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Left Atrial Volume Predicts Atrial Fibrillation Recurrence after Catheter Ablation Only in Obese Patients

A peer-reviewed version of this preprint was published in:
Diagnostics 2024, 14(14), 1570. https://doi.org/10.3390/diagnostics14141570

Submitted:

10 June 2024

Posted:

12 June 2024

You are already at the latest version

Abstract
BACKGROUND: It has been shown that obesity and higher body mass index (BMI) are associated with higher recurrence rate of atrial fibrillation (AF) after successful catheter ablation (CA). The same has been proven for left atrial volume index (LAVI). It has also been shown that there is a correlation between LAVI and BMI. However, whether LAVI prognostic impact on AF recurrence is BMI independent, remains unclear. METHODS: We prospectively included 62 patients with paroxysmal AF who were referred to our institution for CA. All patients underwent radiofrequency CA with standard pulmonary veins isolation. Transthoracic 2-D echocardiography was performed one day after CA to obtain standard measures of cardiac function and morphology. Recurrence was defined as documented AF within 6 months of follow-up period. Patients were also instructed to visit outpatient clinic earlier in case of symptoms suggesting AF recurrence. RESULTS: We observed AF recurrence in 27% of patients after 6 months. The mean BMI in our cohort was 29.65 ± 5.08 kg/cm2 and the mean LAVI was 38.04 ±11.38 ml/m2. We further divided patients into 2 groups according to BMI. Even though LAVI was similar in both groups, we found it to be significant predictor of AF recurrence only in obese patients (BMI ≥ 30), but not in the non-obese group (BMI < 30). There was also no significant difference in AF recurrence between both cohorts. The significance of LAVI as AF recurrence predictor in obesity group was also confirmed in multivariate model. CONCLUSION: According to our results LAVI tends to be significant predictor of AF recurrence after successful catheter ablation in obese patients, but not in normal-weight and overweight patients. This would suggest different mechanisms of AF in non-obese patients in comparison to the obese. Further studies are needed in this regard.
Keywords: 
atrial fibrillation
;  
catheter ablation
;  
left atrial volume index
;  
body mass index
Subject: 
Medicine and Pharmacology  -   Cardiac and Cardiovascular Systems

1. INTRODUCTION

Atrial fibrillation (AF) is chronic degenerative disorder with pandemic proportions. It was stated that it correlates with increasing age, as well as with common cardiovascular risk factors such hypertension, diabetes, hyperlipidaemia and obesity (1). Studies have been conducted to further enlighten the role of body mass index (BMI), body surface area (BSA) as well as height and weight in the pathophysiology of atrial remodelling and subsequent AF incidence and prevalence (2,3). Regarding left atrial remodelling process computed tomography (CT) studies showed that excessive peri-atrial and pericardial adipose tissue could play significant role in loss of atrial architecture and left atrial dilatation (4,5). However, this could be the main pathophysiologic process in obese patients but not in those with normal or near normal weight. It has been also shown that obesity and higher BMI are associated with higher recurrence rate of atrial fibrillation (AF) after successful catheter ablation (CA) (6). The same has been proven for left atrial volume index (LAVI) (7). It was also proven that there is a correlation between LAVI and BMI (8). However, whether LAVI prognostic impact on AF recurrence is BMI independent, remains unclear. The aim of this study was to compare correlations between LAVI and AF recurrence after successful CA in obese and non-obese patients and to further stratify whether LAVI prognostic impact is same across the whole BMI spectrum.

2. METHODS

We prospectively included 62 patients with paroxysmal AF. All patients underwent radiofrequency CA with pulmonary vein isolation (PVI) as primary target of procedure. Sex, age, body height, body weight, body mass index (BMI), and type of antiarrhythmic therapy (AAT) were obtained before the procedure.
Prior to ablation transoesophageal echocardiography was performed in all patients to rule out the presence of thrombus in the LA. Ablation procedure was performed under conscious sedation. Under fluoroscopic guidance transseptal puncture was performed. A detailed bipolar voltage map of left atrium (LA) was then constructed using 20-polar catheter (Pentaray; Biosense-Webster, Irvine, California). Automated 3-D mapping system (Carto, Biosense Webster, Irvine, California) was used in all patients. We used standard respiratory gating to minimize respiratory movement bias. Prior to ablation contact force calibration was performed. Endocardial contact was ensured mainly by local electrogram and contact force measurements. Ablation was done with 3.5-mm irrigated-tipped catheter (SmartTouch Thermocool, Biosense Webster, Irvine, California). PVI was achieved with wide antral circumferential ablation. Isolation of ablated region was then confirmed with entrance and exit block pacing manoeuvres. Direct current cardioversion to restore sinus rhythm was also performed after successful procedure if patients were still in AF. Mapping and CA was performed by single operator.
Standard transthoracic two-dimensional echocardiography was performed one day after CA to obtain standard recording of cardiac function and morphology (Vivid E95, General Electric Vingmed, Milwaukee, Wisconsin, USA). Standard two-dimensional and Doppler measurements were obtained according to the current recommendations (9).

