Background: Arrhythmia in myocardial ischemia has known to be mostly due to focal activity. We assess how focal discharges firing well under ischemic condition interact with rotors in the activation patterns to perpetuate VF. Methods: The rabbit hearts(n=3) were retrogradely perfused and action potentials from the left ventricle free wall were recorded using di-4-ANEPPS with a high speed CMOS camera (100x100 pixels, 1000 f/s). Epicardial optical action potentials were recorded with a photodiode array (26 �� 26 mm). Ischemia was produced by covering central portion of LV with glass and low perfusion flow. Results: The action potential duration(APD) was shortened (158 +/-1 vs.98 +/-4 ms at CL of 220ms) and conduction velocity(CV)(0.92 vs. 0.17m/s) decreased in ischemic heart, compared to non-ischemic heart. APD restitution curve in ischemic heart was less steeper compared to non-ischemic heart. APD, and CV were more heterogeneous and paced wave-front blocked more frequently in the core of ischemic zone, as pacing cycle length(CL) decreased. The highest dominant frequency (DF) of VF was low in ischemic heart than in control (4 vs.15.1Hz). DF,APD, and CV were more decreased in core of ischemic zone, but cycle length and diastolic interval increased during VF. During VF, focal ectopic beats originated intermittently from the ischemic core zone presenting short APD60 (78+/-27ms) and low CV(0.24 m/s) but did not propagated well. Some ectopic beats (10/39) arising from ischemic zone were converted to rotor circulating around the inexcitable ischemic zone, of which tail showed relatively long APD(78+/-13 vs 21+/5ms) and high CV(0.2+/-0.1 vs.0.08+/-0.02 m/s) Conclusions: Our results show that focal ectopic beats by triggered activity can advance to mother rotor of VF with the core in ischemic zone.