There has been much interest in identifying patients who are at risk of sudden death. Specifically, we need to know who is at risk for fatal arrhythmic episodes of ventricular tachycardia and/or ventricular fibrillation. Many studies in both the human electrophysiology laboratory and basic animal laboratory have found that regions of the heart involved with these life threatening arrhythmias are activated later than normal during the cardiac cycle. These so call, """"""""late potentials"""""""", have been observed from directly recorded endocardial and epicardial electrograms and from body surface leads with the special technology of the high resolution ECG (signal averaging). Thus, the promise is great for the wode spread use of this technique in the clinical setting. However, the fundamental bases contributing to the late potentials are not fully understood. This project aims to study late potentials in a well known animal model of late potentials and inducible ventricular arrhythmias. A thin rim of epicardium is the region from which late potentials originate. With multi-electrode mapping and in vitro microelectrode recordings we will characterize the nature of the cardiac generator and attempt to correlate these with the actual recordings of late potentials from the body surface. Such late potential parameters as duration, amplitude, and frequency content will be correlated with derived equivalent dipole generators (via the forward solution). The distribution of cellular properties, e.g., action potential, amplitude, and dV/dt, within the infarct zone will be analyzed with respect to the late potential measurements. Lidocaine, epinephrine, and heart rate will be used as a tool to modulate late potentials in the three recording milieus in order to strengthen our observations and conclusions regarding the fundamental bases of late potentials.
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