2.1. Follow-up

All patients had 12-lead ECG (25 mm/s, 10 mm/mV) recorded at follow-up visit 6 months after CA to evaluate the basic rhythm. Patients were also instructed to visit outpatient clinic earlier in case of symptoms suggesting AF recurrence. Endpoint of our study was to estimate AF recurrence rate diagnosed by ECG. Recurrence was defined as documented AF within 6 months of follow-up period.

2.2. Statistical analysis

Obtained data was analysed using SPSS version 26 (SPSS Inc., Chicago, IL, USA). We used Student’s t-test for evaluating differences between continuous variables and chi-square test for analysis of categorical variables. Continuous data are given as mean ± standard deviation (SD) and categorical variables are expressed as absolute values and percentages. Simple logistic regression method was used to assess the association between LAVI and AF recurrence. The significance for other potential confounders was adjusted via multivariate logistic regression and enter method.

3. RESULTS

The patients’ data is displayed in Table 1. We observed AF recurrence in 27% of patients after 6 months. The mean BMI in our cohort was 29.65 ± 5.08 kg/cm2 and the mean LAVI was 38.04 ± 11.38 ml/m2. We further divided patients into two groups according to BMI (≥ 30 and < 30). We found no statistically significant differences in age, sex, left ventricular ejection fraction, and comorbidities between both groups (Table 2). LAVI was similar in both groups. There was slightly higher percentage of AF recurrences in obese group, however the difference was not statistically significant (Table 2). We found LAVI to be a significant predictor of AF recurrence in all patients. When we further divided patients according to BMI, we found LAVI to be significantly associated with AF recurrence rate only in obese patients (BMI ≥ 30), but not in normal-weight and overweight patients (BMI < 30) (Table 3). The significance of LAVI as AF recurrence predictor according to BMI was also confirmed in a multivariate model in both groups (adjusted for confounding effects of hypertension, diabetes, left ventricular ejection fraction and antiarrhythmic therapy) (Table 3).

4. DISCUSSION

Previous studies demonstrated an association between left atrial (LA) size and the incidence of new-onset AF as well as AF recurrence after CA (3,6,7). However, it is still controversial, whether this is due to the enlargement of LA per se or a consequence of the accompanying risk factors, such as obesity and its metabolic derangements. In a recent study, a CT-derived cut-off value for LAVI of 51.99 ml/m2 was proposed as a prognostic marker for AF recurrence after CA, while the impact of BMI and other measures of obesity was not studied (3). In our study, LAVI was a predictor of AF recurrence only in obese patients, while no association of LAVI with AF recurrence was demonstrated in normal-weight and overweight patients.
Obesity was proven to be an independent risk factor for the incidence of AF with 10–30% higher risk of AF for every 5 kg/m2 increase in BMI (10-12). According to the reported estimations it already accounts for almost one-fifth of AF cases (13,14). Interestingly, Pranata et al. demonstrated a non-linear relationship of BMI with AF recurrence after CA, with a steeper curve in those with BMI >30-35 (6). Besides hemodynamic stress due to persistent volume overload, obesity was found to increase proinflammatory cytokines, induce insulin resistance, alter metabolic pathways, and induce gene expression profiles associated with cardiac hypertrophy, which results in subsequent electrophysiological, mechanical, and structural LA remodelling (12,15-18). Obesity is also commonly associated with other risk factors for LA remodelling and AF, such as arterial hypertension, type 2 diabetes mellitus, and obstructive sleep apnea (19,20). In obese patients compared to non-obese, a lower global LA longitudinal strain revealing LA mechanical dysfunction was also demonstrated (21).
Besides BMI, additional clinical measures, such as waist circumference and waist-to-hip ratio, have been suggested to define regional body fat distribution more precisely and assess visceral fat. A correlation of BMI and waist-to-hip ratio with visceral adiposity was reported, though influenced by gender and race (22–25). Extensive evidence demonstrated more unfavourable metabolic and cardiovascular effects of visceral compared with subcutaneous fat, mediated by its endocrine proinflammatory and immunological mechanisms (26). Most studies evaluated extra-thoracic part of visceral fat, especially its intra-abdominal distribution, and most of them confirmed the association with an adverse metabolic phenotype and an enhanced cardiovascular risk (27,28). In recent years, epicardial adipose tissue (EAT) has been increasingly advocated as a critical part of visceral fat compartment, associated with LA size and function (5,22,29). EAT promotes AF by direct fat infiltration of the underlying atrial myocardium, increased oxidative stress, local autonomic dysfunction, accelerated interstitial atrial fibrosis, and subsequent conduction slowing and heterogeneity (28,30–32). EAT and associated inflammatory cytokines were linked with the incidence, severity, and recurrence of AF (33,34).
As noted in the study by van Rosendael et al, the incidence of paroxysmal AF was the highest in patients with a large amount of EAT, while increased LA size predicted AF persistency (5). Similarly, a recently published metaanalysis confirmed the predictive role of EAT for AF recurrence after CA (35). Based on these results, an increased EAT in normal-sized LA might reflect an early LA disease, followed by LA enlargement and the transition from paroxysmal to persistent/permanent AF. Adding our findings to the recent data, one can expect most frequent AF recurrences in obese patients with a large amount of EAT and subsequent LA enlargement, which warrants further confirmation.
According to our results, LA enlargement unrelated to obesity might have a lower propensity for AF recurrence and the mechanisms behind are crucial. In non-obese patients, LA enlargement is possibly merely a consequence of prolonged hemodynamic stress due to heterogeneous conditions with LA pressure or volume overload, that can be also aggravated by atrial stand-still during AF episodes. On the other hand, genetic factors promoting LA enlargement and AF have also been identified (36, 37). However, LA enlargement in obese patients seems to carry a higher propensity for AF compared to non-obese patients, which highlights the additional proarrhythmogenic impact of local and systemic inflammatory condition mediated by obesity. It is possible that enlarged left atrium in obese patients reflects different and more aggravating pathophysiological circumstances and processes than in non-obese patients. Due to inflammatory as well as direct mechanical impact of adipose tissue and additional deranged atrial position in obese patients it is plausible, that there are vast microscopic and cellular changes taking place. Even though LAVI is similarly enlarged as in non-obese patients, atrial micro-architectonics is probably significantly damaged, thus leading to higher percentage of destructed atrial tissue and hence higher probability of arrhythmic foci outside of pulmonary veins and respective antral regions. Further studies, that would show more specific differences in atrial tissue in reliance to adipose tissue and BMI are needed to prove this hypothesis.
Our results are hypothesis-generating and should be interpreted in context of certain limitations. In our patients, visceral fat was not specifically evaluated, and results are based only on BMI. However, BMI is the most frequently used anthropometric measure in clinical routine and results are easily applied into everyday clinical practice. Since BMI was found to correlate with the amount of visceral fat to a certain degree, we believe that adding more specific measures of visceral fat would not significantly change our results (22). Although the number of included patients was limited, all interventional procedures were performed by same skilled electrophysiologist and echocardiographic examinations were performed by the same experienced echocardiographer on the same ultrasound machine. Thereby we completely avoided the potential interobserver procedural and measurement variability issues.

