Myocardial infarction (MI) is associated with an increased risk of atrial fibrillation (AF). We have shown that MI in rabbits decreases atrial L-type Ca2+ current (ICaL) in the presence of β-adrenergic (β-AR) stimulation (1). However, how MI or ICaL reduction may affect atrial action potentials (AP) in the intact heart is unclear. This study aims to examine effects of MI and pharmacological inhibition of ICaL on atrial electrophysiology in intact rabbit hearts using a voltage sensitive fluorescent dye excited by a light guide system. Methods: MI was induced in New Zealand White rabbits (~2.5 kg, n=6): rabbits were anaesthetised prior to thoracotomy (intravenous midazolam (0.2-0.5mg/kg), and ventilated with N2O/O2/1% isoflurane) with post operative analgesia given (Vetergesic (0.04mg/kg)). After 8 weeks, rabbits were sacrificed by intravenous administration of sodium pentobarbitone (100 mg/kg). Stock animals served as controls (CON, n=10). Hearts were removed and perfused in Langerdorff-mode with Tyrode’s solution in the presence of the mechanical uncoupler blebbistatin (10 μM). Hearts were loaded with the voltage-sensitive dye Di-4-ANEPPS. APs were recorded in the absence and presence of the β-AR agonist isoproterenol (ISO, 1 μM), or with ISO plus the Ca2+ channel blocker nifedipine (NIF, 0.02 and 2 μM). Hearts were either unpaced, or paced (5Hz) with bipolar electrodes. Data are expressed as mean±SEM, and compared by ANOVA or unpaired t-tests. P<0.05 was regarded as significant. Results: In unpaced hearts (mean rate=2.8Hz), MI increased atrial AP duration at 50% repolarisation (APD50), by 40% (66±4 vs 47±4 ms, P<0.01), and APD90 by 41% (117±7 vs 83±5 ms, P<0.01), respectively, vs CON. In paced hearts, MI increased APD50 , by 22% (67±6 vs 55±3 ms, P=0.07), and APD90 by 23% (114±3 vs 93±5 ms, P<0.01), respectively, vs CON. In unpaced CON hearts, ISO also significantly increased APD90, by 22% (101±4 vs 83±5 ms, P<0.05 (mean rate=4.3Hz)), but ISO had no significant effect on APD90 in MI hearts (mean rate= -ISO 2.7Hz, +ISO 4.2Hz). In paced hearts, ISO had no significant effect on APD50 or APD90 in either CON or MI hearts. In the presence of ISO, APD50 or APD90 were not significantly altered by MI in either unpaced or paced hearts. To mimic the reduction in atrial ICaL by MI, in the presence of β-AR stimulation, i.e. 30-40% (1), CON hearts were perfused with NIF at 0.02 μM and 2 μM. NIF significantly decreased APD50 and APD90 (0.02 μM: ~30%; 2 μM: ~50% in unpaced and paced hearts, P<0.01), in CON but not MI. Conclusion: Chronic MI in rabbits increases atrial APD in the absence, but not in the presence of β-adrenergic stimulation. Our data indicate that the atrial ICaL reduction seen in HF is not associated with altered APD.