Cardiac late potential signals and sources.

Most studies of cardiac late potentials (LPs) recorded from the body surface use signal processing definitions to characterize these abnormal ventricular potentials. For many years, the focus of the clinical studies have been on those signals that outlast the QRS complex; however, cardiac mapping studies have clearly identified that the such abnormal activation occurs during the QRS complex as well and can be distinguished from normal QRS potentials using advanced signal processing tools. Thus, both the abnormal intra-QRS potentials and the LP represent a continuum of the same signal sources. The electrogram recordings of these signals are often characterized as multiphasic with ambiguous/multiple depolarization times spanning tens of milliseconds within very short distances (b1.0 mm). The biophysical basis for these ambiguities does not fit conventional theories of cardiac propagation. This work examines the role that myofibroblasts (MFs) may play in facilitating conduction and producing very long conduction delays (10-30 milliseconds) between populations of close but isolated regions of normal cells. The prerequisite element of this hypothesis is that the MF can express gap junction proteins that align with the corresponding proteins in the myocardial cells. Membrane responsiveness studies of the MF did not detect, as expected, any ion channels capable of producing significant transmembrane currents or depolarizing potentials. However, in tissue-cultured preparations of neonatal mouse myocytes, a nonconducting gap (200-400 μm) was seeded with MF, and this gap was electrotonically bridged by the MF resulting in conduction velocities of 0.1 m/s. Such passive cell mediation of cardiac conduction would provide a biophysical explanation of LP as well as forming the basis of several hypothesized mechanisms of cardiac arrhythmias, such as microreentry. A fiber model using a series of coupled Luo-Rudy cardiac cell models was interspersed with a simple resistor-capacitor model of the MF, which then demonstrated a range of conduction disorders including excessive delays (N30 milliseconds) and decremental conduction. Hence, the role of this passive cell coupling in the generation of abnormal patterns of conduction as well as arrhythmogenesis has yet to be fully determined but may in fact define another mechanism of cardiac conduction.