Atrial fibrillation (AF) is the most common sustained arrhythmia, and its prevalence continues to rise globally.1 Due to its frequently asymptomatic and underdiagnosed nature, the associated risk of ischemic stroke (IS) is likely underestimated.2 In a meta-analysis of 50 studies, AF was detected in approximately 24 % (95 % CI, 17 %–31 %) of patients with embolic stroke of undetermined origin, depending on the duration and type of monitoring used.3

Current guidelines for the diagnosis and management of AF recommend classification based on etiology (valvular vs. non-valvular), symptom status (symptomatic vs. asymptomatic), and clinical stage (e.g., “at risk for AF,” “pre-AF,” “paroxysmal,” “persistent,” “long-standing persistent,” “post-successful ablation,” or “permanent AF”).1

The concept of structural, histological, and electrical remodeling of the atria in patients with AF has been well described, both as a cause and a consequence of what is now referred to as atrial cardiomyopathy, which can be evaluated by various cardiac imaging modalities.4,5

AF pathophysiology is complex and involves multiple interacting factors: triggers (initiators of AF), substrates (which maintain AF), and perpetuators (which promote its progression)—summarized in the concept that “AF begets AF” .7,9 Several mechanisms have been proposed, including extracellular matrix remodeling, ion channel dysfunction, and electrical remodeling. Proposed electrophysiological theories include the multiple wavelet hypothesis, macro- and micro-reentry circuits, spiral waves, rotational activity, and focal triggers—primarily from the pulmonary veins (PV) and other atrial regions.

Approximately 90 % of paroxysmal AF cases are driven by PV foci and respond well to PV isolation. However, as the disease progresses, atrial remodeling becomes more extensive and often requires more complex ablation strategies.

Catheter ablation has been established as an effective therapy through multiple randomized trials and large registries, with its use expanding in parallel with technological advances.1 Current guidelines recommend catheter ablation as a first-line treatment in selected patients with symptomatic paroxysmal AF, as part of a shared decision-making strategy focused on rhythm control.6 When implemented early, ablation has been shown to reduce symptoms, recurrence, and AF progression more effectively than antiarrhythmic drugs.

Recurrences within the first three months post-ablation are often attributed to transient inflammatory processes related to the procedure. This period is therefore termed the "blanking period", during which AF episodes are not considered true recurrences.

Emerging evidence also suggests that early rhythm control may reverse atrial remodeling and reduce mitral and tricuspid regurgitation.7 However, some patients are less likely to benefit from ablation—particularly those with significant left atrial enlargement.

Various echocardiographic parameters, such as LA diameter, volume, strain, and tissue Doppler imaging, have been associated with post-ablation outcomes.8 Nevertheless, echocardiographic assessment has limitations, including reliance on geometric assumptions about atrial shape.

Cardiac computed tomography (CT) provides three-dimensional imaging that allows for accurate and reproducible LA volume measurements with minimal interobserver variability. Despite its routine use in pre-ablation evaluations—for assessing LA appendage thrombus, PV anatomy, and anatomical relationships with nearby structures—CT-derived atrial volumetry is not standardized and is not consistently performed.9,10

The aim of this study was to evaluate left atrial volume measured by cardiac CT and assess its prognostic value in predicting AF recurrence after catheter ablation.

Fig. 1, Fig. 2, Fig. 3, Fig. 4