5.1. Histological insights into LACV slowing
The main determinants of myocardial conduction velocity are inter-cellular gap junction function and intracellular depolarization. These are in turn considered to be influenced by tissue fibrosis:9-11 Myocardial tissue with interstitial fibrosis is reported to demonstrates gap junction remodeling, including the depletion and abnormal distribution of gap junctions, which result in conduction disturbance.9 Moreover, myocardial fibrosis promotes myocyte-myofibroblast coupling and elevates myocyte resting membrane potential, causing conduction velocity to decrease by inhibiting the depolarization process of cell membrane.10 In addition, an elevated membrane potential may shorten action potential duration and refractory period. Finally, both conduction disturbance and a short refractory period likely contribute to the development of reentrant circuits and AF persistence.11