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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/cdn\/css\/http\/css_Xg7z6oCTVgud_Q0huYz9x9iiD5H_2YPSJ5z2ZViSWdY.css\u0022 media=\u0022all\u0022 \/\u003E\n\u003Clink rel=\u0027stylesheet\u0027 type=\u0027text\/css\u0027 href=\u0027\/sites\/all\/modules\/contrib\/panels\/plugins\/layouts\/onecol\/onecol.css\u0027 \/\u003E\u003C\/head\u003E\u003Cbody\u003E\u003Cdiv class=\u0022panels-ajax-tab-panel panels-ajax-tab-panel-sageoa-tab-art\u0022\u003E\u003Cdiv class=\u0022panel-display panel-1col clearfix\u0022 \u003E\n  \u003Cdiv class=\u0022panel-panel panel-col\u0022\u003E\n    \u003Cdiv\u003E\u003Cdiv class=\u0022panel-pane pane-highwire-markup\u0022 \u003E\n  \n      \n  \n  \u003Cdiv class=\u0022pane-content\u0022\u003E\n    \u003Cdiv class=\u0022highwire-markup\u0022\u003E\u003Cdiv xmlns=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022 id=\u0022content-block-markup\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\u003Cp id=\u0022p-1\u0022\u003EThe Einthoven Lecture, presented by Prof G\u00fcnter Breithardt, focused on atrial fibrillation (AF) and reviewed the history, mechanisms, and pathogenesis of AF. He focused on the association of metabolic syndrome and obesity with AF. These associations provide evidence that supports treatment strategies designed to prevent the development of AF.\u003C\/p\u003E\u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003Eablation\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Earrhythmias\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Eatrial fibrillation\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Eepicardial adipose tissue\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Eepidemiology\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Emetabolic syndrome\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Eobesity\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Eprimary prevention\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Esleep apnea\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Estroke\u003C\/li\u003E\u003C\/ul\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-1\u0022\u003E\u003Cp id=\u0022p-2\u0022\u003ESince the first electrocardiogram recording of atrial fibrillation (AF) in the late 1800s and early studies showing the link between AF and stroke, much has been learned about this condition. G\u00fcnter Breithardt, MD, Universit\u00e4tsklinikum M\u00fcnster, M\u00fcnster, Germany, discussed how we are expanding our understanding of the influence of comorbid conditions on AF and how to use this understanding to improve patient care.\u003C\/p\u003E\u003Cp id=\u0022p-3\u0022\u003EAF is important given its increasing prevalence in the current era. Although it is a global disease, the epidemiology of the condition varies by region. In 2010, the estimated global burden of AF was 33.5 million, with the United States and Canada having the highest prevalence, whereas Europe and Australia had the highest proportion of deaths associated with AF [Chugh SS et al. \u003Cem\u003ECirculation\u003C\/em\u003E. 2014].\u003C\/p\u003E\u003Cp id=\u0022p-4\u0022\u003EThe clinical management of AF is evolving toward a more personalized approach based on validated parameters that encompass atrial morphology and damage, brain imaging, information on genetic predisposition, systemic or local inflammation, and markers for cardiac strain [Kirchhof P et al. \u003Cem\u003EEuropace\u003C\/em\u003E. 2013].\u003C\/p\u003E\u003Cp id=\u0022p-5\u0022\u003EOf particular interest in the management of AF is the potential impact of appropriately treating comorbid conditions. Results from a 2011 study of 14\u2005598 individuals (mean age, 54.2 years) who had been followed for 17 years in the ARIC study showed that 57% of incident AF events could be associated with risk factors such as hypertension, obesity, diabetes mellitus, smoking, and prior cardiac disease [Huxley RR et al. \u003Cem\u003ECirculation\u003C\/em\u003E. 2011]. Thus, the majority of AF burden is potentially avoidable through the optimization of cardiovascular risk factor levels. As the number of comorbidities\/risk factors for AF increases, there is higher likelihood that AF will progress to being permanent and the risk of stroke increases [Nabauer M et al. \u003Cem\u003EEuropace\u003C\/em\u003E. 2009].