Lifestyle management in the development and treatment of Atrial Fibrillation

C. Fielder Camm (Academic Clinical Fellow (ST1) - Cardiology, John Radcliffe Hospital)


Atrial Fibrillation (AF) is the most common arrhythmia worldwide.1–3 There is a global prevalence of 0.95%,4 and an increasing risk of 3.8-6.2/1000 persons aged 55-64 years, and 62.8-75.9/1000 persons aged 85-94 years.3 AF is a significant cause of morbidity and mortality from thromboembolic stroke.5 An ongoing increase in prevalence of this condition is likely to continue in line with an aging population.3,6

AF is associated with a number of risk factors including coronary heart disease, heart failure, hypertension, diabetes mellitus, age, and valvular heart disease.3 Several modifiable aspects of lifestyle are also thought to play a role in the development of AF, both directly and indirectly. The aims of this paper are threefold; first, to establish the role of common lifestyle factors in the development of AF, secondly to highlight the efficacy of lifestyle modification on prognosis, thirdly to highlight any lifestyle changes that may otherwise impact treatment for AF.


Significant association has been shown between the development of AF and concurrent obesity.7–12 A prospective cohort study with 47,589 participants (mean age 56 years, range 50-64), without pre-existing cardiovascular or endocrine disease, showed a relative risk (RR) increase in the development of AF of 1.08 (95% CI 1.05-1.11) for each unit increase in body mass index.8 Additionally, weight at age 20 and subsequent weight gain have both been strongly associated with the development of AF using a random population sample of 6,903 men.7 A meta-analysis of 123,249 patients across 16 studies showed a 49% increased risk of AF development (RR 1.49, 95% CI 1.36-1.64);10 however, 44,647 of the participants in this analysis were enrolled in post-cardiac surgery studies limiting generalisability.

The correlation between obesity and AF has been shown to occur in patients who have not developed metabolic syndrome.13 Additionally, obesity has been identified as a potential risk factor for the progression of AF from paroxysmal to persistent/permanent.14

Further studies have shown that height as well as weight is an independent risk factor for the development of AF.9 Karas et al. have suggested that the correlation with height highlights a significant limitation in the use of BMI to assess risk of AF.9 Furthermore, in a cohort study of 11,393 post-menopausal women showed a strong correlation between lean body mass and development of incident AF;15 hazard radio 1.24 per 5kg increase (95% CI 1.14-1.34).

The mechanism behind obesity and the development of AF is not clear and is likely to be multifactorial. However, left atrial size has been suggested to play a prominent role. Left atrial (LA) size is known to be increased in obesity.16,17 Additionally this is a known correlate of AF; both in spontaneous development,16,18,19 and recurrence post-ablation.20 A study by Wang et al. has demonstrated that association between BMI and risk of AF was negated once controlled for left atrial size.21 Other proposed roles may include left ventricular (LV) diastolic dysfunction,22 and an increase in pericardial fat.23 Both of these factors are known to be associated with AF.24,25

Reduction in body weight towards normal levels has been shown to improve AF. Pathak et al. have shown that goal directed weight management can lead to a decrease in AF burden.26 Patients with >10% weight loss had decreased symptom severity and arrhythmia free survival (p<0.001) than those with less significant weight loss. It has been further shown that aggressive risk factor management leading to weight loss was associated with significantly increased single-procedure and multiple-procedure post-ablation arrhythmia-free survival.27 There is a pathophysiological correlation with improvement in LA size,28 LV diastolic function,29 and pericardial adiposity seen in obese patients who have lost weight.23


The relationship between smoking and AF is complex. Smoking is known to increase atherosclerosis, ischaemic heart disease, and resulting heart failure;30 all of which are risk factors for the development of AF.3,31,32  However, there is evidence to suggest a direct role of smoking on the development of AF.

A total of six large studies have investigated the link between smoking and the risk of AF.3,8,31–34 Most recently, the Atherosclerosis Risk of Communities (ARIC) study showed an increased risk of AF in both former (HR 1.32, 95% CI 1.10-1.57) and current smokers (HR 2.05, 95% CI 1.71-2.47) when compared to never smokers.33 This correlation remains significant even when controlled for development of coronary heart disease and heart failure. Although, this paper describes a trend towards improved risk of AF development in those that are former smokers compared with current smokers, this was non-significant.

This data is supported by two previous studies,3,34 but no link was found in the remaining three.8,31,32 It has been suggested that the failure of Krahn et al.31 and Frost et al.8 to find a significant correlation was due to combining current and former smokers into a single group for comparison against never smokers.35 A 2016 meta-analysis investigating the association between AF and smoking included 286,217 patients including over a total of 16 prospective studies.36 This analysis by Zhu et al. confirmed a higher prevalence of AF in current smokers (RR 1.25, 95% CI 1.08-1.39) compared with non-smokers. This analysis also showed that current smokers were at increased risk of AF compared with former smokers (RR.121, 95% CI 1.03-1.42) thus supporting the notion that quitting smoking may improve one’s risk of developing AF.

Potential mechanisms for this association have been provided. Nicotine has been shown to increase atrial fibrosis,37 thus providing a potential direct pathological mechanism for the development of AF.37 Furthermore, decreased lung function has been shown to be associated with new AF.38–40 Buch et al. demonstrated that an forced expiratory volume in 1 second (FEV1) <60% had an increased risk of developing atrial fibrillation ( RR 2.14, 95% CI 1.54-2.98, P<0.01) compared with an FEV1 >80%. The role of lung damage has been confirmed by a subgroup analysis of the ARIC study.40 This showed that obstruction (defined as FEV1/Forced vital capacity <70%) was associated with an increased AF incidence versus those without obstruction.

