Electrophysiological, Electroanatomical, and Structural Remodeling of the Atria as Consequences of Sustained Obesity

Mahajan, Rajiv; Lau, Dennis H.; Brooks, A.; Shipp, N.; Manavis, Jim; Wood, John; Finnie, John; Samuel, Chrishan S.; Royce, Simon G.; Twomey, Darragh; Thanigaimani, Shivshankar; Kalman, Jonathan M.; Sanders, Prashanthan

doi:10.1016/j.jacc.2015.04.058

Cited by 348 publications

(232 citation statements)

References 28 publications

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“…Obesity not only creates atrial fibrosis 84 , but also increases epicardial fat 84,85 . Furthermore, obesity leads to the infiltration of fat cells into the atrial tissue and to the activation of atrial fat cells, thus modifying atrial electrical function 22,86 , providing a possible mech anism linking obesity and pericardial fat to AF.…”

Section: Fat-cell Infiltration and Activationmentioning

confidence: 99%

Defining the major health modifiers causing atrial fibrillation: a roadmap to underpin personalized prevention and treatment

et al. 2015

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Despite the important advances that have enabled better stroke prevention in atrial fibrillation (AF) and more effective maintenance of sinus rhythm over the past decades, a large unmet need to improve the prevention and treatment of AF remains. Mortality for AF remains at 3.5% per year, and death is often experienced as sudden death or as a result of heart failure 1,2 . Each year, approximately 20% of patients with AF need to be hospitalized 3,4 , and stroke occurs in 1.5% of patients with AF who are receiving anticoagulant drugs 5 . Furthermore, more than half of the patients with AF are symptomatic despite adequate anticoagulation and rate control 4,6 . In view of the projected increase in the incidence and prevalence of AF 7-9 , as well as the substantial burden of death and dis ability that is still associated with this condition 10 , the status quo is unacceptable.Current management of patients with AF comprises treatment of the accompanying cardiovascular conditions, oral anticoagulation, rate control -with medications that slow atrioventricular nodal recovery or, rarely, with atrioventricular nodal ablation -and rhythm-control therapy with antiarrhythmic drugs, electrical cardioversion, catheter ablation or, at times, AF surgery 11,12 . Unfortunately, most of these current approaches are disconnected from our understanding of the major mechanisms that cause AF 1,13,14 1,2,7,19,20 Abstract | Despite remarkable advances in antiarrhythmic drugs, ablation procedures, and stroke-prevention strategies, atrial fibrillation (AF) remains an important cause of death and disability in middle-aged and elderly individuals. Unstructured management of patients with AF sharply contrasts with our detailed, although incomplete, knowledge of the mechanisms that cause AF and its complications. Altered calcium homeostasis, atrial fibrosis and ageing, ion-channel dysfunction, autonomic imbalance, fat-cell infiltration, and oxidative stress, in addition to a susceptible genetic background, contribute to the promotion, maintenance, and progression of AF. However, clinical management of patients with AF is currently guided by stroke risk parameters, AF pattern, and symptoms. In response to this apparent disconnect between the known pathophysiology of AF and clinical management, we propose a roadmap to develop a set of clinical markers that reflect the major causes of AF in patients. Thereby, the insights into the mechanisms causing AF will be transformed into a format that can underpin future personalized strategies to prevent and treat AF, ultimately informing better patient care.230 | APRIL 2016 | VOLUME 13 www.nature.com/nrcardio CONSENSUS STATEMENT © 2 0 1 6 M a c m i l l a n P u b l i s h e r s L i m i t e d . A l l r i g h t s r e s e r v e d .

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Section: Fat-cell Infiltration and Activationmentioning

confidence: 99%

Defining the major health modifiers causing atrial fibrillation: a roadmap to underpin personalized prevention and treatment

et al. 2015

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“…[4][5][6] The proposed pathophysiological mechanisms on how EAT induces AF, include structural and electric remodeling of the atria by direct (fatty infiltration and fibrosis of the adjacent myocardium) or indirect mechanisms (EAT as source for myocardial inflammation). [7][8][9] Furthermore, EAT could influence trigger formation from the pulmonary veins, which may initiate AF. 10 However, local (and direct) effects are most likely only caused by EAT surrounding the atria rather than surrounding the entire heart.…”

mentioning

confidence: 99%

Association Between Posterior Left Atrial Adipose Tissue Mass and Atrial Fibrillation

Rosendael

Dimitriu-Leen

Rosendael

et al. 2017

Circ: Arrhythmia and Electrophysiology

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“…Weight gain can also induce structural and histological changes in cardiomyocytes, which may predispose patients to chaotic rhythms such as AF (31,32). Furthermore, obesity may also be associated with pericardial fat, causing increased inflammation and local atrial infiltration, leading to increased risk of AF (30).…”

Section: Discussionmentioning

confidence: 99%

Effectiveness and safety of simultaneous hybrid thoracoscopic endocardial catheter ablation of atrial fibrillation in obese and non-obese patients

Phan¹,

Pison

Wang

et al. 2017

J. Thorac. Dis.

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Background: We evaluated the safety and effectiveness of the hybrid thoracoscopic endocardial epicardial ablation technique for the treatment of atrial fibrillation (AF) in obese versus non-obese patients.Methods: Between January 2010 and January 2015, a cohort of 61 patients were retrospectively identified to undergo ablation of AF as a stand-alone procedure using a thoracoscopic, hybrid epicardial-endocardial technique. All patients underwent continuous 7-day Holter monitoring at 3, 6 months, 1 year and yearly thereafter.Results: A total of 40% of the obese cohort had persistent or long-standing AF, compared to 54.9% of the non-obese cohort. There were no deaths or conversion to cardiopulmonary bypass required. At 3-year follow-up, 60% of the obese group were in sinus rhythm (SR) with no episode of AF, atrial flutter or atrial tachycardia lasting 30 s off anti-arrhythmic drugs. This was compared to 70.6% in the non-obese group, with no significant difference between the groups (P=0.468). For success rates on anti-arrhythmic drugs, this was 80% in the obese group compared to 86% in the non-obese group at 3-year follow-up (P=0.637). No patient died and no thromboembolic/bleeding events or procedure-related complications occurred during the follow-up. Conclusions:In a retrospective cohort with approximately half with persistent or long-standing AF, thoracoscopic hybrid epicardial endocardial ablation proved to be equally effective and safe in obese versus non-obese patients. Current preliminary findings require further validation in multi-institutional prospective studies with larger sample sizes.

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Electrophysiological, Electroanatomical, and Structural Remodeling of the Atria as Consequences of Sustained Obesity

Cited by 348 publications

References 28 publications

Defining the major health modifiers causing atrial fibrillation: a roadmap to underpin personalized prevention and treatment

Defining the major health modifiers causing atrial fibrillation: a roadmap to underpin personalized prevention and treatment

Association Between Posterior Left Atrial Adipose Tissue Mass and Atrial Fibrillation

Effectiveness and safety of simultaneous hybrid thoracoscopic endocardial catheter ablation of atrial fibrillation in obese and non-obese patients

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