In contrast to right ventricular pacing that causes dyssynchronous contraction, appropriate left ventricular pacing seems to resynchronize the pattern of contraction when an intrinsic conduction disturbance is present, with the favorable pacing effect dependent, in part, on the site of left ventricular pacing. What is the mechanism by which this pacing-related benefit is achieved? Because hemodynamic improvement follows within a few beats after initiation of left ventricular pacing, it is reasonable to conclude that the direction of electrical depolarization originating from a left ventricular pacing site produces a more synchronous contraction than what exists with the intrinsic intraventricular conduction disturbance. An important question is whether this benefit from cardiac resynchronization therapy persists for some period of time after cessation of left ventricular pacing. Does left ventricular pacing induce favorable changes in the structure, orientation, and/or function of the contractile cardiac proteins that persist when pacing is stopped? This is an important question, for it may be that positive changes in protein expression occur with appropriate left ventricular pacing, and this could be considered a manifestation of favorable cardiac memory.