An additional important link with smoking is the increased risk of stroke. Stroke is a well-known and anticipated risk factor associated with AF.2,5 Smoking is widely accepted as an independent risk factor for the development of ischaemic stroke.41 Nakagawa et al.42 have demonstrated in patients with AF that a history of smoking is an independent risk factor for predicting all-cause mortality (HR 2.7, 95% CI 1.7-4.5), and death from stroke (HR 4.7, 95% CI 1.0-22.3). Current smoking showed an increased risk of intracranial bleeding (HR 4.4, 95% CI 1.1-17.6) suggesting greater risk to smokers on oral anticoagulation.

The above data suggests that patients who are at risk of developing AF should be routinely counselled with regards to smoking cessation. Additionally, patients with already established AF should be advised to quit smoking due to increased risk of stroke in this group.

Alcohol intake

The development of arrhythmias has been long recognised following acute significant alcohol consumption.43 This has specifically been recognised in the case of AF following an ‘alcoholic binge’.44

It is well established that alcohol is arrhythmogenic. A correlation has been established between the development of AF and the regular consumption of very large quantities of alcohol (>69g alcohol/day).45 Furthermore, this risk has been shown repeatedly to be true of high alcohol consumption (>36g alcohol/day);46,47 however, moderate consumption has not been consistently associated with the development of AF.45,47 A Japanese meta-analysis has shown that for each 10g/day increase in alcohol intake there is a relative risk of 1.08 (1.05 – 1.10, p<0.001); 48 a similar correlation is supported by an analysis of the data by Frost et al.8 The correlation of alcohol and the development of AF appears to hold true of patients with established risk factors for AF (blood pressure and left ventricular hypertrophy).49

Overall, evidence suggesting the alcohol reduction can improve AF symptoms has been limited. The ARREST-AF study has shown, in a cohort of 149 patients, that aggressive risk factor management has led to a reduction in AF frequency, duration, symptoms and severity.27 However, only 18% (11 patients) in the intervention group had alcohol consumption in excess of 30g/week prior to intervention.


Caffeine is a stimulant ubiquitous to daily life for many people. Common sense might suggest that increased caffeine consumption should increase the risk of tachyarrhythmias including AF. However, two separate meta-analyses have shown that habitual caffeine consumption leads to a reduction in AF risk.50,51

The first, including 115,993 patients over seven observational studies, showed  that caffeine exposure was not associated with a risk of AF.50 Furthermore, pooling results from only those studies considered high-quality showed a 13% odds reduction in AF risk (OR 0.87, CI 0.78-0.92). The second involving 228,465 patients across six cohort studies demonstrated a trend towards reduced AF risk and increased caffeine intake (RR 0.90, CI 0.81-1.01, P=0.07).51 In addition, in an analysis of sub-groups, low-dose caffeine intake led to an 11% decrease in relative risk (RR 0.89, CI 0.80-0.99, P=0.03). A similar reduction was seen for high dose caffeine consumption.

As such, despite a clear potential mechanism, caffeine does not correlate with AF risk. Notwithstanding this evidence, patients continue to be advised to avoid caffeine intake.52 However, patient anecdotes do suggest that some individuals associate caffeine intake with the development of their own arrhythmias.53 As such, although widespread abstinence from caffeine does not appear necessary, advice regarding this subject should be tailored to the patient’s experience.


Physical activity, in the form of moderate exercise, is regularly recommended for primary and secondary prevention of ischaemic heart disease.54 However, there is also evidence to support the role of physical activity in reducing the risk of AF.11,12,55 Huxley et al.11 showed that patients with ‘ideal’ physical activity (defined as up to 149 min/week of moderate/vigorous exercise) showed an 11% (95% CI 0%-21%) lower risk of AF. This correlation remained when corrected for BMI.

Grundvold et al.12 demonstrated that those with above average physical fitness had reduced risk of AF (RR 0.77, 95% CI 0.60 – 0.99). However, this group also demonstrated that those in the top 1% of age-adjusted physical fitness had an AF incidence of 24%, significantly greater than the next 100 patient with greatest age-adjusted physical fitness. As such, patients who exercise at the very highest level are at increased risk of atrial fibrillation.

Starting a physical fitness programme has also been shown to improve AF. Pathak et al.55 showed that arrhythmia-free survival, both with and without rhythm control strategies, was greatest in those patients with high cardiorespiratory fitness. Furthermore, those patients that had a fitness gain ≥2 METS during the trial had significantly greater arrhythmia survival than those with a gain of <2 METS.


Multiple aspects of modifiable lifestyle play an important role in the development of AF. In particular obesity, smoking, and alcohol intake have all been shown to increase the risk of developing AF. Limited evidence is becoming available showing that modification of these risk factors can reduce the risk of AF development. Importantly, not all likely risk factors have been shown to have a role in AF. Notably, caffeine, despite its stimulant properties, has not been shown to increase the risk of developing AF.

Patient counselling regarding potential lifestyle changes that can be made should play a central role in clinical encounters. This should be the case for both patients who already have AF and those who are likely to be at risk of developing AF.


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