A retrospective evaluation of catheter ablation in atrial flutter post cardiac transplantation

Abstract

Background: Atrial flutter is the most common arrhythmia post cardiac transplantation. Observational studies in the non-transplant population have shown prognostic benefit with catheter ablation; however, there are no data in the heart transplant population.

Frequency, Risk Factors, and Clinical Outcomes of Late-Onset Atrial Flutter in Patients after Heart Transplantation

“…Late-onset post-transplant AFL is a common complication late after HTX and plays an important role in the clinical management of HTX recipients [ 20 ]. Previous studies reported late-onset post-transplant AFL rates ranging from 8.0% to 11.5% [ 25 , 26 , 28 , 29 ]. Pavri and colleagues [ 28 ] published a late-onset post-transplant AFL rate of 8.0% (7 of 88) and Anselmino and colleagues [ 29 ] found a late-onset post-transplant AFL rate of 11.5% (42 of 364).…”

“…While post-transplant atrial fibrillation often occurs in the early stage after HTX, atrial flutter (AFL) is a common atrial arrhythmia late after HTX [ 20 ]. The late onset of AFL after HTX may be the result of chronic changes caused by cardiac allograft vasculopathy and repeated graft rejection episodes [ 20 , 21 , 22 , 23 , 24 , 25 ]. Several authors have described an association between late-onset AFL after HTX and recurring episodes of graft rejection which can lead to myocardial damage including inflammation, edema, fibrosis and scar tissue resulting in cardiac remodeling as well as graft dysfunction [ 20 , 21 , 22 , 23 , 24 , 25 ].…”

“…The late onset of AFL after HTX may be the result of chronic changes caused by cardiac allograft vasculopathy and repeated graft rejection episodes [ 20 , 21 , 22 , 23 , 24 , 25 ]. Several authors have described an association between late-onset AFL after HTX and recurring episodes of graft rejection which can lead to myocardial damage including inflammation, edema, fibrosis and scar tissue resulting in cardiac remodeling as well as graft dysfunction [ 20 , 21 , 22 , 23 , 24 , 25 ]. Areas of atrial fibrosis and scar tissue provide a damaging electrophysiological milieu most conducive to AFL [ 20 , 21 , 22 , 23 , 24 , 25 ].…”

“…Several authors have described an association between late-onset AFL after HTX and recurring episodes of graft rejection which can lead to myocardial damage including inflammation, edema, fibrosis and scar tissue resulting in cardiac remodeling as well as graft dysfunction [ 20 , 21 , 22 , 23 , 24 , 25 ]. Areas of atrial fibrosis and scar tissue provide a damaging electrophysiological milieu most conducive to AFL [ 20 , 21 , 22 , 23 , 24 , 25 ]. In addition, the risk of late-onset AFL is increased in HTX recipients with biatrial anastomosis as this HTX technique results in enlarged atrial cavities with distorted anatomy and two long surgical suture lines of donor and recipient atria providing a highly proarrhythmic substrate [ 17 , 20 , 21 , 22 , 23 , 24 , 25 , 26 ].…”

“…Areas of atrial fibrosis and scar tissue provide a damaging electrophysiological milieu most conducive to AFL [ 20 , 21 , 22 , 23 , 24 , 25 ]. In addition, the risk of late-onset AFL is increased in HTX recipients with biatrial anastomosis as this HTX technique results in enlarged atrial cavities with distorted anatomy and two long surgical suture lines of donor and recipient atria providing a highly proarrhythmic substrate [ 17 , 20 , 21 , 22 , 23 , 24 , 25 , 26 ].…”