['Using a rat in vivo infarct model we tested the hypothesis that fetal cardiomyocyte (FCM) implantation would increase repolarization heterogeneity.', 'Four groups of rats were studied: two groups served as controls and underwent injection with FCM or culture medium in a region of the left ventricle (LV) supplied by the left anterior descending artery (LAD), and two groups underwent LAD ligation followed 3 weeks later by the injection of either FCM or culture medium. Epicardial monophasic action potential (MAP) recordings were obtained 4 to 5 weeks after cell injection from the right ventricle (RV), LV infarction region and LV region remote from the LAD. The maximum difference in action potential duration (MAPD90) between the three sites was defined as repolarization heterogeneity.', 'LAD ligation (in the control media injection group) resulted in an increase in repolarization heterogeneity from 6.9 +/- 0.9 to 13.8 +/- 1.2 ms (p < 0.005). Similarly, injection of FCM without coronary ligation resulted in an increase in heterogeneity from 6.9 +/- 3.9 to 20.7 +/- 1.3 ms (p = 0.001). However, injection of FCM into regions of infarction did not result in an increase in heterogeneity when compared with the control media group (13.8 +/- 1.9 vs 13.0 +/- 2.6 ms, respectively, p = 0.752).'] Does cardiac myocyte transplantation increase global epicardial repolarization heterogeneity in a rat infarct model?