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16, 2017
STATE-OF-THE-ART REVIEW
Carl J. Lavie, MD,a Ambarish Pandey, MD,b Dennis H. Lau, MBBS, PHD,c Martin A. Alpert, MD,d
Prashanthan Sanders, MBBS, PHDc
ABSTRACT
Both obesity and atrial brillation (AF) are increasing in epidemic proportions, and both increase the prevalence of
cardiovascular disease events. Obesity has adverse effects on cardiovascular hemodynamics and cardiac structure and
function, and increases the prevalence of AF, partly related to electroanatomic remodeling in obese patients. However,
numerous studies, including in AF, have demonstrated an obesity paradox, where overweight and obese patients with
these disorders have a better prognosis than do leaner patients with the same degree of severity of cardiovascular
disease/AF. In this paper, the authors discuss special issues regarding AF in obesity, as well as the evidence that
despite the presence of an obesity paradox, there are benets of weight loss, physical activity/exercise training,
and increases in cardiorespiratory tness on the prognosis of obese patients with AF. (J Am Coll Cardiol 2017;70:202235)
2017 by the American College of Cardiology Foundation.
From the aDepartment of Cardiovascular Diseases, John Ochsner Heart and Vascular Institute, Ochsner Clinical School-The
University of Queensland School of Medicine, New Orleans, Louisiana; bDivision of Cardiology, University of Texas South-
western Medical Center, Dallas, Texas; cCentre for Heart Rhythm Disorders, South Australian Health and Medical Research
Institution, University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia; and the dDivision of Cardiovascular Medicine,
Listen to this manuscripts University of Missouri School of Medicine, Columbia, Missouri. Dr. Sanders is supported by a Practitioner Fellowship from the
audio summary by National Health and Medical Research Council of Australia. Dr. Lavie is author of the book The Obesity Paradox; and has served as
JACC Editor-in-Chief a promotional speaker and consultant for Bristol-Myers Squibb, Pzer, and Boehringer Ingelheim. Dr Lau has received lecture and/
Dr. Valentin Fuster. or consulting fees from St. Jude Medical, Boehringer Ingelheim, Bayer, and Pzer. Dr. Sanders has been on advisory boards of
Biosense Webster, Medtronic, St. Jude Medical, Boston Scientic, and CathRx; has received lecture and/or consulting fees from
Biosense Webster, Medtronic, St. Jude Medical, and Boston Scientic; and has received research funding from Medtronic, St. Jude
Medical, Boston Scientic, Biotronik, and Sorin. All other authors have reported that they have no relationships relevant to the
contents of this paper to disclose.
Manuscript received April 5, 2017; revised manuscript received August 23, 2017, accepted September 1, 2017.
JACC VOL. 70, NO. 16, 2017 Lavie et al. 2023
OCTOBER 17, 2017:202235 Obesity and Atrial Fibrillation
The estimated prevalence in the United States is coming decades given its burgeoning ABBREVIATIONS
approximately 5.2 million, and is expected to increase epidemic worldwide (16). A recent large study AND ACRONYMS
to 12.1 million by the year 2030 (4,5). Although reports the association between genetically
AF = atrial brillation
numerous factors contribute to this epidemic of AF, predicted obesity and AF incidence, making
BMI = body mass index
the obesity epidemic, which leads to left atrial (LA) the case that primordial prevention may be
CHD = coronary heart disease
remodeling by various mechanisms (4,6,7), is associ- needed in the AF epidemic (17).
