The heart has the capability to adjust to dynamic circumstances. This can be acute (e.g. during exercise) or chronic (as a result of a disease). In the latter, the new "steady state" is called ventricular remodeling and encompasses (molecular and functional) adaptations at the structural, contractile and electrical level. Besides benign adaptations responsible for maintaining cardiac output (compensation) and wall stress (cardiac hypertrophy), these remodeling processes also may be arrhythmogenic (electrical remodeling). In this presentation, the focus will be on electrical remodeling and arrhythmogenesis in a canine model of compensated hypertrophy: dogs with chronic AV block. The adaptations will be described on a functional and molecular level leading to 1) an unstable prolongation of ventricular repolarization, and 2) an enhanced susceptibility for drug induced Torsade de Pointes arrhythmias. Furthermore, a new surrogate parameter to identify repolarization lability will be introduced: beat to beat variability of ventricular repolarization (BVR).