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      Relation of overweight and symptomatic atrial fibrillation: A case report

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          Abstract

          Introduction KEY TEACHING POINTS • Weight reduction and lifestyle management are important in the treatment of symptomatic atrial fibrillation. • Strict weight management using a cardiac rehabilitation program is a treatment option for obese patients before invasive treatment modalities are deployed. Over the past few decades, obesity has become a global epidemic and represents a major challenge for current and future health. 1 Although the pathogenesis of atrial fibrillation (AF) is not completely understood, there is compelling evidence that obesity increases the risk for new-onset and recurrences of AF and increases progression to more persistent forms of AF. 2 Weight reduction in patients with AF reduces the burden and number of AF-episodes and cumulative AF duration. 3 These findings support therapy directed at reducing weight and controlling risk factors in the treatment of AF. We present the case of a 46-year-old male patient with symptomatic AF and a temporal relation between weight changes and recurrences of AF. Case report A 46-year-old Caucasian male patient with a history of hypertension and 10 years paroxysmal AF was referred to our center. Treatment with class IC and III antiarrhythmic drugs had failed, and the patient experienced progressive frequency and severity of palpitations and fatigue (European Heart Rhythm Association score = 3). The calculated CHA2DS2-VASc (acronym for congestive heart failure, hypertension, age ≥75 y [double points], diabetes mellitus, prior stroke or thromboembolism [double points], vascular disease, age 65–74 years, sex category) score was 1 (hypertension). The patient’s body mass index was 28.3 kg/m2 (97 kg, 185 cm) at time of referral. In the workup for pulmonary vein isolation (PVI), transthoracic echocardiography results showed normal cardiac function, and a left atrial volume indexed of 29.1 mL/m2. The transcatheter PVI using radiofrequency energy was performed. After the PVI, the patient lost 10 kg with the help of our institutional patient-tailored 3-month cardiac rehabilitation program, which constituted low-intensity exercise guided by a physiotherapist, a balanced diet supported by our institutional nutritionist, and nutritional psychoeducation provided by a psychologist. Thereafter, the patient was free of atrial arrhythmias during the first 6 months. In the next 6 months, the patient lost another 4 kg, arriving at 83 kg. The variance in the patient’s weight over time is depicted in Figure 1. Two years after the first PVI, the patient regained weight up to 98 kg and experienced a symptomatic recurrence of paroxysmal AF, which was confirmed by 24-hour Holter monitoring. A second electrophysiological examination and PVI were scheduled, but with physical exercise the patient managed to lose weight to 89 kg. From that point, he was asymptomatic and in sinus rhythm. The re-PVI was therefore not performed. The patient was in sinus rhythm for over 1 year, until he regained weight up to a total of 100 kg. This time, the recurrent AF episode was classified as persistent, which was confirmed by 24-hour Holter monitoring. The patient underwent elective electrocardioversion, and flecainide was restarted. Another year later, weighing 103 kg, the patient continued to have severely symptomatic AF, with an AF burden on 24-hour Holter monitoring of 39%. The patient was again referred to our cardiac rehabilitation facility; the patient lost 15 kg again, and symptomatic AF disappeared. Since then, neither AF nor other atrial arrhythmias have been seen on 24-hour Holter monitoring. Discussion Obesity is associated with multiple cardiovascular risk factors, for example, hypertension, dyslipidemia, insulin resistance, obstructive sleep apnea syndrome, pericardial fat deposition, and a systemic inflammatory state. 4 After adjustment for other risk factors, obesity and is associated with an increased risk of cardiovascular diseases, such as ischemic heart diseases, heart failure, and AF. 5 There is abundant evidence for the involvement of obesity in the development of AF. Obese individuals have up to 2.4-fold increased risk for new-onset AF. 6 The dynamic association of weight with AF prevalence was previously presented in the Women׳s Health Study. 7 Mechanisms underlying the relation between obesity and new-onset AF, may relate to structural remodeling caused by elevated end-diastolic pressure, inflammation, and increased plasma volume.8, 9 Also, obesity is known to be associated with sleep apnea syndrome, an independent risk factor for AF. 10 Our case underscores the direct (12-year) temporal relation between weight and symptomatic AF. In this particular case, when weight was >95 kg, the patient experienced symptomatic AF recurrences. All 24-hour electrocardiogram registrations performed, in total 360 hours’ worth, are depicted in Figure 1. After testing, no obesity-associated comorbidities, such as diabetes, metabolic syndrome, and sleep apnea syndrome, appeared to be present in our case. The finding that obesity itself may also induce AF or increase AF burden has been reported in previous studies. 11 It is unknown whether this risk factor is attributable only to body composition or also to the level of physical activity. 12 Also, the role of epicardial fat remains to be thoroughly investigated as a risk factor. 13 Obesity is a modifiable risk factor, although its management can be very challenging in clinical practice. A recent randomized trial compared intervention with active weight management to modification with general lifestyle advice. Results of this pivotal paper show that weight reduction with intensive risk-factor management causes a significant reduction in AF symptom burden and severity. 3 The recent ARREST-AF trial showed that aggressive risk-factor management improves long-term outcomes of AF ablation. 14 Furthermore, if this weight loss is sustained at long-term follow-up, reduction of AF burden and maintenance of sinus rhythm are significantly higher compared to those in patients with weight fluctuation. 15 In fact, our case nicely illustrates the relation of overweight and recurrence of symptomatic AF, and it stresses the importance of weight counseling in patients referred for symptomatic AF, especially before considering invasive treatment modalities such as transcatheter or surgical PVI. A cardiac rehabilitation program is an option for such patients. Conclusions Weight reduction and lifestyle management are important in the treatment of symptomatic AF and warrant more attention.

