[Behavior of late ventricular potentials in acute experimental myocardial ischemia].

Locally retarded depolarizations of the ischaemic myocardium are regarded as frequent trigger mechanisms of dangerous ventricular arrhythmias. Up to now, however, there are scarcely systematic investigations concerning their concrete developmental conditions in man, since late potentials can be made evident only by means of expensive invasive methods or signal mediation techniques. Therefore, an animal model should be built, which is suitable for the control of new therapy conceptions with antiarrhythmic drugs. The investigations were performed on 22 pigs in whom under insufflation anaesthesia altogether 10 pressure, flow and contractility parameters as well as 6 epicardial ECG signals were continuously recorded. The episodes of ischaemia were caused by LAD occlusions of different duration and intensity. Typical late potentials could be registered in 5 animals who all had survived complete interruptions of the coronary blood flow of longer than 10 min. The mean duration of the late potentials was 20 +/- 9.2 ms, their amplitudes reached from 150 to 600 microV. Also with regard to time and cycle constancy, the delay of the late Q-potential and the morphology they corresponded to the homogeneous phenomenon, known from man. They always could be derived only from electrodes outside the immediate zone of ischaemia. Neither partial occlusions nor complete interruption of the coronary blood flow in intervals shorter than 10 minutes led to the development of a late potential. The animal model used altogether appears very suitable to investigate the medicamentous influencibility of arrhythmogenic areas of the myocardium under direct control of the dynamic behaviour of ventricular late potentials.