\u003C\/p\u003E\u003Cp id=\u0022p-6\u0022\u003EAlthough the current European Society of Cardiology (ESC) guidelines encourage early treatment of AF using a variety of treatment modalities [Camm AJ et al. \u003Cem\u003EEur Heart J\u003C\/em\u003E. 2011], Prof Breithardt believes that we are still not paying enough attention to primary prevention. He is currently involved in the EAST trial, run by AFNET jointly with EHRA, a prospective study designed to test the hypothesis that an early, structured rhythm control therapy based on antiarrhythmic drugs and catheter ablation can prevent AF-related complications in patients with AF when compared with usual care.\u003C\/p\u003E\u003Cp id=\u0022p-7\u0022\u003EWhen studying AF, it is important not to bundle AF patients together as there are a variety of clinical subgroups, including a large group of patients with unclassified AF. Among these are patients with obesity, increased body mass index, and the metabolic syndrome. In a meta-analysis of nearly 6000 cases of AF, increasing body mass index was associated with a significant increase in AF incidence, whereas sustained weight loss was associated with significant reduction of AF burden [Pathak RK et al. \u003Cem\u003EJ Am Coll Cardiol\u003C\/em\u003E. 2015]. Importantly, as the number of components of the metabolic syndrome increase, so does the probability of AF (\u003Ca id=\u0022xref-fig-1-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F1\u0022\u003EFigure 1\u003C\/a\u003E) [Chamberlain AM et al. \u003Cem\u003EAm Heart J\u003C\/em\u003E. 2010].\u003C\/p\u003E\u003Cdiv id=\u0022F1\u0022 class=\u0022fig pos-float  odd\u0022\u003E\u003Cdiv class=\u0022highwire-figure\u0022\u003E\u003Cdiv class=\u0022fig-inline-img-wrapper\u0022\u003E\u003Cdiv class=\u0022fig-inline-img\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/15\/22\/4\/F1.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022Incidence of Atrial Fibrillation Associated With Increasing Components of Metabolic SyndromeFigure adjusted for the following covariates at baseline: age (45 to \u0026amp;lt;\u0026#x2005;50, 50 to \u0026amp;lt;\u0026#x2005;55, 55 to \u0026amp;lt;\u0026#x2005;60, \u0026#x2265;\u0026#x2005;60), sex, race, center, educational attainment, smoking status and cigarette-years of smoking (quartiles).Reprinted from Chamberlain AM et al, Metabolic syndrome and incidence of atrial fibrillation among blacks and whites in the Atherosclerosis Risk in Communities (ARIC) Study, Am Heart J, 2010, Vol 159, Issue 5, Pages 850-856, with permission from 2010 Mosby, Inc.\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-1535134800\u0022 data-figure-caption=\u0022\u0026amp;lt;div xmlns=\u0026amp;quot;http:\/\/www.w3.org\/1999\/xhtml\u0026amp;quot;\u0026amp;gt;Incidence of Atrial Fibrillation Associated With Increasing Components of Metabolic SyndromeFigure adjusted for the following covariates at baseline: age (45 to \u0026amp;amp;lt;\u0026#x2005;50, 50 to \u0026amp;amp;lt;\u0026#x2005;55, 55 to \u0026amp;amp;lt;\u0026#x2005;60, \u0026#x2265;\u0026#x2005;60), sex, race, center, educational attainment, smoking status and cigarette-years of smoking (quartiles).Reprinted from Chamberlain AM et al, Metabolic syndrome and incidence of atrial fibrillation among blacks and whites in the Atherosclerosis Risk in Communities (ARIC) Study, \u0026amp;lt;em\u0026amp;gt;Am Heart J, 2010\u0026amp;lt;\/em\u0026amp;gt;, Vol 159, Issue 5, Pages 850-856, with permission from 2010 Mosby, Inc.\u0026amp;lt;\/div\u0026amp;gt;\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003E\u003Cimg class=\u0022fragment-image\u0022 alt=\u0022Figure 1.\u0022 src=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/15\/22\/4\/F1.medium.gif\u0022\/\u003E\u003C\/a\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cul class=\u0022highwire-figure-links inline\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/15\/22\/4\/F1.large.jpg?download=true\u0022 class=\u0022highwire-figure-link highwire-figure-link-download\u0022 title=\u0022Download Figure 1.