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Atrial Fibrillation Ablation In Obesity ‚ Size Matters


Atrial Fibrillation Ablation In Obesity – Size Matters
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Credits:Li-Fern Hsu1, Prashanthan Sanders2
Department of Cardiology, National Heart Centre, Singapore;1 and the Cardiovascular Research Centre, Department of Cardiology, Royal Adelaide Hospital, and the Disciplines of Medicine and Physiology, University of Adelaide, Adelaide, Australia.2

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.

References

1.  World Health Organization. Obesity: Preventing and managing the global epidemic report of a WHO consultation on obesity. Geneva, Switzerland. World Health Organization Report 1998:1-276

2.  Braunwald E. Shattuck Lecture Cardiovascular medicine at the turn of the millennium: triumphs, concerns and opportunities. N Engl J Med 1997;337:1360-1369

3.  Wang TJ, Parise H, Levy D, et al. Obesity and the risk of new-onset atrial fibrillation. JAMA 2004;292:2471-2477

4.  Wanahita N, Messerli MH, Bangalore S, et al. Atrial fibrillation and obesity results of a meta-analysis. Am Heart J 2008;155:310-315

5.  Dublin S, French B, Glazer NL, et al. Risk of new-onset atrial fibrillation in relation to body mass index. Arch Intern Med 2006;166:2322-2328

6.  Vaziri SM, Larson MG, Benjamin EJ, et al. Echocardiographic predictors of nonrheumatic atrial fibrillation. The Framingham Heart Study. Circulation 1994;89:724-730

7.  Benjamin EJ, Levy D, Vaziri SM, et al. Independent risk factors for atrial fibrillation in a population-based cohort. The Framingham Heart Study. JAMA 1994;271:840-844

8.  Iacobellis G, Ribaudo MC, Leto G, et al. Influence of excess fat on cardiac morphology and function: studying uncomplicated obesity. Obes Res 2002;10:767-773

9.  Engelis S, Sharma AM. The renin-angiotensin system and natriuretic peptides in obesity-associated hypertension. J Mol Med 2001;79:21-29

10.  Pelat M, Verwaerde P, Merial C, et al. Impaired atrial M(2)-cholinoceptor function in obesity-related hypertension. Hypertension 1999;34:1066-1072

11.  Gami AS, Pressman G, Caples SM, et al. Association of atrial fibrillation and obstructive sleep apnea. Circulation 2004;110:364-367

12.  Gami AS, Hodge DO, Herges, RM, et al. Obstructive sleep apnea, obesity, and the risk of incident atrial fibrillation. J Am Coll Cardiol 2007;49:565-571

13.  Pritchett AM, Jacobsen SJ, Mahoney DW, et al. Left atrial volume as an index of left atrial size: a population-based study. J Am Coll Cardiol 2003;41:1036-1043

14.  Kanagala R, Murali NS, Friedman PA, et al. Obstructive sleep apnea and the recurrence of atrial fibrillation. Circulation 2003;107:2589-2594

15.  Jongnarangsin K, Chugh A, Good E,et al. Body mass index, obstructive sleep apnea, and outcomes of catheter ablation of atrial fibrillation. J Cardiovasc Electrophysiol 2008. (In Press. EPub March 2008)

16.  Lakkireddy DR, Blake GE, Patel D, et al. Success of radiofrequency catheter ablation of atrial fibrillation: Does obesity influence the outcomes? JAFIB 2008:1:12-19.

17.  Wachtell K, Lehto M, Gerdts E, et al. Angiotensin II receptor blockade reduces new-onset atrial fibrillation and subsequent stroke compared to atenolol: the Losartan Intervention For End Point Reduction in Hypertension (LIFE) study. J Am Coll Cardiol 2005;45:712-719

18.  Ducharme A, Swedberg K, Pfeffer MA, et al. Prevention of atrial fibrillation in patients with symptomatic chronic heart failure by candesartan in the Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM) program. Am Heart J 2006;152:86-92

19.  Anand K, Mooss AN, Hee TT, et al. Meta-analysis: inhibition of renin-angiotensin system prevents new-onset atrial fibrillation. Am Heart J 2006;152:217-222

20.  Madrid AH, Bueno MG, Rebollo JMG. Use of irbesartan to maintain sinus rhythm in patients with long-lasting persistent atrial fibrillation. Circulation 2002;106:331-336


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