Effect of the Epicardial Adipose Tissue Volume on the Prevalence of Paroxysmal and Persistent Atrial Fibrillation

Oba, Kageyuki; Maeda, Minetaka; Maimaituxun, Gulinu; Yamaguchi, Satoshi; Arasaki, Osamu; Fukuda, Daiju; Yagi, Shusuke; Hirata, Yoshihiro; Nishio, S.; Igarashi, Takashi; Sugiyama, Takao; Kusunose, Kenya; Yamada, Hirotsugu; Soeki, Takeshi; Wakatsuki, Tetsuzo; Harada, Masafumi; Masuzaki, Hiroaki; Sata, Masataka; Shimabukuro, Michio

doi:10.1253/circj.cj-18-0021

Cited by 30 publications

(20 citation statements)

References 34 publications

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“…The available evidence supports this pathophysiological framework. Epicardial adipose tissue is increased in patients with HFpEF and in those with AF, 17,[22][23][24][25][26][27][28] and is particularly prominent when HFpEF and AF coexist, 24 particularly if patients have evidence of systemic inflammation or are at risk of adverse outcomes. 21,27 Coronary microvascular dysfunction is exceptionally common in HFpEF and, when present, is associated with a two-fold increase in the prevalence of AF.…”

Section: Pathophysiological Mechanisms Leading To Hfpefmentioning

confidence: 99%

“…17,22 Accordingly, epicardial fat volume predicts the incidence of AF in the community, even in the absence of prior evidence of cardiovascular disease. 23 Furthermore, epicardial adipose tissue mass increases as AF evolves from a paroxysmal to a persistent arrhythmia; 26 such expansion presages an exaggerated risk for thromboembolic events. 27 The strong association between obesity and AF in epidemiological studies is entirely explained by changes in LA geometry, which reflect the underlying atrial myopathy.…”

Section: Epidemiological and Clinical Evidence Supporting Atrial Fibrmentioning

confidence: 99%

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Do most patients with obesity or type 2 diabetes, and atrial fibrillation, also have undiagnosed heart failure? A critical conceptual framework for understanding mechanisms and improving diagnosis and treatment

Packer

2019

European J of Heart Fail

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Obesity and diabetes can lead to heart failure with preserved ejection fraction (HFpEF), potentially because they both cause expansion and inflammation of epicardial adipose tissue and thus lead to microvascular dysfunction and fibrosis of the underlying left ventricle. The same process also causes an atrial myopathy, which is clinically evident as atrial fibrillation (AF); thus, AF may be the first manifestation of HFpEF. Many patients with apparently isolated AF have latent HFpEF or subsequently develop HFpEF. Most patients with obesity or diabetes who have AF and exercise intolerance have increased left atrial pressures at rest or during exercise, even in the absence of diagnosed HFpEF. Among patients with AF, those who also have latent HFpEF have increased risk for systemic thromboembolism and death. The identification of HFpEF in patients with obesity or diabetes alters the risk‐to‐benefit relationship of commonly prescribed treatments. Bariatric surgery and statins can ameliorate AF and reduce the risk for HFpEF. Conversely, antihyperglycaemic drugs that promote adipogenesis or cause sodium retention (insulin and thiazolidinediones) may increase the risk for heart failure in patients with an underlying ventricular myopathy. Patients with obesity and diabetes who undergo catheter ablation for AF are at increased risk for AF recurrence and for post‐ablation increases in pulmonary venous pressures and worsening heart failure, especially if HFpEF coexists. Therefore, AF may be the earliest indicator of HFpEF in patients with obesity or type 2 diabetes, and recognition of HFpEF alters the management of these patients.

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Section: Pathophysiological Mechanisms Leading To Hfpefmentioning

confidence: 99%

Section: Epidemiological and Clinical Evidence Supporting Atrial Fibrmentioning

confidence: 99%

Do most patients with obesity or type 2 diabetes, and atrial fibrillation, also have undiagnosed heart failure? A critical conceptual framework for understanding mechanisms and improving diagnosis and treatment

Packer

2019

European J of Heart Fail

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“…The severity of electroanatomical abnormalities is closely related to the volume and inflammatory state of adjacent epicardial fat . Epicardial fat mass predicts the incidence of AF in the general population, and epicardial adiposity increases as AF progresses from a paroxysmal to a persistent arrhythmia …”

Section: Mechanisms Leading To Af In Obesity and Diabetesmentioning

confidence: 99%

“…6,7 Epicardial fat mass predicts the incidence of AF in the general population, and epicardial adiposity increases as AF progresses from a paroxysmal to a persistent arrhythmia. 8,9 The management of obesity and diabetes can influence epicardial adipose tissue and the development of atrial myopathy and AF. Marked weight loss decreases epicardial fat mass, improves LA geometry, and alleviates the burden of AF.…”

Section: Mechanisms Leading To Af In Obesity and Diabetesmentioning

confidence: 99%

Heightened risk of intensive rate control in patients with atrial fibrillation who are obese or have type 2 diabetes: A critical review and re‐evaluation

