To the Editor:
We read with
interest the article from Bitter et al. (1) published in the last volume of
JAFIB.
This
non-systematic review covers some of the most important physiopathological
aspects of the link between sleep disordered breathing (SDB) and atrial
fibrillation (AFib). We do agree with the authors on the role of hypertension,
endothelial dysfunction and inflammation. These topics were, to our
understanding and perspective, very well covered by the authors on this review.
However, despite
that the authors mentioned atrial remodeling a couple of times during their
review, we are not sure that this topic and specifically atrial electrical
remodeling, was properly discussed and referenced.
The
pathophysiology linking SDB to AF is multifactorial and may involve repetitive
hypoxemia, increased sympathetic drive, fluctuations in intrathoracic pressure
and systemic inflammation (2). These physiologic changes may induce structural
and electrical remodeling serving as a substrate to the development of AFib.
An indirect marker
for such electrical remodeling is the prolongation of atrial conduction time,
represented by increased maximum P-wave duration in the surface ECG. In a prior
study, we showed that an increased P-wave duration has been associated with SDB
(3). Interatrial block (IAB), defined as a surface P-wave duration > 120 ms,
was more prevalent in patients with moderate-severe SDB (34.7% SDB vs. 0%
controls, p <0.001). P-wave dispersion, a measurement that was linked to
development of new AFib, was also increased in patients with SDB (14.6±7.5 vs.
8.9±3.1, p<0.001). In linear regression, age and AHI (apnea/hypopnea index) >
25 were independent predictors of maximum P-wave duration (p=0.001 and p<0.001
respectively) (3).
Another
non-invasive method to determine atrial electrical remodeling is the Signal-averaged
P-wave (SAPW) duration. The SAPW duration represents the average of all P-wave
durations in a given number of consecutive heartbeats. We recently postulated
that SAPW would be useful to identify atrial electrical remodeling in patients
with severe SDB and that treatment with C-PAP for 4-6 weeks may induce reverse
atrial electrical remodeling (4). The results of this study have shown that
patients with severe SDB have a longer SAPW duration than controls (131.9 ±
10.4 vs 122.8 ± 10.5 ms; p = 0.04)
and that a significant reduction of the SAPW duration occurs after treatment
with C-PAP (131.9 ± 10.4 to 126.2 ± 8.8 ms; p < 0.001) (Figure 1) (4).
The shortening of
SAPW duration and surface P-wave duration represents more rapid inter-atrial
conduction and provides evidence for reverse atrial electrical remodeling. This
may indicate an additional benefit of treating patients with C-PAP, as this
evidence suggests that C-PAP may improve the anatomical and electrical
substrate for AFib. Reverse atrial electrical remodeling is a concept in
evolution, and several cardiovascular treatments may improve atrial dynamics
(5). It is of utmost importance, in the times of considering AFib ablation as
first line therapy for recurrent AFib; to be familiarized with the impact of
non-recognized/non-treated SDBs over the cardiac electrical system. Conventional
treatment for SDB as C-PAP may also represent a benefit in terms of
facilitating normal atrial conduction and reducing the risks associated with
AFib.
Credits: Adrian Baranchuk; Diego Conde