ated with a marked increase in the risk of developing The ARIC (Atherosclerosis Risk In Commu- CRET = cardiac rehabilitation
and exercise training
AF. As with other CVDs, however, there is evidence nities) study estimates that almost 1 in 5 cases
CRF = cardiorespiratory tness
that although obesity increases the risk for the devel- of AF can be attributable to overweight or
CVD = cardiovascular disease
opment of AF, overweight and obese patients with AF obesity (16), and another report from the ARIC
seem to have a better prognosis, including CVD and study showed that trajectories of various CVD EAT = epicardial adipose tissue
all-cause survival, compared to lean AF patients, risk factors many years before the diagnosis of HF = heart failure
indicating an apparent obesity paradox (2,7,8). AF impacted the subsequent development of LA = left atrial
Although we and others have reviewed the AF (18). A recent meta-analysis of 51 studies LAE = left atrial enlargement
association and impact of obesity on AF (911), we involving more than 600,000 individuals has LV = left ventricle/ventricular
believe that this current state-of-the-art review of evaluated the impact of obesity on AF in LVH = left ventricular
AF and obesity most comprehensively reviews the different clinical scenarios (19). Specically, hypertrophy
adverse effects of obesity on cardiovascular hemody- every 5-unit increment in BMI was found to MET = metabolic equivalent
namics, cardiac structure and function, the electro- confer an additional 19% to 29% risk of of task
physiological effects of obesity, and other mechanisms incident AF, a 10% risk of post-operative AF, PV = pulmonary vein
that may increase the prevalence of AF. We review and a 13% risk of post-ablation AF (19). Not RV = right ventricle/ventricular
data on the impact of obesity on prognosis in AF, surprisingly, longitudinal cohort data from SVR = systemic vascular
special management issues in the obese patient with the Womens Health Study and Olmsted resistance
AF, and implications for weight loss and increases in County both demonstrated that the obese state con-
physical activity, exercise training, and improvements tributes to disease progression, whereby increasing
in cardiorespiratory tness (CRF) on prognosis of AF. BMI was associated with incremental risk of devel-
oping a persistent or permanent form of AF (20,21).
OBESITY AND AF:
EPIDEMIOLOGICAL CONSIDERATIONS IMPACT OF OBESITY ON CARDIAC
PERFORMANCE AND MORPHOLOGY
Early epidemiological studies have uncovered a host
of established cardiovascular conditions that are EFFECTS OF OBESITY ON CARDIAC PERFORMANCE
independently associated with the development AND MORPHOLOGY: GENERAL CONSIDERATIONS.
of AF. More recently, obesity has emerged as an in- Obesity is associated with a variety of hemodynamic
dependent risk factor for AF (1215). For example, alterations that predispose to changes in cardiac
long-term prospective data from the Framingham morphology, which may result in ventricular
Heart Study with almost 14 years of follow-up has dysfunction (2224). The effects of obesity on hemo-
identied obesity as an important modiable risk dynamics and cardiac structure and function are
factor for AF (12). Importantly, the association summarized in Table 1 and Figure 1. These alterations
between obesity and AF has been shown to be are most pronounced in severely obese patients, but
independent of obstructive sleep apnea, a common may occur to a lesser extent in those with mild-to-
comorbid condition in obese individuals (13). moderate obesity. Excessive adipose accumulation,
Furthermore, data from the Womens Health Study in association with increased lean body mass,
have elegantly demonstrated the dynamic nature of produces an increase in total and central blood
the risk for AF with weight changes (14). Specically, volume. In most obese individuals, these alterations
short-term weight gain to BMI >25 kg/m2 was found promote an increase in cardiac output, a response
to be associated with substantial risk of developing that is facilitated by a decrease in systemic vascular
AF, and obese individuals who lost weight to resistance (SVR). Because there is little change in
BMI <30 kg/m 2 over 5 years were found to have heart rate, the rise of cardiac output is attributable
reduced AF risk similar to those who maintained predominantly to an increase in left ventricular (LV)
BMI <30 kg/m 2 over the same period of time (14). stroke volume. Augmentation of cardiac output
Obesity represents the second highest population- predisposes to LV enlargement and eccentric LV
attributable risk for AF behind hypertension and hypertrophy (LVH). Recent studies suggest that
will likely escalate the global burden of AF in the central obesity is not always associated with elevated
2024 Lavie et al. JACC VOL. 70, NO. 16, 2017
LV Dilation
in Some
RV Failure Hypertension
Neurohormonal
and
LA Pressure LV Hypertrophy
Metabolic
and Volume Alterations
Inadequate Adequate
LV Systolic LV Diastolic
Dysfunction Dysfunction
LV Failure
Proposed pathophysiology of obesity cardiomyopathy. This diagram shows the central hemodynamic alterations that result from
excessive adipose accumulation in severely obese patients and their subsequent effects on cardiac morphology and ventricular function.