Packer

2019

Cardiovasc electrophysiol

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Atrial fibrillation (AF) is common in patients with obesity and diabetes; the arrhythmia (if long‐standing) is typically managed by rate control and anticoagulation. However, the coexistence of these two metabolic disorders complicates therapeutic options for rate control. The likely pathogenesis of AF in these patients is an expansion of epicardial adipose tissue whose inflammation is transmitted to the left atrium causing electromechanical remodeling. However, this same process is also transmitted to the left ventricle (LV), impairing its distensibility and its ability to tolerate volume, leading to heart failure with preserved ejection fraction. Unfortunately, the latter diagnosis (although commonly present in patients with AF and a coexistent metabolic disorder) is often ignored. To achieve rate control, physicians prescribe intensive treatment with atrioventricular (AV) nodal–blocking drugs, often at doses that are titrated to blunt exercise as well as resting heart rate responses. However, strict rate control (target rate, <80/min) is associated with somewhat worse outcomes than lenient rate control (target rate, <110/min). Furthermore, any rate slowing that facilitates diastolic filling may aggravate filling pressures that are already disproportionately increased because the LV is stiff and overfilled as a result of cardiac inflammation. Rate slowing in AF with beta blockers may not achieve the benefit expected from the blockade of adrenergically mediated cardiotoxicity, and some AV nodal–blocking drugs (digoxin and dronedarone) can increase the risk of death in patients with AF. Finally, cardiac fibrosis in obesity and diabetes may affect the conduction system, which can predispose to serious bradyarrhythmias if patients are prescribed AV nodal–blocking drugs.

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“…Epicardial adipose tissue (EAT), a metabolically active visceral fat reservoir surrounding and in ltrating myocardium and vessels, is recognized as a source of pro-in ammatory mediators involved in the onset and development of various cardiovascular diseases (CVD), such as coronary artery disease (CAD) and arrhythmias 8,9 . And the increase in EAT volume or thickness is associated with DM and is correlated with left atrial enlargement, atrial brosis, abnormal electrical conduction between cardiomyocytes, and results in the onset of AF 10,11 .…”

Section: Introductionmentioning

confidence: 99%

MiR-21-3p regulation FGFR1/FGF21/PPARγ pathway induces atrial fibrosis by targeting FGFR1 in diabetes

Pan¹,

Lin

et al. 2020

Preprint

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Background: A relationship between the abundance of epicardial adipose tissue (EAT) and the risk of atrial fibrosis and atrial fibrillation (AF) in diabetes mellitus (DM) has been reported. And previous studies have shown that MicroRNA-21 (miR-21) is a regulatory factor in atrial fibrosis and AF. The aim of this study was to examine the role of different subtypes of miR-21 in EAT browning and atrial fibrosis under hyperglycemia conditions.Methods: In vivo, C57BL/6 wild type (WT) and miR-21 knockout (KO) mice were used to establish the diabetic model by intraperitoneal injection of streptozotocin (STZ). In vitro, the EAT adipocytes from miR-21 KO mice were cultured and transfected with miR-21-3p mimic or miR-21-5p mimic and co-cultured with atrial fibroblasts in both HG or LG conditions. The browning of EAT and the fibrosis of fibroblasts were assessed by western blotting, immunofluorescence, Masson staining, and ELISA. The gain- and loss-of-function experiments were used to identified fibroblast growth factor receptor 1 (FGFR1) as the target gene of miR-21-3p.Results: In patients with DM and/or AF, serum hsa-miR-21-3p, instead of hsa-miR-21-5p, was significantly up-regulated. And miR-21 KO clearly ameliorated the atrial fibrosis in the diabetic mice. miR-21-3p as a key regulator that controls EAT browning and participates in atrial fibrosis under hyperglycemia conditions. Moreover, our gain- and loss-of-function experiments showed that FGFR1, as a direct target of miR-21-3p identified a regulatory pathway in EAT adipocytes. Conclusions: MiR-21-3p regulated EAT browning and participated the process of hyperglycemia-induced atrial fibrosis by targeting FGFR1.

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Effect of the Epicardial Adipose Tissue Volume on the Prevalence of Paroxysmal and Persistent Atrial Fibrillation

Abstract: The EATV index is associated with the prevalence of PAF and PeAF, and its cutoff values are predictive for PAF and PeAF development independently of other AF risk factors.

Cited by 30 publications

References 34 publications

Do most patients with obesity or type 2 diabetes, and atrial fibrillation, also have undiagnosed heart failure? A critical conceptual framework for understanding mechanisms and improving diagnosis and treatment

Do most patients with obesity or type 2 diabetes, and atrial fibrillation, also have undiagnosed heart failure? A critical conceptual framework for understanding mechanisms and improving diagnosis and treatment

Heightened risk of intensive rate control in patients with atrial fibrillation who are obese or have type 2 diabetes: A critical review and re‐evaluation

MiR-21-3p regulation FGFR1/FGF21/PPARγ pathway induces atrial fibrosis by targeting FGFR1 in diabetes

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