© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Repolarizing currents in ventricular myocytes from young patients with tetralogy of Fallot
aInstitut für Medizinische Physik und Biophysik, Universität Graz, Harrachgasse 21, A-8010 Graz, Austria
bUniversitätsklinik für Chirurgie, Universität Graz, Auenbruggerplatz 5, A-8036 Graz, Austria
* Corresponding author. Tel.: +43-316-3807741; fax: +43-316-3809660 Schaffer{at}balu.kfunigraz.ac.at
Objective: It was the aim of our study to describe repolarizing currents in ventricular myocytes isolated from children with tetralogy of Fallot. This is the first report on outward currents in ventricular myocytes from children. Methods: Ventricular myocytes were isolated from tissue samples of the outflow tract of the right ventricle which were obtained during corrective surgery of tetralogy of Fallot. Action potentials and whole-cell currents were recorded with the patch clamp technique at a temperature of 36–37°C. Results: The mean resting potential was –71.7±1.92 mV, action potential amplitude was 110±2.96 mV and action potential duration at 90% repolarization was 794±99.5 ms (n=12). In four out of 12 myocytes early afterdepolarizations (EADs) were observed. Upon hyperpolarization Ba2+-sensitive inward currents similar to the inward rectifier current (IK1) could be observed. The current density at –120 mV was –22.8±2.47 pA/pF (n=14). A transient outward current (Ito1) could be recorded in all myocytes studied, the current density varied from 0.3 to 8.6 pA/pF with a mean of 3.77±0.47 pA/pF at +40 mV (n=38). Recovery of Ito1 from inactivation was fast (70% recovery within 100 ms), rate-dependent reduction amounted to 38.2% at 4 Hz. A delayed rectifier current was seen in only two out of 38 myocytes (rapid component IKr). Conclusions: The electrophysiological characteristics of right ventricular myocytes isolated from children with tetralogy of Fallot resemble in most cases subendocardial myocytes from adults. The most prominent difference is a fast recovery from inactivation as well as a small rate dependent reduction of Ito1. The observed EADs may have clinical implications.
KEYWORDS Arrhythmia (mechanisms); Congenital defects; Ion channels; Myocytes
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