Severity of tricuspid regurgitation predicts risk of atrial fibrillation recurrence after pulmonary vein isolation

Dimitrios Bismpos (Homburg/Saar)1, J. Wintrich (Homburg/Saar)1, A. Teusch (Homburg/Saar)1, V. Pavlicek (Homburg/Saar)1, P. Fischer (Homburg/Saar)2, F. Mahfoud (Homburg/Saar)1, M. Böhm (Homburg/Saar)1, C. Ukena (Homburg/Saar)1

1Universitätsklinikum des Saarlandes Innere Medizin III - Kardiologie, Angiologie und internistische Intensivmedizin Homburg/Saar, Deutschland; 2Universitätsklinikum des Saarlandes Innere Medizin III - Kardiologie, Angiologie und internistische Intensivmedizin, Universitätsklinikum des Saarlandes, Homburg/Saar Homburg/Saar, Deutschland


Background: Atrioventricular valve regurgitation (AVVR) results in atrial remodeling, thus promoting the formation of a substrate for atrial fibrillation (AF). On the other hand, AF may cause functional AVVR by annular dilatation of the atria. In this vicious circle, the identification of the leading pathomechanism and consequently the optimization of treatment can be challenging.  

Purpose: Our aim was to investigate whether the presence of significant AVVR and especially of tricuspid regurgitation (TR) affects the efficacy of catheter-based pulmonary vein isolation (PVI) for AF. Furthermore, we evaluated whether rhythm control for AF through PVI could lead to an improvement of AVVR severity. Finally we examined the effect of concomitant right atrial flutter on the arrhythmic outcome in patients with significant TR .

Methods: We enrolled patients undergoing first-time PVI for symptomatic AF. We compared the severity of AVVR at the time of the procedure as well as after 6 months, using transthoracic echocardiography. Moderate to severe AVVR was defined as significant. Moreover, we evaluated whether the presence of significant AVVR, at baseline and 6 months after the procedure, could serve as an independent predictor for AF recurrence. 

Results: Out of 320 consecutive patients (mean age 66.3 ± 10 years, 61.6% male, 60% paroxysmal AF) , significant TR at baseline was documented in 13.1%, while significant mitral regurgitation (MR) in 10.9%. Six months after PVI, the proportion of patients with moderate to severe TR (13.1% to 7.2%; p<0.001) and MR (10.9% to 6.6%; p<0.001) decreased significantly. Compared to patients with post-interventional improvement of significant TR, right atrial (RA) dilatation at baseline was more pronounced in patients with persistent significant TR (RA area 20.2 ± 4.4 vs. 26.6 ± 8.3 cm2; p=0.002). The presence of significant TR, particularly without improvement during the follow-up, independently increased the risk of atrial fibrillation recurrences. Even after propensity-score matching, TR at baseline remained an independent risk predictor regarding recurrent atrial fibrillation (HR 2.2 [95% CI, 1.1 - 4.9]; p=0.045). Among patients with significant TR, those with documented right atrial flutter were at high risk for recurrence of atrial arrhythmia (HR 2.69 [95% CI, 1.0 – 6.9]; p=0.039), despite the additional ablation of the cavo-tricuspid isthmus. Significant MR was not associated with increased risk of atrial arrhythmias.  

Conclusion: In patients with symptomatic AF undergoing PVI, the presence of moderate to severe TR, particularly without improvement 6 months after the procedure, was associated with a worse arrhythmic outcome. Further investigations to enhance the understanding of the underlying electrophysiological substrate and the need for tailored ablation strategies are warranted.
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