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload figure\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/15\/22\/4\/F1.large.jpg\u0022 class=\u0022highwire-figure-link highwire-figure-link-newtab\u0022 target=\u0022_blank\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EOpen in new tab\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/16750\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003Cdiv class=\u0022fig-caption\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cspan class=\u0022fig-label\u0022\u003EFigure 1.\u003C\/span\u003E \u003Cp id=\u0022p-8\u0022 class=\u0022first-child\u0022\u003EIncidence of Atrial Fibrillation Associated With Increasing Components of Metabolic Syndrome\u003C\/p\u003E\u003Cp id=\u0022p-9\u0022\u003EFigure adjusted for the following covariates at baseline: age (45 to \u0026lt;\u200550, 50 to \u0026lt;\u200555, 55 to \u0026lt;\u200560, \u2265\u200560), sex, race, center, educational attainment, smoking status and cigarette-years of smoking (quartiles).\u003C\/p\u003E\u003Cp id=\u0022p-10\u0022\u003EReprinted from Chamberlain AM et al, Metabolic syndrome and incidence of atrial fibrillation among blacks and whites in the Atherosclerosis Risk in Communities (ARIC) Study, \u003Cem\u003EAm Heart J, 2010\u003C\/em\u003E, Vol 159, Issue 5, Pages 850-856, with permission from 2010 Mosby, Inc.\u003C\/p\u003E\u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cp id=\u0022p-11\u0022\u003EExcess weight is also a predictor of sleep-disordered breathing, or sleep apnea, which is itself an independent predictor of stroke [Yaggi HK et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E. 2005]. Indices of sleep-disordered breathing are positively correlated with visceral fat [Vgontzas AN et al. \u003Cem\u003EJ Clin Endocrinol Metab\u003C\/em\u003E. 2000], as well as higher plasma concentrations of the tumor necrosis factor-\u03b1 and the proinflammatory cytokine interleukin-6, both of which are markers of inflammation [Vgontzas AN et al. \u003Cem\u003ESleep Med Rev\u003C\/em\u003E. 2005].\u003C\/p\u003E\u003Cp id=\u0022p-12\u0022\u003EThere is also a relationship between sleep-disordered breathing, overweight\/obesity, and heart failure (HF). It has recently been suggested that HF with preserved ejection fraction (HFpEF) may be another manifestation of the metabolic syndrome in which myocardial dysfunction and remodeling are driven by inflammation (\u003Ca id=\u0022xref-fig-2-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F2\u0022\u003EFigure 2\u003C\/a\u003E) [Paulus WJ, Tschope C. \u003Cem\u003EJ Am Coll Cardiol\u003C\/em\u003E. 2013].\u003C\/p\u003E\u003Cdiv id=\u0022F2\u0022 class=\u0022fig pos-float  odd\u0022\u003E\u003Cdiv class=\u0022highwire-figure\u0022\u003E\u003Cdiv class=\u0022fig-inline-img-wrapper\u0022\u003E\u003Cdiv class=\u0022fig-inline-img\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/15\/22\/4\/F2.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022New Paradigm for Heart Failure With HFpEF: Importance of ComorbiditiesComorbidities induce a systemic proinflammatory state with elevated plasma levels of interleukin (IL)-6, tumor necrosis factor (TNF)-a, soluble ST2 (sST2), and pentraxin 3. Coronary microvascular endothelial cells reactively produce reactive oxygen species (ROS), vascular cell adhesion molecule (VCAM), and E-selectin. Production of ROS leads to formation of peroxynitrite (ONOO) and reduced nitric oxide (NO) bioavailability, both of which lower soluble guanylate cyclase (sGC) activity in adjacent cardiomyocytes. Lower sGC activity decreases cyclic guanosine monophosphate concentration and protein kinase G (PKG) activity. Low PKG activity increases resting tension (Fpassive) of cardiomyocytes because of hypophosphorylation of titin and removes the brake on prohypertrophic stimuli inducing cardiomyocyte hypertrophy. VCAM and E-selectin expression in endothelial cells favors migration into the subendothelium of