Obesity results in progressive atrial structural and electrical remodeling: Implications for atrial fibrillation

Abed, H.; Samuel, Chrishan S.; Lau, Dennis H.; Kelly, Darren J.; Royce, Simon G.; Alasady, M.; Mahajan, Rajiv; Kuklik, Paweł; Zhang, Yuan; Brooks, A.; Nelson, Adam; Worthley, Stephen G.; Abhayaratna, Walter P.; Kalman, J.; Wittert, Gary; Sanders, Prashanthan

doi:10.1016/j.hrthm.2012.08.043

Cited by 331 publications

(169 citation statements)

References 29 publications

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“…The potential mechanism may be that eccentric and concentric left ventricular hypertrophy with resultant progressive atrial enlargement [22], [23]. The elevated circulating volume and enhanced neurohormonal activation (obliged by a larger body mass) may also contribute to the left atrium dilation and electrical instability [21], [24]. Although the exact significance of decreased NT-proBNP levels in overweight or obese state of AF patients are not yet understood, it at least raises the possibility that there may be lesser natriuretic-mediated vasodilation and antagonism of the rennin-angiotensin system, or loss of natriuretic ability in overweight or obese patients, which may also play a role in the development of the AF in overweight or obese patients.…”

Section: Discussionmentioning

confidence: 99%

Impact of Body Mass Index on Plasma N-Terminal ProB-Type Natriuretic Peptides in Chinese Atrial Fibrillation Patients without Heart Failure

Zheng

Yao

et al. 2014

PLoS ONE

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BackgroundAn inverse relationship between body mass index (BMI) and circulating levels of N-terminal proB-type natriuretic peptide (NT-proBNP) has been demonstrated in subjects with and without heart failure. Obesity also has been linked with increased incidence of atrial fibrillation (AF), but its influence on NT-proBNP concentrations in AF patients remains unclear. This study aimed to investigate the effect of BMI on NT-proBNP levels in AF patients without heart failure.MethodsA total of 239 consecutive patients with AF undergoing catheter ablation were evaluated. Levels of NT-proBNP and clinical characteristics were compared in overweight or obese (BMI≥25 kg/m2) and normal weight (BMI<25 kg/m2) patients.ResultsOf 239 patients, 129 (54%) were overweight or obese. Overweight or obese patients were younger, more likely to have a history of nonparoxysmal AF, hypertension, and diabetes mellitus. Levels of NT-proBNP were significantly lower in overweight or obese than in normal weight subjects (P<0.05). The relationship of obesity and decreased NT-proBNP levels persisted in subgroup of hypertension, both gender and both age levels (≥65 yrs and <65 yrs).Multivariate linear regression identified BMI as an independent negative correlate of LogNT-proBNP level.ConclusionsAn inverse relationship between BMI and plasma NT-proBNP concentrations have been demonstrated in AF patients without heart failure. Overweight or obese patients with AF appear to have lower NT-proBNP levels than normal weight patients.

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Section: Discussionmentioning

confidence: 99%

Impact of Body Mass Index on Plasma N-Terminal ProB-Type Natriuretic Peptides in Chinese Atrial Fibrillation Patients without Heart Failure

Zheng

Yao

et al. 2014

PLoS ONE

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“…In sheep fed a high-fat diet, increased adiposity was associated with atrial fibrosis and dilation accompanied by accentuated expression of fibrogenic mediators (28). These findings may explain the association of obesity with atrial dysrhythmias (29).…”

Section: Cardiac Fibrosis In Animal Models Of Obesitymentioning

confidence: 99%

“…Fibrogenic actions of TGF-β are primarily mediated through effects involving Smad signaling (88), although Smad-independent actions have also been implicated. Increased expression of myocardial TGF-β is consistently noted in experimental models of obesity and is associated with cardiac fibrosis (89), (28), (79). Upregulation of TGF-β in obesity-associated cardiomyopathy may be due to angiotensin II signaling (79), but may also involve angiotensin-independent pathways mediated through the direct stimulatory effects of high glucose and leptin on TGF-β transcription and activation (90), (91).…”

Section: The Molecular Signals Regulating Obesity-associated Fibrosismentioning

confidence: 99%

“…First, fibrotic myocardial remodeling may impair ventricular diastolic function contributing the development of heart failure with preserved ejection fraction. Second, development of atrial fibrosis may predispose obese subjects to atrial tachyarrhythmias (28). Third, collagen deposition in the ventricular myocardium may contribute to the increased incidence of ventricular arrhythmias and sudden death observed in obese individuals (131).…”

Section: Therapeutic Perspectivesmentioning

confidence: 99%

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Obesity, metabolic dysfunction, and cardiac fibrosis: pathophysiological pathways, molecular mechanisms, and therapeutic opportunities

Cavalera

Wang

Frangogiannis

2014

Translational Research

217

155

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Cardiac fibrosis is strongly associated with obesity and metabolic dysfunction and may contribute to the increased incidence of heart failure, atrial arrhythmias and sudden cardiac death in obese subjects. Our review discusses the evidence linking obesity and myocardial fibrosis in animal models and human patients, focusing on the fundamental pathophysiologic alterations that may trigger fibrogenic signaling, the cellular effectors of fibrosis and the molecular signals that may regulate the fibrotic response. Obesity is associated with a wide range of pathophysiologic alterations (such as pressure and volume overload, metabolic dysregulation, neurohumoral activation and systemic inflammation); their relative role in mediating cardiac fibrosis is poorly defined. Activation of fibroblasts likely plays a major role in obesity-associated fibrosis; however, inflammatory cells, cardiomyocytes and vascular cells may also contribute to fibrogenic signaling. Several molecular processes have been implicated in regulation of the fibrotic response in obesity. Activation of the Renin-Angiotensin-Aldosterone System, induction of Transforming Growth Factor-β, oxidative stress, advanced glycation end-products (AGEs), endothelin-1, Rho-kinase signaling, leptin-mediated actions and upregulation of matricellular proteins (such as thrombospondin-1) may play a role in the development of fibrosis in models of obesity and metabolic dysfunction. Moreover, experimental evidence suggests that obesity and insulin resistance profoundly affect the fibrotic and remodeling response following cardiac injury. Understanding the pathways implicated in obesity-associated fibrosis may lead to development of novel therapies to prevent heart failure and to attenuate post-infarction cardiac remodeling in obese patients.

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“…The difficulty in evaluating the role of obesity in AF is confounded by the coexistence of other cardiometabolic RFs and OSA. Abed et al 15 demonstrated that in sheep excessive caloric intake leading to weight gain was associated with adverse atrial remodeling marked by increased left atrial mass, fibrosis, inflammation, slower and more heterogeneous atrial conduction, and greater burden of AF. When the sheep were subjected to caloric restriction leading to weight reduction, this resulted in favorable structural and electric atrial changes, that is, reverse remodeling.…”

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confidence: 99%

Fitness and the Development of Atrial Fibrillation

Bhatt

Monahan

2015

Circulation

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Obesity results in progressive atrial structural and electrical remodeling: Implications for atrial fibrillation

Cited by 331 publications

References 29 publications

Impact of Body Mass Index on Plasma N-Terminal ProB-Type Natriuretic Peptides in Chinese Atrial Fibrillation Patients without Heart Failure

Impact of Body Mass Index on Plasma N-Terminal ProB-Type Natriuretic Peptides in Chinese Atrial Fibrillation Patients without Heart Failure

Obesity, metabolic dysfunction, and cardiac fibrosis: pathophysiological pathways, molecular mechanisms, and therapeutic opportunities

Fitness and the Development of Atrial Fibrillation

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