4 Discussion
AF is a disease characterized by the disruption of cardiac mechanical
functions due to irregular atrial activation. There are initiating
factors that cause the onset of AF and an anatomical substrate that
maintains it. An important feature of AF is to an important feature of
AF is that the arrhythmia sustains itself when it begins. This is
possibly caused by remodeling occurring in the atrium. Atrial remodeling
occurs at electrophysiological, cellular, and anatomic levels [21,
15]. Many studies have shown the association between intra- and
interatrial conduction blocks and AF [22, 23]. It is thought that a
shortening in the atrial effective refractory period, inconsistency of
the atrial effective refractory period with changes in heart rate, and a
prolongation in atrial conduction time occur as a result of electrical
remodeling in AF [24]. Delay in interatrial and intra-atrial
conduction causes atrial refractoriness to be inhomogeneous.
In a study by Deniz et al. [25], it was shown that left intra-atrial
mechanical delay increased in patients with PAF and it was an
independent risk factor of PAF. Kumagai et al [26] showed that inter
and intra-atrial conduction was prolonged following electrical
cardioversion in patients with lone AF. In a study by Evranos et al.
[27] with patients who underwent cryoballoon, the intra-atrial delay
before and 3 months after the procedure was found to be a predictor of
late AF recurrence.
There may be fibrosis in the left atrium in AF, which causes anisotropy,
maintain anisotropic atrial conduction delay, changes intra-atrial
refractoriness, and leads to the continuity of reentrant arrhythmia. The
persistence of AF during the structural atrial remodeling process leads
to a reduction in the amount of connexin 40 and thus causing regional
conduction abnormalities that lead to reentrant pathways to maintain
themselves [28]. Radiofrequency (RF) catheter ablation has recently
been introduced as an important therapeutic option in patients with
drug-resistant atrial fibrillation (AF), with about a 75% success rate
[29, 30]. In our study, significant decreases were observed in
intra- and interatrial conduction times after RF ablation (PA lateral p:
0.022; PA septum p: 0.002; PA tricuspid p: 0.019; interatrial conduction
delay p:0.012; and intra-atrial conduction delay p:0.029). This result
suggests that providing stable sinus rhythm by the elimination of the AF
triggering mechanisms with RF ablation of pulmonary vein isolation may
slow down, stop or even improve structural remodeling at substrate level
secondary to AF even in patients who did not yet develop atrial fibrosis
and permanent structural changes. There is a linear relationship between
electrophysiological, structural, and cellular remodeling with the
increase of AF duration during the day in PAF patients, and this process
progresses towards permanent AF [15]. However, it is unclear whether
AF can produce additional forms of remodeling, especially when
arrhythmia remains sustained for long periods [31]. As also seen in
our study, preservation of sinus rhythm after pulmonary vein RF ablation
is expected to affect this process.
Sex differences may affect diagnostic and therapeutic interventions in a
wide variety of medical conditions including cardiac arrhythmias
[32]. In our study, when atrial conduction times were compared
before and after RF ablation according to sexes; no significant
difference was observed between the two groups in male patients, while
there were significant differences in all parameters except for
intra-atrial conduction delay in female patients. The reason was
probably due to the low number of male patients (14 patients; 28%) who
had atrial conduction time measurement after the procedure.