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