Abstract
Spontaneous electrical activity in the atria, primarily
near the pulmonary veins (PVs), is strongly linked with
triggers for atrial fibrillation (AF). However, mechanisms
of such triggered activity are incompletely understood.
In this study, we use electrophysiologically detailed atrial
cell models to investigate the role of late sodium current,
INaL, in the mechanisms of triggered activity. The model
simulations show that increases of this inward current
(seen in several conditions that predispose to AF) can
play a key role in the initiation of spontaneous diastolic
depolarisation in atrial cells. Sustained triggered activity
also requires contributions of other factors − increased
L-type calcium current and decreased potassium currents
− which are associated with -adrenergic stimulation of
atrial cells. The proposed mechanism is in agreement
with experiments showing that triggered activity can be
induced in the PVs primarily by -adrenergic stimulation
and stopped by ranolazine, a blocker of INaL. Triggered
activity in the model can be halted in fibrotic conditions,
when myocytes are coupled to fibroblasts. Hence, the
mechanism may be more relevant to paroxysmal AF.
| Original language | English |
|---|---|
| Title of host publication | Computing in Cardiology |
| Publisher | Computing in Cardiology (CINC) |
| Pages | 1021-1024 |
| Number of pages | 4 |
| Volume | 41 |
| ISBN (Electronic) | 978-1-4799-4347-0 |
| ISBN (Print) | 978-1-4799-4346-3 |
| Publication status | Published - 2014 |