Background The abnormal transmembrane action potentials of subendocardial Purkinje fibers that survive 24 to 48 hours after coronary artery occlusion can be a source of the multiform ventricular tachycardias that occur during this time. A change in the density or function of either or both the T-type and L-type cardiac Ca2+ channels may contribute to the altered electrical activity of these Purkinje myocytes.Methods and Results The purpose of this study was to determine the function of the T- and L-type Ca2+ currents (iCatand iCaL, respectively) in Purkinje myocytes dispersed from the subendocardium of the left ventricle 24 and 48 hours after coronary artery occlusion (IZPC24and IZPC48, respectively). To do this we compared whole-cell Ca2+ currents from Purkinje myocytes enzymatically dispersed from free-running fiber bundles (SPCs), from the subendocardium of the noninfarcted canine heart (NZPCs), and from IZPC24and IZPC48. ICaLand iCatwere recorded with Cs sup + - and EGTA-rich pipettes and in Na sup + -K sup + -free external solutions to eliminate overlapping currents. ICaLdensity was significantly reduced in IZPC48compared with NZPC or IZPC sub 24. This was not accompanied by a shift in the current-voltage relation or by a change in the time course of decay of iCaL. Replacement of Ca sup 2+ with equimolar Ba2+ increased iCaLdensity in all cell types, but peak iBaLof IZPC48remained reduced compared with control iBaLvalues. T-type Ca2+ currents were recorded in all SPCs and NZPCs. In IZPC24and IZPC48there was a reduction in peak iCatamplitudes and densities. This was not accompanied by a shift in the current-voltage relation or by a change in the time course of decay of peak iCat. However, there was a hyperpolarizing shift in the steady-state availability relations in both IZPC24and IZPC48. In addition, the maximally available iCatin IZPC24was not different from control, whereas it was significantly reduced in IZPC48.Conclusions The L-type ICadensity in subendocardial Purkinje myocytes that survive in the infarcted heart is significantly decreased by 48 hours after the time of coronary artery occlusion. The peak T-type ICadensity is decreased in subendocardial Purkinje myocytes that survive in the infarcted heart at 24 hours, but further reduction occurs in these myocytes by 48 hours. This loss in Ca2+ channel function could contribute to the abnormal transmembrane potentials of these myocytes surviving in the infarcted heart. (Circulation. 1994;89: 2747-2759.)