RESUMEN
OBJECTIVE: The aim was to investigate the antifibrillatory effects of two concentrations of propafenone by means of signal analysis of epicardial ECG recordings in isolated, Langendorff-perfused guinea-pig hearts. METHODS: Isolated Langendorff-perfused guinea-pig hearts were used as a model for sustained ventricular fibrillation (VF) during reperfusion after global ischaemia. ECG signals were recorded for the first 20 min of reperfusion. The recording was divided into episodes of 1 s and the median frequency (FM) of the dynamic power spectrum was computed for each episode. Cardiac electrical activity was monitored for an additional 10 min. Additionally steady state conditions (i.e. constant FM values for the remaining observation period) were analysed and the effects of 0.1 microM and 1.0 microM propafenone added at reperfusion on the FM were examined. RESULTS: After initial irregularities, FM remained on a high steady state level in the control group. The addition of propafenone 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 microM propafenone caused spontaneous conversion to stable sinus rhythm 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 microM propafenone, 5 out of 6 hearts spontaneously converted to stable sinus rhythm. The sixth heart showed repeated switching between VF and periods 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 stability of the sinus rhythm was correlated inversely with the FM immediately 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.
Asunto(s)
Antiarrítmicos/farmacología , Pericardio/efectos de los fármacos , Propafenona/farmacología , Animales , Relación Dosis-Respuesta a Droga , Electrocardiografía/efectos de los fármacos , Femenino , Cobayas , Masculino , Perfusión , Pericardio/fisiopatología , Procesamiento de Señales Asistido por Computador , Fibrilación Ventricular/tratamiento farmacológico , Fibrilación Ventricular/fisiopatologíaRESUMEN
Verapamil is supposed to suppress the initiation of circus movement supraventricular tachycardia by affecting the atrioventricular node. In electrophysiological tests, programmed stimulation is usually performed by using the same location for pacing and premature stimulus. Spontaneous ectopic activity starts from a different location than the sinus node and can therefore find altered re-entry conditions. In this study a 3D computer model based on Huygen's principle is used for simulation of the spread of excitation in the human heart in combination with a posterobasal, right or left lateral accessory pathway (AP). The effect of verapamil on properties of the atrioventricular node were modelled by prolonging the effective refractory period and basal conduction time. For each of the three APs, ectopic foci at the atrial base and between sinus node and AP were modelled at various coupling intervals for investigating re-entrant activation. In the control state (without verapamil) only orthodromic echoes were found. The maximum echo zone (EZ) range was found near the AP. If stimuli were selected further away from the AP on the atrial basis, the EZ range decreased until no EZ was found. The EZ range decreased from it's maximum value near the AP, towards the difference of the effective refractory periods between AP and AV-node near the sinus node Verapamil abolished the EZ in case of a posteroseptal AP. For a lateral AP the administration of verapamil resulted in an orthodromic and antidromic EZ depending on the atrial premature activation site. A maximum orthodromic EZ was found for premature stimuli near the AP. As stimulus site moved away from the AP, the EZ range first decreased continuously to zero leading eventually to an antidromic EZ. These findings suggest the important influence of the site of premature stimuli with respect to the accessory pathway and AV-node on the inducibility of atrial re-entry.
Asunto(s)
Antiarrítmicos/uso terapéutico , Nodo Atrioventricular/efectos de los fármacos , Simulación por Computador , Modelos Cardiovasculares , Verapamilo/uso terapéutico , Síndrome de Wolff-Parkinson-White/tratamiento farmacológico , Complejos Atriales Prematuros/fisiopatología , Nodo Atrioventricular/fisiopatología , Estimulación Cardíaca Artificial , Estimulación Eléctrica , Sistema de Conducción Cardíaco/fisiopatología , Humanos , Periodo Refractario Electrofisiológico/efectos de los fármacos , Nodo Sinoatrial/efectos de los fármacos , Nodo Sinoatrial/fisiopatología , Síndrome de Wolff-Parkinson-White/fisiopatologíaRESUMEN
A computer simulation study is performed to investigate the method of current density reconstruction to localise myocardial ischaemia. A computer model of the entire human heart is used to simulate the excitation and repolarisation process in eight topographically different cases of myocardial ischaemia. The associated magnetocardiogram is calculated at 37 positions of the KRENIKON biomagnetic measurement equipment. The method of current density reconstruction is applied at the S-point (the last discernible deviation from the ST-segment at the end of the QRS-complex) of the MCG to find characteristics of the myocardial ischaemia simulated by the model. The results show that it is possible to determine the location of the ischaemia. The current density distribution may be interpreted physiologically in terms of the so-called 'injury-current'. This indicates that magnetocardiography might be a suitable method for noninvasive ischaemia diagnosis, and further investigations of the current density reconstruction method for the injury current should be performed on patients with ischaemic heart disease.