monocytes. These monocytes release transforming growth factor b (TGF-b). The latter stimulates conversion of fibroblasts to myofibroblasts, which deposit collagen in the interstitial space. COPD\u0026#x2005;=\u0026#x2005;chronic obstructive pulmonary disease; HPEF\u0026#x2005;=\u0026#x2005;heart failure with preserved ejection fraction.Reprinted from J Am Coll Cardiol. Vol 62, A novel paradigm for heart failure with preserved ejection fraction: comorbidities drive myocardial dysfunction and remodeling through coronary microvascular endothelial inflammation. Pages 263-7, Copyright 2013, with permission from American College of Cardiology Foundation.\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-1535134800\u0022 data-figure-caption=\u0022\u0026amp;lt;div xmlns=\u0026amp;quot;http:\/\/www.w3.org\/1999\/xhtml\u0026amp;quot;\u0026amp;gt;New Paradigm for Heart Failure With HFpEF: Importance of ComorbiditiesComorbidities induce a systemic proinflammatory state with elevated plasma levels of interleukin (IL)-6, tumor necrosis factor (TNF)-a, soluble ST2 (sST2), and pentraxin 3. Coronary microvascular endothelial cells reactively produce reactive oxygen species (ROS), vascular cell adhesion molecule (VCAM), and E-selectin. Production of ROS leads to formation of peroxynitrite (ONOO) and reduced nitric oxide (NO) bioavailability, both of which lower soluble guanylate cyclase (sGC) activity in adjacent cardiomyocytes. Lower sGC activity decreases cyclic guanosine monophosphate concentration and protein kinase G (PKG) activity. Low PKG activity increases resting tension (Fpassive) of cardiomyocytes because of hypophosphorylation of titin and removes the brake on prohypertrophic stimuli inducing cardiomyocyte hypertrophy. VCAM and E-selectin expression in endothelial cells favors migration into the subendothelium of monocytes. These monocytes release transforming growth factor b (TGF-b). The latter stimulates conversion of fibroblasts to myofibroblasts, which deposit collagen in the interstitial space. COPD\u0026#x2005;=\u0026#x2005;chronic obstructive pulmonary disease; HPEF\u0026#x2005;=\u0026#x2005;heart failure with preserved ejection fraction.Reprinted from \u0026amp;lt;em\u0026amp;gt;J Am Coll Cardiol\u0026amp;lt;\/em\u0026amp;gt;. Vol 62, A novel paradigm for heart failure with preserved ejection fraction: comorbidities drive myocardial dysfunction and remodeling through coronary microvascular endothelial inflammation. Pages 263-7, Copyright 2013, with permission from American College of Cardiology Foundation.\u0026amp;lt;\/div\u0026amp;gt;\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003E\u003Cimg class=\u0022fragment-image\u0022 alt=\u0022Figure 2.\u0022 src=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/15\/22\/4\/F2.medium.gif\u0022\/\u003E\u003C\/a\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cul class=\u0022highwire-figure-links inline\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/15\/22\/4\/F2.large.jpg?download=true\u0022 class=\u0022highwire-figure-link highwire-figure-link-download\u0022 title=\u0022Download Figure 2.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload figure\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/15\/22\/4\/F2.large.jpg\u0022 class=\u0022highwire-figure-link highwire-figure-link-newtab\u0022 target=\u0022_blank\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EOpen in new tab\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/16751\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003Cdiv class=\u0022fig-caption\u0022\u003E\u003Cspan class=\u0022fig-label\u0022\u003EFigure 2.