Left ventricular (LV) hypertrophy in severe obesity may be eccentric or concentric. Factors inuencing LV remodeling and geometry
include severity and duration of obesity, duration and severity of adverse LV loading conditions (particularly hypertension), and, possibly,
neurohormonal and metabolic abnormalities such as increased sympathetic nervous system tone, activation of the renin-angiotensin-
aldosterone system, insulin resistance with hyperinsulinemia, leptin resistance with hyperleptinemia, adiponectin deciency, lipotoxicity,
and lipoapoptosis. These alterations may contribute to the development of LV failure. LV failure, facilitated by pulmonary arterial
hypertension from sleep apnea/obesity hypoventilation, may subsequently lead to right ventricular (RV) failure. Adapted from
Alpert et al. (22). CVD cardiovascular disease; LA left atrial.
2026 Lavie et al. JACC VOL. 70, NO. 16, 2017
presence of LVH (eccentric or concentric) in associa- 113), adipocytokines (adiponectin, leptin, resistin,
tion with LV diastolic dysfunction (9,2228,32). visfatin, omentin), inammatory cytokines and
The hypercirculatory state serves as both a direct chemokines and various interleukins (including IL1 b
contributor to LAE and as a major cause of LVH, and IL6), plasminogen activator inhibitor-1, tumor
LV diastolic dysfunction, and elevated LA pressure necrosis factor alpha, monocyte chemotactic protein 1,
(9,2228,32). Hypertension occurs in nearly one-half chemokine ligands, adrenomedullin, and phospholi-
of obese patients and more than 60% of severely pase A2 (36,37). Pericardial fat is also biologically
obese patients (2224). Hypertension is a well- active and is a depot of visceral adipose tissue
established cause of LAE, increased LA pressure, and (27,36,37). As such, it provides endocrine, paracrine,
LA hypertrophy. This is due primarily to the devel- and autocrine functions that are similar to those of
opment of LVH and LV diastolic dysfunction, but also visceral adipose tissue elsewhere in the body
to comorbidities, such as diabetes mellitus, CHD, and (27,36,37). Cardiac adipose is most pronounced over
obstructive sleep apnea. All of these comorbidities the RV, but can also be found to a lesser extent over the
are commonly associated with obesity and may surface of the LV, in the atrioventricular grooves,
contribute to LA remodeling and LV diastolic and along the posterior surface of the LA (2224,36).
dysfunction by various mechanisms (2227,33). Pericardial fat and EAT have been shown to wrap
Recently, abnormal LA strain has been described around the pulmonary veins (PVs) as they enter
during diastole in obese subjects (2224). Increased LA the LA (36,37). EAT contains a dense network
stretch and insufcient LA emptying have also been of autonomic ganglia (consisting predominantly of
reported in obese patients (27). Various neurohor- parasympathetic nerve bers) (27,28,36,37).
