Exploring the role of atrial arrhythmias in adults with congenital heart disease

In a comprehensive review about the role of atrial fibrillation (AF) in adults with congenital heart disease (CHD), Waldmann et al. [1] highlighted its association with adverse events and the need of further understanding its physiopathological mechanisms in order to improve outcomes. This should be even more emphasized from the recent evidence that atrial arrhythmias (AA) are the only modifiable predictor of sudden cardiac death and late mortality in patients with transposition of great arteries after atrial switch operation (TGA-ASO) [2]. TGA-ASO is the adult congenital heart condition with the highest risk of cardiac arrest [3]. The mechanisms through which AA potentially cause morbidity and mortality in CHD are multiple, including 1:1 conduction throughout atrio-ventricular node or accessory pathways, ischemia, preload reduction, embolism, systemic ventricle remodeling and consequent heart failure (HF) or ventricular arrhythmias. The interplay between AA and systemic ventricular dysfunction is noteworthy, not only among the sequelae of AA, but also among their triggers. This concept has been better studied in the wider spectrum of HF, in which AF affects over 20% of patients [4]. The question of whether the AF is a cause of ventricular dysfunction rather than merely one of its consequence, is relevant, especially in the era of catheter ablation as rhythm control option. At the same time, this has implications for the monitoring strategy of adults with CHD, since AA occurrence could be considered a clinical expression of impaired ventricular function [5] and lead to further patient assessment and a more accurate risk stratification.