204 from the National Institutes of Health, the Dwan Family Fund and a grant from the American Heart Association, Minnesota Affiliate.


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