monal, and metabolic factors, growth factors, adipo- Multiple controlled studies employing cardiac
cytokines, and inammatory markers were described imaging techniques (primarily computed tomography)
in a study of 30 obese sheep (29). Abed et al. (29) re- have demonstrated an association of pericardial
ported increases in LA volume (p 0.01), transforming fat and AF (3638). Most of these studies did not
growth factor 1 (p 0.02), platelet-derived growth distinguish between pericardial fat and EAT. It is
factor (p 0.02), LA brosis (p 0.02), LA inamma- thought however, that fat deposits directly in contact
tory inltrates (p 0.01), and lipidosis (p 0.02) in LA with LA myocardium (EAT) are more likely to
myocardium (33). It has been proposed that many of contribute to the development of AF (3638). Nearly all
these factors contribute to LA remodeling and of these studies showed that greater volumes or
dysfunction in humans, and as such may serve as both thicknesses of pericardial fat were associated with a
triggers and substrates for AF. EAT is thought to be a higher prevalence of paroxysmal and persistent AF
source of many of these factors. This is discussed in (3639). In one study, each SD increase in pericardial
more detail in the following section. The changes in fat volume was associated with a 28% increase in
LA morphology may provide a substrate for electro- the prevalence of AF (38). In another study, a 10%
physiological remodeling of the LA, which may pre- increase in pericardial fat volume increased the odds
dispose to and perpetuate AF, affecting its severity of AF by 13% (37). Several studies have reported an
and the response to catheter ablation. association between pericardial fat volume and
severity of AF (trends toward persistent AF and
RELATION OF EAT AND PERICARDIAL FAT TO AF. more symptoms) (27,3639). Multiple studies have
In recent years, there has been increasing interest in identied excessive pericardial fat as a predictor of
the role of cardiac fat in the development of AF, a higher recurrence rate of AF after catheter ablation
particularly EAT and pericardial fat (3640). EAT is (27,3639). In one study, respective pericardial
located between the visceral pericardium and the thicknesses of 6.0 and 6.9 mm identied patients who
epicardial layer of myocardium (36,37). Pericardial were at higher risk of recurrence of paroxysmal
adipose tissue or pericardial fat is located beyond the and nonparoxysmal AF after catheter ablation (37).
parietal pericardium (36,37). Both forms of cardiac Indeed, a recent meta-analysis has suggested that the
fat are derived from brown fat, but are embryologically associations of AF with pericardial fat were stronger
distinct (36,37). EAT is highly biologically active. than those with abdominal or overall adiposity (40).
It secretes metabolic factors (free fatty acids and Pericardial fat volumes correlated with complex frag-
uncoupling protein-1), angiogenic factors (angio- mented LA electrograms in patients with AF (37).
tensin, endostatin, vascular endothelial growth Excessive interatrial adiposity may also predispose
factor-1, thrombospondin-2, angiopoetin), growth and to AF (41).
remodeling factors (activing A, follistatin, trans- Obesity, particularly central obesity, is associated
forming growth factors 13, matrix metalloproteinases with increased pericardial fat volumes (2224).
JACC VOL. 70, NO. 16, 2017 Lavie et al. 2027
OCTOBER 17, 2017:202235 Obesity and Atrial Fibrillation
F I G U R E 2 Obesity and AF
Cardiometabolic
Abnormalities
HTN
Obesity
Dyslipidemia
Metabolic Syndrome/
DM
Adiposity
Mechanical Effects Inflammation EAT
Hemodynamics Adipocytokines Metabolic and
OSA Paracrine Effects Neurohormonal
Ventricular
LA Remodeling
Abnormalities
Dilation/stretch
LV Remodeling
Fatty infiltration
LVH
Fibrosis
HF
Conduction slowing
CHD
Atrial
Fibrillation
Proposed mechanisms explaining the increased risk of atrial brillation in obesity. CHD coronary heart disease; DM diabetes mellitus;
EAT epicardial adipose tissue; HF heart failure; HTN hypertension; LVH left ventricular hypertrophy; OSA obstructive sleep apnea;
other abbreviations as in Figure 1.
