Introduction: We hypothesized that drugs which alter ventricular refractoriness or excitability produce quantifiable changes in ventricular fibrillation.
Methods And Results: We used a 528-channel mapping system to quantify the effects of the beta-antagonist, propranolol, and the beta-agonist, isoproterenol, on activation patterns in ventricular fibrillation. A plaque of 506 (22 x 23) electrodes spaced 1.
Cardiac activation sequences are normally determined by (i) the detection and timing of local activations in cardiac electrograms, (ii) the grouping together of activations in different electrodes that are generated by the same activation fronts, and (iii) the construction by interpolation of isochronal maps showing the pathways of the activation fronts. This process is typically carried out by manual or semiautomated methods. These methods are usually adequate for stable, repeatable rhythms in normal hearts.
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