\u003C\/span\u003E \u003Cp id=\u0022p-13\u0022 class=\u0022first-child\u0022\u003ENew Paradigm for Heart Failure With HFpEF: Importance of Comorbidities\u003C\/p\u003E\u003Cp id=\u0022p-14\u0022\u003EComorbidities induce a systemic proinflammatory state with elevated plasma levels of interleukin (IL)-6, tumor necrosis factor (TNF)-a, soluble ST2 (sST2), and pentraxin 3. Coronary microvascular endothelial cells reactively produce reactive oxygen species (ROS), vascular cell adhesion molecule (VCAM), and E-selectin. Production of ROS leads to formation of peroxynitrite (ONOO) and reduced nitric oxide (NO) bioavailability, both of which lower soluble guanylate cyclase (sGC) activity in adjacent cardiomyocytes. Lower sGC activity decreases cyclic guanosine monophosphate concentration and protein kinase G (PKG) activity. Low PKG activity increases resting tension (Fpassive) of cardiomyocytes because of hypophosphorylation of titin and removes the brake on prohypertrophic stimuli inducing cardiomyocyte hypertrophy. VCAM and E-selectin expression in endothelial cells favors migration into the subendothelium of monocytes. These monocytes release transforming growth factor b (TGF-b). The latter stimulates conversion of fibroblasts to myofibroblasts, which deposit collagen in the interstitial space. COPD\u2005=\u2005chronic obstructive pulmonary disease; HPEF\u2005=\u2005heart failure with preserved ejection fraction.\u003C\/p\u003E\u003Cp id=\u0022p-15\u0022\u003EReprinted from \u003Cem\u003EJ Am Coll Cardiol\u003C\/em\u003E. Vol 62, A novel paradigm for heart failure with preserved ejection fraction: comorbidities drive myocardial dysfunction and remodeling through coronary microvascular endothelial inflammation. Pages 263-7, Copyright 2013, with permission from American College of Cardiology Foundation.\u003C\/p\u003E\u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cp id=\u0022p-16\u0022\u003EAnimal studies have also demonstrated the relationship between sleep apnea and AF. A recent study in rats showed that chronic obstructive sleep apnea (OSA) leads to AF-promoting cardiac remodeling, with conduction abnormalities related to connexin dysregulation and increased fibrosis playing a prominent role [Iwasaki YK et al. \u003Cem\u003EJ Am Coll Cardiol\u003C\/em\u003E. 2014].\u003C\/p\u003E\u003Cp id=\u0022p-17\u0022\u003EProf Breithardt noted that adipose tissue induces fibrosis in the atria, whereas visceral adipose tissue (pericardial fat) volume is highly associated with paroxysmal and persistent AF independent of traditional risk factors, including left atrial enlargement [Al Chekakie MO et al. \u003Cem\u003EJ Am Coll Cardiol\u003C\/em\u003E. 2010]. Pericardial fat is also associated with AF severity, chronicity, and LA volume. Additionally, it is also predictive of long-term AF recurrence after ablation [Wong CX et al. \u003Cem\u003EJ Am Coll Cardiol\u003C\/em\u003E. 2011]. Very recent experimental studies have shown that human epicardial adipose tissue, but not subcutaneous fat tissue, induces fibrosis of the atrial myocardium through the secretion of adipo-fibrokines, thereby creating a substrate for AF [Venteclef N et al. \u003Cem\u003EEur Heart J\u003C\/em\u003E. 2015]. Thus, epicardial adipose tissue may be an important modifier linking obesity, sleep apnea, and HF to AF. Higher plasma concentration of resistin, a hormone associated with obesity, inflammation, and HF, has been implicated in incident AF [Rienstra M et al. \u003Cem\u003EAm Heart J\u003C\/em\u003E. 2012] and may be a good marker.\u003C\/p\u003E\u003Cp id=\u0022p-18\u0022\u003EKnowledge of these cause-and-effect mechanisms supports new preventive measures. Sleep apnea as an expression of obesity can also predict the risk of recurrent AF after ablation and cardioversion, whereas the use of continuous positive airway pressure can reduce the incidence of OSA-related arrhythmias and AF [Abe H et al. \u003Cem\u003EHeart Vessels\u003C\/em\u003E. 2010]. Other studies suggest that interventions can prevent or reduce AF occurrence. In overweight or obese patients undergoing weight and cardiometabolic risk factor management, significant reduction in AF symptom burden, severity scores, inflammation, and improved cardiac remodeling were reported [Abed HS et a. \u003Cem\u003EJAMA\u003C\/em\u003E. 2013], as well as improved long-term success of AF ablation [Pathak RK et al. \u003Cem\u003EJ Am Coll Cardiol\u003C\/em\u003E. 2014].