EFFECTS OF PROPAFENONE ON THE MEDIAN FREQUENCY OF VENTRICULAR-FIBRILLATION IN LANGENDORFF PERFUSED GUINEA-PIG HEARTS

Citation
U. Eggenreich et al., EFFECTS OF PROPAFENONE ON THE MEDIAN FREQUENCY OF VENTRICULAR-FIBRILLATION IN LANGENDORFF PERFUSED GUINEA-PIG HEARTS, Cardiovascular Research, 31(6), 1996, pp. 926-931
Citations number
25
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
00086363
Volume
31
Issue
6
Year of publication
1996
Pages
926 - 931
Database
ISI
SICI code
0008-6363(1996)31:6<926:EOPOTM>2.0.ZU;2-#
Abstract
Objective: The aim was to investigate the antifibrillatory effects of two concentrations of propafenone by means of signal analysis of epica rdial ECG recordings in isolated, Langendorff-perfused guinea-pig hear ts. Methods: Isolated Langendorff-perfused guinea-pig hearts were used as a model for sustained ventricular fibriliation (VF) during reperfu sion after global ischemia. ECG signals were recorded for the first 20 min of reperfusion. The recording was divided into episodes of 1 s an d the median frequency (FM) of the dynamic power spectrum was computed for each episode. Cardiac electrical activity was monitored for an ad ditional 10 min. Additionally steady state conditions (i.e. constant F M values for the remaining observation period) were analysed and the e ffects of 0.1 mu M and 1.0 mu M propafenone added at reperfusion on th e FM were examined. Results: After initial irregularities, FM remained on a high steady state level in the control group. The addition of pr opafenone altered the steady state value of FM in a dose-dependent and significant manner but had no effects on the time until steady state was reached. During reperfusion without propafenone, 1 out of 6 hearts spontaneously converted to a stable sinus rhythm. Reperfusion with 0. 1 mu M propafenone caused spontaneous conversion to stable sinus rhyth m in 1 out of 6 hearts and intermittent periods of sinus rhythms in 2 additional hearts. During the first 30 min of reperfusion with 1.0 mu M propafenone, 5 out of 6 hearts spontaneously converted to stable sin us rhythm. The sixth heart showed repeated switching between VF and pe riods of non-sustained sinus rhythm. Conclusion: Propafenone caused a dose-dependent decrease of FM at steady state conditions. The rate of spontaneous termination of VF appeared to be dose dependent and the st ability of the sinus rhythm was correlated inversely with the FM immed iately before spontaneous defibrillation. Therefore, in this model the FM value prior to spontaneous termination of VF may be useful in the estimation of defibrillation success.