Electrical restitution hysteresis: good memory or delayed response?

Abstract

The action potential duration (APD) of ventricular myocytes depends on the length of the preceding diastolic interval (DI) in a relationship termed “electrical restitution.” The APD shortens with decreasing cycle length and thus with decreasing DI.1 The teleological advantage of this phenomenon is that it provides increased time for excitation-contraction coupling at long cycle lengths while preserving diastolic time for coronary perfusion and ventricular filling at short cycle lengths. Restitution of the APD may also lead to rich behavior in beat-to-beat APD fluctuations. At a fixed cycle length, a perturbation in action potential that shortens the APD results in concomitant lengthening of the next DI, given that CL=APD+DI. The restitution relationship dictates that a prolonged DI will lead to lengthening of the next APD. Thus, the initial perturbation results in alternation in APD between values that are shorter or longer than the steady-state APD. Whether the APD oscillations grow or decay depends on whether the slope of the restitution curve in the region near the steady state is greater than or less than unity.2 In the case of growing APD alternans, regions of myocardium may develop sufficiently long APD on some beats as to be rendered refractory to activation on the subsequent beat. This results in wavebreak and the substrate for reentry and fibrillation.3–5 But there is further complexity in electrical restitution in that the shape and duration of the action potential depend on more than just the DI of the preceding beat.6–9 The APD observed at any given DI is not unique and depends on the history of activation sequence leading up to that beat. In this issue of Circulation Research , Wu and Patwardhan10 report on APD restitution in canine isolated ventricular tissue preparations using oscillatory sequences of DI. These investigators made use …