PROGNOSIS OF AF RELATED TO BODY COMPOSITION- In contrast to the higher risk of AF recurrence and
OBESITY PARADOX. There has been increasing inter- progression with increasing adiposity, recent cohort
est in evaluating the impact of obesity on long-term studies have demonstrated the phenomenon of an
clinical outcomes among individuals with estab- obesity paradox for risk of mortality among
lished AF. Several studies have implicated obesity in patients with prevalent AF, such that overweight
progression of AF and recurrence after ablation or and obesity (vs. normal BMI) was associated with a
cardioversion. Recent studies have demonstrated a signicantly lower risk of all-cause mortality on long-
strong graded association between higher overall term follow-up (5355). In a study from the ORBIT-AF
adiposity, as measured by BMI, and risk of persistent registry (Outcomes Registry for Better Informed
and post-ablation AF (40,52). Similar associations Treatment of Atrial Fibrillation), a contemporary
have also been reported for measures of site-specic cohort of patients with prevalent AF, Pandey et al.
adiposity, such as epicardial fat and visceral (55) demonstrated a 35% lower risk of all-cause
adiposity, and risk of AF progression and recurrence mortality among Class I obese patients with AF
(51). as compared with those with normal BMI. Similar
JACC VOL. 70, NO. 16, 2017 Lavie et al. 2029
OCTOBER 17, 2017:202235 Obesity and Atrial Fibrillation
involved cardiac surgery patients (37,74,75). A meta- these ndings suggest that substantial amount of
analysis of 6 studies of patients undergoing coro- weight loss may be needed to signicantly lower the
nary artery bypass surgery suggested that posterior AF incidence in at-risk patients.
pericardiectomy signicantly reduced the incidence Among patients with established AF, lifestyle
of post-operative AF (74). More recently, a study interventions with sustained weight loss have been
assessing injections of botulinum toxin into the associated with reduction in the AF burden and
epicardial fat pad reduced the recurrence rate of AF symptom severity in a dose-dependent fashion. In a
after cardiac surgery (75). randomized controlled trial with 248 prevalent AF
IMPLICATIONS REGARDING WEIGHT LOSS IN AF patients, Abed et al. (72) demonstrated that weight
AND PROGNOSIS. Substantial weight loss in normo- reduction through participation in a structured
tensive persons with expanded total and central weight management program was associated with
blood volume is capable of reducing total and central signicant reduction in AF symptom burden and
blood volume, LV stroke volume, and cardiac output lower risk of AF recurrence. Similarly, in the obser-
(2224). Weight loss in such individuals increases SVR vational LEGACY (Long-Term Effect of Goal Directed
in most, but this depends on the blood pressure Weight Management on Atrial Fibrillation Cohort:
response, but regardless produces regression in LVH. A 5 Year Follow-Up Study) cohort, Pathak et al. (73)
The effects on LV end-diastolic pressure and LA demonstrated that AF patients with signicant
pressure are more variable, with reduction in some intentional weight loss over a 5-year follow-up
patients and no signicant change in others (2224). (>10%) had 6-fold higher likelihood of arrhythmia-
Impaired noninvasive LV diastolic lling parameters free survival, as compared with those with modest-
generally improve with weight loss (2224). LV sys- to no-weight change (<3%). Similar ndings were also
tolic function usually does not change with weight observed in a Mediterranean cohort of AF patients,
loss or slightly decreases (2224). However, LV sys- where individuals with higher and increasing
tolic function may improve in patients with a reduced BMI over long-term follow-up had higher risk of AF
LV ejection function (2224). Symptoms and signs of recurrences (79).
HF generally improve in those with obesity cardio- Structured physician-directed risk factor and
myopathy (24). The effect of weight loss on pulmo- weight management programs have also been shown
nary artery pressure, pulmonary vascular resistance, to improve long-term success of AF ablation with
and right heart pressures is variable, depending on better symptom control and recurrence-free survival
the contributions of left-sided HF and the hemody- (80). The mechanism underlying the favorable impact
namic response to sleep apnea and obesity hypo- of weight loss on AF related outcomes are related to
ventilation (2224). In many patients, pulmonary both indirect effects on CVD risk factors and direct
hemodynamics and right heart pressures improve as effects on cardiac structure and function (73,80,81).