\u003C\/p\u003E\u003Cp id=\u0022p-19\u0022\u003EIn summary, obesity and its associated comorbidities are likely contributors to the expanding epidemic of AF. Patients with untreated OSA have a higher recurrence of AF after cardioversion, which can be reduced with continuous positive airway pressure. Weight reduction and cardiometabolic risk factor management also are associated with reductions in symptomatic AF burden, higher percentage of time in sinus rhythm after ablation, improvement in cardiac structure, and reductions in pericardial adipose tissue.\u003C\/p\u003E\u003Cp id=\u0022p-20\u0022\u003E\u003Ca id=\u0022xref-fig-3-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F3\u0022\u003EFigure 3\u003C\/a\u003E outlines Prof Breithardt\u2019s current understanding regarding metabolic syndrome and AF.\u003C\/p\u003E\u003Cdiv id=\u0022F3\u0022 class=\u0022fig pos-float  odd\u0022\u003E\u003Cdiv class=\u0022highwire-figure\u0022\u003E\u003Cdiv class=\u0022fig-inline-img-wrapper\u0022\u003E\u003Cdiv class=\u0022fig-inline-img\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/15\/22\/4\/F3.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022Metabolic Syndrome and Atrial FibrillationAF, atrial fibrillation; EF, ejection fraction; LA, left atrium.Reproduced with permission from G Breithardt, MD.\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-1535134800\u0022 data-figure-caption=\u0022Metabolic Syndrome and Atrial FibrillationAF, atrial fibrillation; EF, ejection fraction; LA, left atrium.Reproduced with permission from G Breithardt, MD.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003E\u003Cimg class=\u0022fragment-image\u0022 alt=\u0022Figure 3.\u0022 src=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/15\/22\/4\/F3.medium.gif\u0022\/\u003E\u003C\/a\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cul class=\u0022highwire-figure-links inline\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/15\/22\/4\/F3.large.jpg?download=true\u0022 class=\u0022highwire-figure-link highwire-figure-link-download\u0022 title=\u0022Download Figure 3.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload figure\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/15\/22\/4\/F3.large.jpg\u0022 class=\u0022highwire-figure-link highwire-figure-link-newtab\u0022 target=\u0022_blank\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EOpen in new tab\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/16752\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003Cdiv class=\u0022fig-caption\u0022\u003E\u003Cspan class=\u0022fig-label\u0022\u003EFigure 3.\u003C\/span\u003E \u003Cp id=\u0022p-21\u0022 class=\u0022first-child\u0022\u003EMetabolic Syndrome and Atrial Fibrillation\u003C\/p\u003E\u003Cp id=\u0022p-22\u0022\u003EAF, atrial fibrillation; EF, ejection fraction; LA, left atrium.\u003C\/p\u003E\u003Cp id=\u0022p-23\u0022\u003EReproduced with permission from G Breithardt, MD.\u003C\/p\u003E\u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cp id=\u0022p-24\u0022\u003ETo translate this new knowledge into clinical practice, there is a need to highlight the impact of obesity on various cardiovascular entities such as myocardial infarction and vascular stroke, HFpEF, and sleep apnea, all of which lead to AF. In addition, it is important to align with the WHO and WHF targets of achieving a 25% relative reduction in premature mortality from noncommunicable diseases by 2025.\u003C\/p\u003E\u003C\/div\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2015 SAGE Publications\u003C\/li\u003E\u003C\/ul\u003E\u003Cspan class=\u0022highwire-journal-article-marker-end\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Cspan id=\u0022related-urls\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Ca href=\u0022http:\/\/mdc.sagepub.com\/content\/15\/22\/4.abstract\u0022 class=\u0022hw-link hw-link-article-abstract\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView Summary\u003C\/a\u003E\u003C\/div\u003E  \u003C\/div\u003E\n\n  \n  \u003C\/div\u003E\n\u003C\/div\u003E\n  \u003C\/div\u003E\n\u003C\/div\u003E\n\u003C\/div\u003E\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_figures.js?nzl3eq\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_openurl.js?nzl3eq\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}