Premature beats undergo transmural conduction slowing due to intrinsic APD dispersion

Intrinsic regional differences in myocardial cell characteristics play an important role in the safety of intramural propagation for premature beats. A diseased condition which further reduces intramural coupling may exacerbate this heterogeneity leading to higher dispersion of refractoriness and vulnerability to reentry. Using a computer model of the ventricle, we demonstrate that this heterogeneity is sufficient to produce significant slowing of activation away from the stimulus site which is believed to increase the vulnerability of the heart to arrhythmia