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Aim and Methods: To analyze the relationship of Purkinje and endocardial focal VT versus epicardial reentry VT to varying ischemic size (IS), one hundred seven alpha chloralose anesthetized dogs were studied with 3-D mapping before and after coronary artery occlusion (CAO) with or without collateral ligation (LIG) to vary IS and distribution. IS was measured as % of all electrograms recorded which had voltage drop >45% with CAO. Mapping localized the origin of reproducibly induced VT. Results: VT was similar in the LIG (77%, n=65) and non-LIG groups (75%, n=42). IS was larger in the LIG group 51±3% vs 34±2% (p<0.05). Epicardial reentry was more prevalent in LIG (80%) than non-LIG (24%, p<0.01). However, focal VT dominated in non-LIG group (63%, p<0.05). Regardless of infarct size, Purkinje focal VT originated from sites with ischemia in Purkinje (50%) or muscle (25%) recorded on the same electrode as Purkinje, while the additional 25% were only adjacent to ischemia <10 mm away. Endocardial focal VT was similar. Dogs without focal VT had 50% fewer ischemic Purkinje sites (p<0.01). In vitro data confirmed action potentials from ischemic sites showing depolarization, triangulation and triggered activity compared to normal tissue. Conclusions: Infarct size plays a major role in mechanism of VT. Larger infarcts have more epicardial reentry; small infarcts facilitate focal VT because of ischemia in endocardium and Purkinje. [ABSTRACT FROM AUTHOR]