Financial Support : Dr. Sanders is supported by National Heart Foundation of Australia

Disclosure : Dr. Hsu has received lecture fees from Biosense-Webster and St Jude Medical. Dr. Sanders has served on advisory board of and received lecture fees and research funding from Bard Electrophysiology, Biosense-Webster, Medtronic and St Jude Medical.

Corresponding Author : Prashanthan Sanders, Cardiovascular Research Centre,Department of Cardiology,Royal Adelaide Hospital, Adelaide, SA 5000,Australia Tel: +61 8 8222 2723. Fax:+61 8 8222 2722. Email: prash.sanders@adelaide.edu.au

Received : 2008-05-10 Accepted : 2008-05-13

Copyright: Copyright belongs to Dr. Hsu et.al., under Open Access License details available online at http://creativecommons.org

doi : 10.4022/jafib.v1i1.407

Both obesity and atrial fibrillation (AF) have a significant negative impact on morbidity and mortality. In recent times, these conditions have become growing public health problems, being described separately as emerging epidemics.^1,2 Obesity is increasingly recognized as a risk factor for developing AF, with the risk escalating with increasing body mass index (BMI).^3,4 In addition, this association is greater for long-standing and permanent AF, suggesting a possible role for obesity in the maintenance of AF as well.⁵

Although often attributed to left atrial dilatation,^3,6 the pathogenesis of AF in obese patients is likely to be more complex and involve a combination of the many comorbid conditions associated with obesity. In general, obese individuals are more likely to suffer from concomitant hypertension, diabetes mellitus, coronary artery disease and heart failure, all of which are established predisposing conditions for AF.⁷ Left atrial enlargement may result from ventricular diastolic dysfunction,⁸ excess or inappropriate neurohormonal activation,⁹ autonomic dysfunction,¹⁰ or a combination of them. In addition, obstructive sleep apnea (OSA) is highly prevalent in obesity and has been implicated in the development of AF.^11,12 Finally, BMI itself has a strong correlation with left atrial size.¹³

The negative effect of obesity and OSA has extended to AF therapy as well. Patients with OSA have demonstrated a higher recurrence rate after cardioversion for AF compared to those without OSA.¹⁴ As catheter ablation of AF offers the best chance of achieving a long-term cure, and advances in techniques and technology enable more widespread adoption of the procedure, it should be logical to evaluate the impact of this therapy in various high-risk subgroups, including obesity. Recently, Jongnarangsin and colleagues studied the outcomes of 324 consecutive patients who underwent AF ablation classed according to their BMI and the presence of OSA.¹⁵ At baseline, obese patients had larger left atrial diameters, and higher prevalence of chronic AF, OSA and hypertension. Their fluoroscopy and procedural durations were also longer compared to patients with normal BMI. With univariate analysis, obese patients (BMI ≥30 kg/m²) demonstrated a 2.48-fold increase in the probability of recurrent AF, and each unit increase in BMI was found to increase the probability of recurrent AF by 5%. However, multivariate analysis revealed that BMI was not predictive of recurrent AF. Instead, the strongest independent predictor was the presence of OSA.

In this issue of the Journal, Lakkireddy and colleagues evaluated the outcomes of AF ablation in 511 patients classified according to their BMI.¹⁶ Similarly, they also found that overweight and obese patients had larger left atrial diameters and a higher prevalence of persistent and permanent AF, and in addition, a higher prevalence of diabetes mellitus and coronary artery disease. In concordance with the previous study, they found a significant correlation between increasing BMI class and AF recurrence during long-term (1-year) follow-up after catheter ablation. In addition, while no formal evaluation was performed for OSA, the investigators found that a history for OSA was not an independent predictor of arrhythmia recurrence.

Although possessing several limitations, these 2 studies present important information. They confirm previous observations on obesity and its association with left atrial dilatation, and the higher prevalence of persistent and permanent AF. They demonstrate that catheter ablation in obese patients was more difficult, as evidenced by the longer fluoroscopy and procedure durations. The exact reason remains unclear, although possible factors are the larger atrial sizes, and the higher prevalence of persistent and permanent AF among this group, requiring more complex ablation. Importantly, they demonstrate that obesity with its attendant comorbities negatively affects the outcome of AF ablation. The exact roles of BMI, OSA and other factors remain to be determined.

What is more important to us is that many of these factors and comorbidities can be modified or treated. Treatment of OSA with continuous positive airway pressure (CPAP) was associated with an almost 50% reduction in recurrent AF after cardioversion.¹⁴ Pharmacological therapy of hypertension and heart failure, especially with drugs blocking the renin-angiotensin system, has been demonstrated to reduce the incidence of new-onset AF,^17-19 the addition of an angiotensin II receptor blocker was associated with a significant reduction in AF recurrence after cardioversion.²⁰ Although the effect of weight loss in patients with AF has not been determined, it would be logical to include aggressive weight management as part of current AF therapy, as many of these comorbidities like hypertension and OSA can improve with weight loss.

In conclusion, the management of AF demands a multifaceted approach. Although the results of catheter ablation have improved greatly in recent years, much more can be done to give the patient the best chance to maintain sinus rhythm after the procedure. Better understanding of the role of risk factors for AF, such as obesity, and their aggressive management, constitute the first step in the right direction.

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