5. CONCLUSION

According to our results LAVI tends to be significant predictor of AF recurrence after CA in obese patients, but not in normal-weight and overweight patients. This would suggest different mechanisms of AF in patients with normal weight or slightly over-weighted patients in comparison to obese patients. Further studies are needed in this regard.

Conflicts of Interests

Authors have nothing to disclose.

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Table 1. Patient characteristics.
Table 1. Patient characteristics.
Parameter Mean and standard deviation
Age (years) 61.52 ± 9.87
Body height (cm) 175.00 ± 9.43
Body weight (kg) 92.13 ± 15.58
LAVI (mL/m2) 38.04 ±11.38
BMI (kg/m2) 29.65 ± 5.08
Legend (Table 1): LAVI, left atrial volume index; AF, atrial fibrillation; BMI, body mass index.
Table 2. Comparison of patients stratified according to BMI.
Table 2. Comparison of patients stratified according to BMI.
BMI ≥ 30 kg/cm2 BMI < 30 kg/cm2 P value
Number of patients 27 35
Age (years) 61.3±11.5 61.7±7.3 0.9
Sex (female) 11(40.7%) 6(17.1%) 0.06
LAVI (mL/m2) 38.2±13.2 37.8±8.8 0.9
AF recurrence after 6 months (%) 9(33.3%) 8(22.9%) 0.4
Antiarrhythmic treatment after CA 26(89.7%) 32(84.2%) 0.7
Left ventricular ejection fraction (%) 58.7±2.5 59.3±2.8 0.4
Hypertension 18(66.6%) 19(54.3%) 0.5
Diabetes 1(4.0%) 2(5.7%) 1.0
Legend (Table 2): LAVI, left atrial volume index; AF, atrial fibrillation; BMI, body mass index; CA, catheter ablation.
Table 3. LAVI as a predictor of AF recurrence after catheter ablation in both groups.
Table 3. LAVI as a predictor of AF recurrence after catheter ablation in both groups.
Number of patients Odds ratio for AF recurrence Confidence interval P value
LAVI (BMI < 30 kg/cm2) - unadjusted 35 1.08 0.87 – 1.17 0.1
LAVI (BMI < 30 kg/cm2) – adjusted* 35 1.07 0.97 – 1.17 0.16
LAVI (BMI ≥ 30 kg/cm2) - unadjusted 27 1.29 1.07 – 1.54 0.007
LAVI (BMI ≥ 30 kg/cm2) – adjusted* 27 1.35 1.02 – 1.78 0.03
Legend (Table 3): LAVI, left atrial volume index; AF, atrial fibrillation; BMI, body mass index; *Adjustment for confounding effects of hypertension, diabetes, left ventricular ejection fraction, beta blocker and antiarrhythmic therapy.
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