Background - Our objective was to create an animal preparation displaying long term electrical alterations following chronic regional energetic stress without myocardial scarring. Methods - An ameroid (AM) constrictor was implanted around the left circumflex coronary artery (LCx) two weeks before initiating chronic rapid ventricular pacing (CRP) at 240/min for 4 weeks (CRP-AM). Comparisons were made with healthy canines (H) and canines with either AM or CRP. Unipolar electrograms were recorded from 191 sites in the LCx territory in open-chest, anesthetized animals during sinus rhythm and while pacing at 120-150/min, with bouts of transient rapid pacing (TRP: 240/min). Results - In CRP-AM and AM, ST segment elevation was identified at central, and ST depression at peripheral sites, both increasing with TRP. In CRP-AM and CRP, -dV/dt_max of activation complexes were significantly depressed and activation-recovery intervals (ARI) prolonged. Areas of inexcitability as well as irregular isocontour patterns displaying localized ARI shortening and gradients >20ms between neighboring sites were identified in one third of CRP-AM at slow rate, with increasing incidence and magnitude in response to TRP. In CRP-AM, programmed stimulation induced marked conduction delay and block as well as polymorphic ventricular tachycardias, which stabilized into monomorphic under lidocaine or procainamide. Whole-cell Na⁺ current and channel protein expression were reduced in CRP-AM and CRP. Despite complete constrictor closure, small areas of necrosis were detected in a minority of CRP-AM. Conclusion - Long term electrical alterations and their exacerbation by TRP contribute to arrhythmia formation in collateraldependent myocardium subjected to chronic tachycardic stress.