The goal of the proposed research is to map the onset of ventricular fibrillation in a conscious animal model consisting of an old infarct plus acute ischemia. Activation wavefronts during fibrillation will be determined by recording from 126 chronically implanted intramural electrodes. The 3D anatomy of the old infarct, the degree of ischemia, and the status of the autonomic nervous system at the time of fibrillation will be determined. The investigators will determine the mechanism by which a pre-existing infarct increases the incidence of fibrillation caused by acute ischemia. They will determine (1) the site of origin of the initiating beat of fibrillation, e.g., the endocardial border, lateral border or central portion of the ischemic bed, (2) the mechanism by which this first beat occurs, e.g., reentry or focal, (3) the mechanism by which the old infarct makes fibrillation more likely, e.g., directly, by forming secondary reentrant circuits in the infarcted region, or indirectly by changing autonomic tone so that secondary reentry occurs more readily outside to infarcted region. Initial studies will be carried out in models in which time of the arrhythmias can be predicted to within one hour and, hence, can be performed using currently available mapping instrumentation. In order to study more realistic sudden death, the investigators proposes to develop telemetry methods to record and analyze data from chronically implanted electrodes for up to several months. They will use this technology to record long-term from instrumented animals that are untethered. This will allow the monitoring of animals in which the time of fibrillation cannot be anticipated, such as sudden death in which there is an old infarct or chronic heart failure but no acute ischemia.
| Johnson, Philip L; Newton, Jonathan C; Rollins, Dennis L et al. (2003) Adaptive pacing during ventricular fibrillation. Pacing Clin Electrophysiol 26:1824-36 |
| Kong, Wei; Walcott, Gregory P; Smith, William M et al. (2003) Emission ratiometry for simultaneous calcium and action potential measurements with coloaded dyes in rabbit hearts: reduction of motion and drift. J Cardiovasc Electrophysiol 14:76-82 |
| Zhou, Xiaohong; Huang, Jian; Ideker, Raymond E (2002) Transmural recording of monophasic action potentials. Am J Physiol Heart Circ Physiol 282:H855-61 |
| Johnson, Philip L; Newton, Jonathan C; Rollins, Dennis L et al. (2002) Intelligent multichannel stimulator for the study of cardiac arrhythmias. Ann Biomed Eng 30:180-91 |
| Smith, W M; Barr, R C (2001) The forward and inverse problems: what are they, why are they important, and where do we stand? J Cardiovasc Electrophysiol 12:253-5 |
| Cates, A W; Smith, W M; Ideker, R E et al. (2001) Purkinje and ventricular contributions to endocardial activation sequence in perfused rabbit right ventricle. Am J Physiol Heart Circ Physiol 281:H490-505 |
| Porras, D; Rogers, J M; Smith, W M et al. (2000) Distributed computing for membrane-based modeling of action potential propagation. IEEE Trans Biomed Eng 47:1051-7 |
| Fotuhi, P C; Chattipakorn, N; Rollins, D L et al. (2000) Effect of altering the left ventricular pressure on epicardial activation time in dogs with and without pacing-induced heart failure. J Interv Card Electrophysiol 4:561-8 |
| Rollins, D L; Killingsworth, C R; Walcott, G P et al. (2000) A telemetry system for the study of spontaneous cardiac arrhythmias. IEEE Trans Biomed Eng 47:887-92 |
| Barnette, A R; Bayly, P V; Zhang, S et al. (2000) Estimation of 3-D conduction velocity vector fields from cardiac mapping data. IEEE Trans Biomed Eng 47:1027-35 |
Showing the most recent 10 out of 77 publications