HF and sleep-disordered breathing improves (2224). Weight loss has been associated with favorable
These weight loss-related alterations have been cardiac structural remodeling, with decreases in LA
associated with reductions in the frequency, symp- volumes, LV wall thickness, and improvements in LV
tom burden, and severity of AF (72,73). diastolic function (73,80,81). Furthermore, recent
Findings from large prospective cohort studies, studies have also demonstrated that intentional
such as the Womens Health Study and the ARIC weight loss is associated with signicant reduction
study, have shown that weight gain is associated with in EAT, a well-established mediator of AF through
increased risk of AF (14,76). Similarly, several lifestyle proinammatory and brotic paracrine effects
intervention studies have demonstrated that lifestyle (52,81,82). Taken together, these studies provide
risk factor modication with intentional weight loss strong evidence in favor of management strategies
has a favorable impact on the epidemiology of AF. aimed at weight loss and associated cardiac substrate
In a cohort study of Swedish Obese Subjects, Jamaly modication among symptomatic AF patients.
et al. (77) demonstrated that weight loss through Future studies are needed to determine if weight
bariatric surgery is associated with lower incidence of loss strategies can lower long-term risk of adverse
AF among individuals with severe obesity (77). This is clinical outcomes, such as mortality, stroke, and HF
in contrast to the ndings from the Look AHEAD hospitalization.
(Look AHEAD: Action for Health in Diabetes) study, IMPLICATIONS REGARDING PHYSICAL ACTIVITY,
where modest weight loss from intensive lifestyle EXERCISE, CRF, AND AF. Physical inactivity and
interventions was not associated with lower risk of low CRF have been traditionally associated with
AF in subjects with diabetes (78). Taken together, higher risk of CVD, such as CHD and HF (8387).
JACC VOL. 70, NO. 16, 2017 Lavie et al. 2031
OCTOBER 17, 2017:202235 Obesity and Atrial Fibrillation
Proposed mechanism of benets of weight loss and exercise training to reduce atrial brillation. AF atrial brillation; CV cardiovascular.
The relationship between PA levels and risk of AF more recent review suggests a modest benet of
is more complex. Multiple longitudinal and case physical activity at approximately 1,000 to 1,500
control studies have reported that a higher risk of AF metabolic equivalents of task (MET) minutes per
is particularly present among athletes who participate week (99). Taken together, ndings from these
in endurance sports (8891). Among healthy, but studies suggest that higher levels of PA within the
nonathletic, individuals, the association between optimal range may be benecial and not associated
physical activity and risk of AF is less well estab- with increased risk of AF.
lished. Some studies have reported a higher risk of AF Recent studies have also explored the association
with increased PA levels over a lifetime, whereas between CRF levels, an accurate and objective mea-
others have reported an inverse or J-shaped associa- sure of exercise capacity, and risk of AF in the general
tion between physical activity levels and risk of AF population. These studies have demonstrated a
(76,90,9297). In a recent meta-analysis of 19 cohort consistent dose-dependent inverse association
studies, Kwok et al. (98) observed no association be- between CRF and risk of AF (100102). Thus, low CRF
tween physical activity and risk of AF, although a could represent an important modiable risk factor
2032 Lavie et al. JACC VOL. 70, NO. 16, 2017
for AF that could be targeted with exercise to determine if the benecial effects of exercise in
interventions. However, in a recent study from the AF patients in the short-term may translate into
Look AHEAD trial, Alonso et al. (78) did not observe a favorable CVD outcomes in the long-term follow-up.
signicant association between improvement in CRF LIMITATIONS AND FUTURE RESEARCH.
