Dhein S, Müller A, Klaus W
Institute of Pharmacology, University of Cologne, FRG.
Basic Res Cardiol. 1990 May-Jun;85(3):285-96. doi: 10.1007/BF01907117.
The aim of our studies was to examine the electrophysiological conditions prior to the onset of arrhythmia in order to analyze in more detail whether arrhythmia is a sudden event or whether there are early signs preceding arrhythmia. For this purpose a computer-assisted mapping system equipped with 256 AgCl-electrodes for unipolar epicardial multichannel-recording was constructed that provided high temporal and spatial resolution (4 kHz/channel; 1 mm interelectrode distance). The electrodes were fixed to the surface of an isolated rabbit heart (prepared according to the Langendorff-technique; constant perfusion pressure 70 cm H2O; Tyrode solution equilibrated with 95% O2 and 5% CO2 at 37 degrees C) covering nearly the whole heart's surface. The activation times at each electrode were determined as the timepoints of the fastest negative deflection of the epicardial potentials. From these data the origins of epicardial activation were determined ("breakthrough points", BTP), and for each electrode a vector was constructed giving direction and velocity of the epicardial activation. This analysis was carried out for single heart beats under control conditions, under arrhythmogenic conditions (induced either by lowering the K+ concentration from initially 5.4 to finally 2.0 mmol/l or by application of ouabain 0.1, 0.2 or 0.3 mumol/l) or during manifest arrhythmia. By comparison of heart beats under these various conditions with control conditions we determined the percentage of identical BTP (deviating less than 1 mm) and of similar vectors (deviating less than 5 degrees). Under control conditions 80% BTP remained unchanged over a period of 60 min and about 30% of the vectors were similar. Reduction of the extracellular K(+)-concentration or treatment with ouabain resulted in a progressive, concentration-dependent decline in BTP- or vector-similarity (in still rhythmically beating hearts). In some cases these treatments finally lead to variant forms of arrhythmia. Critical values for the onset of arrhythmia were a reduction to 45% BTP-similarity and 18% vector-field-similarity. From these results it is concluded that arrhythmia is preceded by a state characterized by a derangement of the typical activation pattern which may be called prearrhythmia.