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          Most cited references10

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          Body size and fat distribution as predictors of coronary heart disease among middle-aged and older US men.

          Obesity, android fat distribution, and other anthropometric measures have been associated with coronary heart disease in long-term prospective studies. However, fluctuations in weight due to age-related hormonal changes and changes in lifestyle practices may bias relative risk estimates over a long follow-up period. The authors prospectively studied the association between body mass index (BMI) (kg/m2), waist-to-hip ratio, and height as independent predictors of incident coronary heart disease in a 3-year prospective study among 29,122 US men aged 40-75 years in 1986. The authors documented 420 incident coronary events during the follow-up period. Body mass index, waist-to-hip ratio, short stature, and weight gain since age 21 were associated with an increased risk of coronary heart disease. Among men younger than 65, after adjusting for other coronary risk factors, the relative risk was 1.72 (95% confidence interval (CI) 1.10-2.69) for men with BMI of 25-28.9, 2.61 (95% CI 1.54-4.42) for BMI of 29.0-32.9, and 3.44 (95% CI 1.67-7.09) for obese men with BMI > or = 33 compared with lean men with BMI or = 65 years of age, the association between BMI and risk of coronary heart disease was much weaker. However, in this age group, the waist-to-hip ratio was a much stronger predictor of risk (relative risk = 2.76, 95% CI 1.22-6.23 between extreme quintiles). These results suggest that for younger men, obesity, independent of fat distribution, is a strong risk factor for coronary heart disease. For older men, measures of fat distribution may be better than body mass index at predicting risk of coronary disease.
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            Obesity as a risk factor for the progression of paroxysmal to permanent atrial fibrillation: a longitudinal cohort study of 21 years.

            Obesity has been shown to be a risk factor for first atrial fibrillation (AF), but whether it is associated with progression from paroxysmal to permanent AF is unknown. In this longitudinal cohort study, Olmsted County, MN residents confirmed to have developed paroxysmal AF during 1980-2000 were identified and followed passively to 2006. The interrelationships of body mass index (BMI), left atrial (LA) size, and progression to permanent AF were analysed. Of a total of 3248 patients (mean age 71 +/- 15 years; 54% men) diagnosed with paroxysmal AF, 557 (17%) progressed to permanent AF (unadjusted incidence, 36/1000 person-years) over a median follow-up period of 5.1 years (interquartile range 1.2-9.4). Adjusting for age and sex, BMI independently predicted the progression to permanent AF (hazard ratio, HR 1.04, CI 1.03-1.06; P or=35 kg/m(2)) were associated with increased risk for progression [HR 1.54 (CI 1.2-2.0; P = 0.0004) and 1.87 (CI 1.4-2.5; P < 0.0001, respectively)]. BMI remained highly significant even after multiple adjustments. In the subgroup with echocardiographic assessment (n = 744), LA volume was incremental to BMI for independent prediction of progression after multiple adjustments, and did not weaken the association between BMI and progression to permanent AF (HR 1.04; CI 1.02-1.05; P < 0.0001). There was a graded risk relationship between BMI and progression from paroxysmal to permanent AF. This relationship was not weakened by LA volume, which was independent of and incremental to BMI for the prediction of progression to permanent AF.
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              Epicardial adipose tissue and atrial fibrillation.

              Atrial fibrillation (AF) is the most frequent cardiac arrhythmia in clinical practice. AF is often associated with profound functional and structural alterations of the atrial myocardium that compose its substrate. Recently, a relationship between the thickness of epicardial adipose tissue (EAT) and the incidence and severity of AF has been reported. Adipose tissue is a biologically active organ regulating the metabolism of neighbouring organs. It is also a major source of cytokines. In the heart, EAT is contiguous with the myocardium without fascia boundaries resulting in paracrine effects through the release of adipokines. Indeed, Activin A, which is produced in abundance by EAT during heart failure or diabetes, shows a marked fibrotic effect on the atrial myocardium. The infiltration of adipocytes into the atrial myocardium could also disorganize the depolarization wave front favouring micro re-entry circuits and local conduction block. Finally, EAT contains progenitor cells in abundance and therefore could be a source of myofibroblasts producing extracellular matrix. The study on the role played by adipose tissue in the pathogenesis of AF is just starting and is highly likely to uncover new biomarkers and therapeutic targets for AF.
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                Author and article information

                Contributors
                Journal
                HeartRhythm Case Rep
                HeartRhythm Case Rep
                HeartRhythm Case Reports
                Elsevier
                2214-0271
                22 June 2015
                September 2015
                22 June 2015
                : 1
                : 5
                : 342-344
                Affiliations
                [0005]Department of Cardiology and Cardiothoracic Surgery, University Medical Centre Groningen, Groningen, The Netherlands
                Author notes
                [* ] Address reprint requests and correspondence: Dr Isabelle C Van Gelder, Department of Cardiology, Thoraxcenter, University of Groningen, University Medical Center Groningen, P.O. Box 30.001, 9700 RB Groningen, The Netherlands i.c.van.gelder@ 123456umcg.nl
                Article
                S2214-0271(15)00125-6
                10.1016/j.hrcr.2015.06.002
                5419659
                727b04da-8e4e-43b0-a74a-44ddb25e93c7
                Published by Elsevier Inc.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Categories
                Case Report

                af, atrial fibrillation,pvi, pulmonary vein isolation,sr, sinus rhythm,atrial fibrillation,obesity,risk factors,pulmonary vein isolation

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