with intensive lifestyle interventions and risk of AF
among individuals with diabetes. This could be Current data on the obesity paradox and mortality
related to the only relatively modest changes in CRF outcomes are statistically adjusted from non-
levels among Look AHEAD study participants with matched cohorts with very different baseline
lifestyle intervention (<1 MET by the end of the characteristics, including age, CVD risk prole, and
study) and relatively small number of incident AF medications usage.
events in this large study. There is a clear lack of dedicated research in obese
Among patients with existing AF, however, higher individuals, with limited data available to guide
CRF levels have been associated with greater safe use of various antiarrhythmic and anti-
arrhythmia-free survival. In the CARDIOFIT (Impact coagulation therapies.
of Cardiorespiratory Fitness on Arrhythmia Recur- More work is needed to evaluate the impact of
rence in Obese Individuals With Atrial Fibrillation) epicardial adiposity on AF pathogenesis to guide
study, Pathak et al. (103) demonstrated that 1-MET potential specic therapeutics.
higher CRF at baseline was associated with 13% It is unknown whether intentional weight loss
lower risk of AF recurrence. Furthermore, improve- and exercise in obese individuals with AF may
ment in CRF on long-term follow-up was also asso- confer mortality benets in addition to improved
ciated with signicantly lower AF symptom burden AF outcomes and quality of life.
and AF recurrence. Similarly, in a recent randomized
controlled trial, Malmo et al. (104) showed that CONCLUSIONS
aerobic interval exercise training was associated with
signicantly lower burden of AF among patients Obesity and AF have been increasing in epidemic
in short-term follow-up. They also observed a trend proportions in the United States and in most of the
towards improvement in clinical outcomes, such as Westernized world. These disorders are strongly
need for cardioversion and hospitalization among interrelated, and the risk of AF is markedly increased
exercise participants. in the setting of obesity and weight gain. However, as
Several factors may underlie the observed with other established CVDs, a strong obesity paradox
benecial effects of exercise and higher CRF in in AF has been reported in many individual trials and
lowering AF burden, including improvement in car- large meta-analyses, showing that overweight and
diometabolic risk factor prole, lower sympathetic obese with AF appear to have a better prognosis than
drive, and favorable changes in cardiac structure do their leaner counterparts with AF. Nevertheless,
and function (103,105). This is consistent with the recent evidence indicates that weight-loss programs,
previously reported favorable pleiotropic effects of as well as programs increasing physical activity, ex-
exercise among healthy individuals, as well as those ercise, and levels of CRF, reduce recurrences of AF in
with HF (106108). patients with a history of AF, and higher levels of CRF
Cardiac rehabilitation and exercise training (CRET) appear to be associated with the primary prevention
programs have been shown to improve exercise of AF. Future studies are needed to assess the impacts
capacity, symptom burden, and lower hospitalization of CRET and other weight-loss programs, as well as
rates in patients with other CVD conditions, such as physical activity/exercise, on the prevention of
CHD and HF (108,109). The American College of other major CVD events, including CHD and HF, as
Cardiology/American Heart Association guidelines well as CVD- and all-cause mortality, among patients
have strong recommendations for CRET as a key with AF.
component of management of these CVDs (110,111).
However, the role of exercise for management of AF ADDRESS FOR CORRESPONDENCE: Dr. Carl J. Lavie,
is not well dened in the current guidelines. Findings Cardiac Rehabilitation, Exercise Laboratories, John
from the studies discussed above provide strong ev- Ochsner Heart and Vascular Institute, Ochsner
idence in favor of incorporating exercise as an adjunct Clinical School - The University of Queensland School
strategy for AF management (Central Illustration). of Medicine, 1514 Jefferson Highway, New Orleans,
Future large randomized controlled trials are needed Louisiana 70121-2483. E-mail: clavie@ochsner.org.
JACC VOL. 70, NO. 16, 2017 Lavie et al. 2033
OCTOBER 17, 2017:202235 Obesity and Atrial Fibrillation
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