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.