The central point: A DECAAF II data analysis evaluated 119 patients with persistent atrial fibrillation and left ventricular dysfunction (ejection fraction ≤50%). The main finding: 60.5% of these patients had arrhythmia-induced cardiomyopathy, defined as ejection fraction reaching ≥50% after ablation with an absolute improvement of at least 10 points, or an absolute improvement ≥15 points. The most important predictor for identifying these patients before the procedure was the amount of interatrial septal fibrosis assessed by MRI. Patients with less septal fibrosis were more likely to recover heart function.
The clinical dilemma: did the arrhythmia cause heart failure, or is it the reverse?
Patients with persistent atrial fibrillation and reduced ejection fraction represent a common clinical scenario. The challenge is determining whether ventricular dysfunction was caused by the arrhythmia (arrhythmia-induced cardiomyopathy, also known as tachycardiomyopathy) or whether the arrhythmia is a consequence of a heart already diseased for another reason.
This distinction directly affects treatment decisions. When atrial fibrillation causes ventricular dysfunction, ablation can significantly restore heart function. Trials such as CASTLE-AF and CASTLE-HTx have demonstrated benefit from ablation in this population, leading to a class I indication in current guidelines. However, until now there was no reliable marker to predict before the procedure which patients would recover.
Main study data
- 119 patients with persistent AF and ejection fraction ≤50% (DECAAF II data)
- 72 patients (60.5%) classified as arrhythmia-induced cardiomyopathy (LVEF ≥50% after ablation with improvement ≥10 points, or improvement ≥15 points)
- 47 patients (39.5%) without significant recovery of ventricular function
- Main predictor: regional fibrosis in the interatrial septum (OR 0.917; 95% CI, 0.871 to 0.965; P = 0.001)
- Septal fibrosis: 12.2% in the AIC group vs 20.7% in the non-AIC group (P < 0.001)
- Post-ablation LVEF: 58.9% in the AIC group vs 44.0% in the non-AIC group
- Septal fibrosis cutoff: 15.8% (AUC 0.80; P < 0.001) for predicting AIC
How the study was conducted
The authors used DECAAF II trial data, selecting patients who had both persistent AF and left ventricular systolic dysfunction (ejection fraction ≤50% by transthoracic echocardiography or cardiac MRI cine sequence). All patients had undergone late gadolinium-enhanced cardiac MRI before ablation, allowing total and regional atrial fibrosis to be quantified.
Arrhythmia-induced cardiomyopathy was defined as ejection fraction reaching at least 50% after ablation with an absolute improvement of at least 10 percentage points, or an absolute improvement of at least 15 points regardless of the final value. The 119 patients were then divided into two groups: those who recovered ventricular function (AIC group, 72 patients) and those who did not (non-AIC group, 47 patients).
Atrial fibrosis was analyzed not only as a total value but regionally, including the anterior, posterior and lateral walls, interatrial septum, left atrial appendage, left pulmonary vein ostia and right pulmonary vein ostia. This segmented approach identified differences in fibrosis distribution between the groups.
Main results
Most patients had arrhythmia-induced cardiomyopathy
Of the 119 patients analyzed, 72 (60.5%) met the criterion for arrhythmia-induced cardiomyopathy. Baseline ejection fraction was similar in both groups (approximately 39%), but the difference after ablation was marked: the AIC group reached a mean ejection fraction of 58.9%, while the non-AIC group remained at 44.0%.
Septal fibrosis as a predictor: the central finding
Total atrial fibrosis did not differ significantly between the two groups. What distinguished patients with arrhythmia-induced cardiomyopathy was the regional distribution of fibrosis: the AIC group had significantly less interatrial septal fibrosis than the non-AIC group.
In multivariable analysis, regional fibrosis in the interatrial septum was the only independent predictor of arrhythmia-induced cardiomyopathy (OR 0.917; 95% CI, 0.871 to 0.965; P = 0.001). Each 1% increase in septal fibrosis reduced the likelihood of arrhythmia-induced cardiomyopathy by approximately 8%. Mean septal fibrosis was 12.2% in the AIC group versus 20.7% in the non-AIC group (P < 0.001).
The authors identified a 15.8% cutoff for regional septal fibrosis using grid search, with an AUC of 0.80 for predicting AIC (P < 0.001). Patients with septal fibrosis below this value were significantly more likely to have arrhythmia-induced cardiomyopathy and therefore to recover ventricular function after ablation.
Reduction in AF burden and ventricular recovery
Reduction in atrial fibrillation burden after ablation correlated with improvement in ejection fraction in the combined group (r = -0.23; P = 0.02). The authors also found that an AF burden below 3.8% after ablation strongly predicted AIC (AUC 0.706; P = 0.024). In addition, left atrial volume decreased significantly in both groups after the procedure (mean 36.2 ml; P < 0.001).
Study limitations
Post-hoc analysis
This study was not prospectively designed to answer the question of arrhythmia-induced cardiomyopathy. The data come from DECAAF II, which had a different primary objective. The results should therefore be interpreted as hypothesis-generating rather than definitive evidence.
Arbitrary definition of arrhythmia-induced cardiomyopathy
The definition of AIC as improvement in ejection fraction to ≥50% with a gain of at least 10 points (or improvement ≥15 points), although used in previous studies, is an arbitrary choice. Patients may have varying degrees of arrhythmia contribution to ventricular dysfunction rather than a binary division.
Limited sample size
The analysis included 119 patients, relatively few for a robust multivariable analysis. This may explain why other clinical variables did not reach statistical significance in the final model.
Follow-up and imaging method
Follow-up was limited to the DECAAF II protocol. In addition, quantifying fibrosis by late-enhancement MRI depends on standardization across centers, and acquisition and processing variations can influence results.
Implications for clinical practice
The main contribution of this study is a potential tool for resolving a specific clinical dilemma. When a patient presents with persistent AF and reduced ejection fraction, MRI with regional fibrosis quantification may help estimate the likelihood of ventricular recovery after ablation.
The fact that total fibrosis did not differ between groups while septal fibrosis did reinforces the importance of segmented analysis. The authors suggest the interatrial septum is especially informative because its fibrosis may reflect intrinsic myocardial disease rather than only arrhythmia-induced remodeling.
Another relevant finding is the proportion: 60.5% of patients with persistent AF and ventricular dysfunction had arrhythmia-induced cardiomyopathy. This indicates that, in most of these patients, arrhythmia is probably the main cause rather than merely a consequence of cardiac dysfunction, strengthening the indication for ablation in this population.
My view as an electrophysiologist: In practice, the dilemma between “the heart is weak because of the arrhythmia” and “the arrhythmia appeared because the heart was already weak” is one of the most frequent we face. Until now, our ability to predict who would recover ventricular function was based on indirect clinical criteria. This study offers an interesting perspective by showing that regional atrial fibrosis distribution, specifically in the septum, may carry prognostic information. The 60.5% rate of arrhythmia-induced cardiomyopathy is consistent with what we observe in practice and reinforces that ablation should be considered proactively in these patients. The results require prospective validation, but the pathophysiological logic is consistent: less septal fibrosis suggests an atrium with less intrinsic structural disease, where the arrhythmia is the primary problem and therefore treatable.
