  In this numerical study, we investigate the role of intrinsic heterogeneities
of cardiac tissue due to M cells in the generation and maintenance of reentrant
excitations using the detailed Luo-Rudy dynamic model. This model has been
extended to include a description of the long QT 3 syndrome, and is studied in
both one dimension, corresponding to a cable traversing the ventricular wall,
and two dimensions, representing a transmural slice. We focus on two possible
mechanisms for the generation of reentrant events. We first investigate if
early-after-depolarizations occurring in M cells can initiate reentry. We find
that, even for large values of the long QT strength, the electrotonic coupling
between neighboring cells prevents early-after-depolarizations from creating a
reentry. We then study whether M cell domains, with their slow repolarization,
can function as wave blocks for premature stimuli. We find that the inclusion
of an M cell domain can result in some cases in reentrant excitations and we
determine the lifetime of the reentry as a function of the size and geometry of
the domain and of the strength of the long QT syndrome.
