Abstract 16685: Obstructive Fibrosis Related to Transverse Conduction Slowing in Chronic Atrial Fibrillation
Introduction: Patients with paroxysmal atrial fibrillation (AF) often transition between sinus rhythm and AF. For AF to initiate there must be both a trigger and a substrate that facilitates reentrant activity. This trigger is often caused by a premature atrial contraction or focal activations within the atrium.
Hypothesis: We hypothesize long strands of continuous fibrosis act as a substrate that slows conduction, but only after a premature contraction.
Methods: A high density electrode plaque was placed on 13 controls and 6 chronic AF goats (an average of 6 months of rapid pacing induced AF). Conduction slowing following a premature contraction was quantified. Atrial fibrosis was quantified into two groups, non-obstructive and obstructive fibrosis. Obstructive fibrosis was considered fibrosis that was at least the length of a myocyte (100 μm), thus potentially disrupting transverse cell to cell conduction. Non-obstructive fibrosis had a length less than 100 μm.
Results: Conduction velocity of the AF goats was significantly slowed compared to the control goats in the transverse direction (0.40±0.03 m/s vs. 0.53±0.15 m/s, p<0.05) but not in the longitudinal direction (0.70±0.27 m/s vs. 0.76±0.18 m/s, p = N.S.) following a premature atrial contraction. The AF goats had more obstructive fibrosis than the controls (18±8 fibers/mm2 vs. 9±3 fibers/mm2, p<0.05). The control group trended towards more non-obstructive, diffuse fibrosis than the AF animals (1109±309 fibers/mm2 vs. 718±380 fibers/mm2, p = 0.07, N.S).
Conclusions: Structural and electrophysiological remodeling in chronic AF leads conduction velocity slowing transverse to fiber orientation. Histology from goats with a history of chronic AF had more obstructive fibrosis, which may lead to the conduction slowing and alteration in conduction pathways to make the tissue more susceptible to AF. The amount of obstructive fibrosis may be more important to AF outcomes than the total density of fibrosis.
Author Disclosures: N.A. Angel: None. L. Li: None. R.S. MacLeod: None. N. Marrouche: None. R. Ranjan: None. D.J. Dosdall: None.
- © 2015 by American Heart Association, Inc.