EFFECTS OF ACTIVATION SEQUENCE ON THE SPATIAL-DISTRIBUTION OF REPOLARIZATION PROPERTIES

The electrotonic effects of activation spread on the spatial distribut ion of repolarization properties were studied in animal experiments an d with computer simulations. Refractory periods (RPs) were measured at 36 sites within a 1.0 cm(2) region of the epicardial surface of the c anine pulmonary conus during 37 drives in 11 experiments. In each expe riment three or four sites along the perimeter of the region bounding the RP test sites were driven. Activation propagated uniformly during some and nonuniformly during other drives in the same animals. In gene ral, RPs were distributed uniformly when activation spread uniformly a nd nonuniformly when activation spread nonuniformly. The authors obser ved RP differences as large as 16 ms between sites with 2 mm separatio n during drive from some epicardial sites in these normal canine heart s. Indices of nonuniformity of activation and of relative RP values we re used to quantify the relation between nonuniformity of activation s pread and the spatial distribution of the RP. There was a significant negative correlation between nonuniformity of activation and RP indice s during the 19 drives in which activation spread nonuniformly. This i ndicated that RPs were relatively long at sites where activation sprea d decelerated and relatively short at sites where activation spread ac celerated. When nonuniform activation spread was simulated by introduc ing high-resistance barriers in a model with fixed anisotropic conduct ivities, there were marked spatial variations in action potential dura tion. The spatial variations in action potential duration were negativ ely correlated to acceleration and deceleration of activation spread. The major new finding of this study is that the spatial distributions of RPs are markedly affected by activation spread. Since both char act eristics of activation sequence and nonuniformity of RP distributions have roles in reentrant arrhythmias, the findings suggest that some si tes of origin of premature activity may be more arrhythmogenic than ot hers. The findings may also explain why ventricular tachycardia can so metimes be initiated from one but not from other sites in patients und ergoing electrophysiologic testing.