# Characterization of Cardiac Fat in Atrial Fibrillation Patients Prior to Ablation Treatment
## 4 Discussion  
Our findings indicate that obesity and its subsequent deposition of cardiac fat significantly impacts both the anatomical and functional characteristics of the heart, predisposing to atrial fibrillation. All cardiac fat parameters, including EAT, PAT, and total cardiac fat area, are substantially associated with an increase in BMI. Moreover, an increase in BMI was also associated with a decrease in functionality, as indicated by reduced cardiac indices in obese patients. Our findings demonstrate that BMI is significantly associated with EAT, PAT, and total cardiac fat area, making obesity pivotal in atrial fibrillation. In the context of cardiovascular diseases, including AF, EAT has been shown to have a direct relationship with obesity and BMI [21; 22]. The relationship stems from the shared embryological origin of EAT with the epicardial layer of the myocardium, resulting in no connective tissue layer separating the two [22]. Therefore, excessive deposition of EAT causes direct fibrofatty infiltration and the release of inflammatory mediators such as interleukin-1-beta, interleukin-6, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 that, via paracrine mechanism, cause atrial fibrosis and AF [21]. Furthermore, EAT contains abundant ganglionated plexi that might contribute to the recurrence of AF [23; 24; 25; 26]. In our study, overweight and obese AF patients showed higher recurrence compared to normal. EAT inflammatory activity has been reported as being higher in patients with AF than in controls, and it was shown to be greater in the left main artery than in the subcutaneous or visceral thoracic tissue [23]. An increased EAT could affect the ganglia function and impact the atrial substrate remodeling, and thereby, the maintenance of AF [25]. The association of the regional distribution of fat was not evaluated in the current study. However, regional EAT increment may be associated with AF nesting [25]. The latter remains an important question to address in future studies. Our study also reveals an association between PAT and BMI in the setting of paroxysmal AF. On the other hand, [PERSON] et al. demonstrated significant associations of PAT with AF presence, severity, and post-ablation outcomes, independent of systemic adiposity measures like BMI and BSA, suggesting that PAT may be a possible independent biomarker of AF [27]. However, this might be attributable to the use of volume measurements compared to area measurements in our study. Sex and age also impact cardiac fat and AF. Our findings reveal slight sex differences for EAT and PAT deposition, with male sex having a stronger correlation to PAT area than EAT. In fact, across all BMI groups, males had significantly higher PAT areas compared to females. Men tend to have higher visceral fat deposition, which includes EAT and PAT,  
Figure 4: Kaplan–Meier survival analysis curve for atrial fibrillation recurrence in relation to BMI. The Log Rank (Mantel-Cox) \(p\)-value for overall comparison is 0.552.  
whereas women have more subcutaneous fat deposits [28]. [PERSON] et al. also illustrated that PAT volume is positively associated with BMI and is significantly higher in men than in women. However, in the context of metabolic syndrome and other cardiometabolic risk measures that are similar for various cardiovascular diseases including AF, the association of PAT was found to be stronger in women compared to men [29]. Nonetheless, sex seems to play less of a role in EAT than PAT, as in our study, there was no significant difference between the area of EAT in the hearts of normal, overweight, or obese males and their female counterparts. Conversely, [PERSON] et al. demonstrated higher total EAT volume in male AF patients and higher peri-atrial/total EAT ratio in post-menopausal females, alongside a greater rate of post-ablation AF recurrence [30]. Further exploration into sex differences in cardiac fat deposition is needed. Advancing age, a well-established AF risk factor, may affect cardiac fat dynamics [2].