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Disease-treatment interactions in the management of patients with obesity and diabetes who have atrial fibrillation: the potential mediating influence of epicardial adipose tissue.
Cardiovascular Diabetology ( IF 8.5 ) Pub Date : 2019-09-24 , DOI: 10.1186/s12933-019-0927-9
Milton Packer 1, 2
Affiliation  

Both obesity and type 2 diabetes are important risk factors for atrial fibrillation (AF), possibly because they both cause an expansion of epicardial adipose tissue, which is the source of proinflammatory adipocytokines that can lead to microvascular dysfunction and fibrosis of the underlying myocardium. If the derangement of epicardial fat adjoins the left atrium, the result is an atrial myopathy, which is clinically manifest as AF. In patients with AF, there is a close relationship between epicardial fat volume and the severity of electrophysiological abnormalities in the adjacent myocardial tissues, and epicardial fat mass predicts AF in the general population. The expansion of epicardial adipose tissue in obesity and type 2 diabetes may also affect the left ventricle, impairing its distensibility and leading to heart failure with a preserved ejection fraction (HFpEF). Patients with obesity or type 2 diabetes with AF often have HFpEF, but the diagnosis may be missed, if dyspnea is attributed to increased body mass or to the arrhythmia. The expected response to the treatment for obesity, diabetes or AF may be influenced by their effects on epicardial inflammation and the underlying atrial and ventricular myopathy. Bariatric surgery and metformin reduce epicardial fat mass and ameliorate AF, whereas insulin promotes adipogenesis and cardiac fibrosis, and its use is accompanied by an increased risk of AF. Rate control strategies for AF may impair exercise tolerance, because they allow for greater time for ventricular filling in patients who cannot tolerate volume loading because of cardiac fibrosis and HFpEF. At the same time, both obesity and diabetes decrease the expected success rate of rhythm control strategies for AF (e.g., electrical cardioversion or catheter ablation), because increased epicardial adipose tissue volumes and cardiac fibrosis are important determinants of AF recurrence following these procedures.

中文翻译:

房颤的肥胖症和糖尿病患者管理中的疾病治疗相互作用:心外膜脂肪组织的潜在介导影响。

肥胖和2型糖尿病都是心房纤颤(AF)的重要危险因素,可能是因为它们都引起心外膜脂肪组织扩张,而后者是促炎性脂肪细胞因子的来源,可导致微血管功能障碍和基础心肌纤维化。如果心外膜脂肪的紊乱伴有左心房,则结果是房性肌病,临床上表现为房颤。在患有AF的患者中,心外膜脂肪量与邻近心肌组织中电生理异常的严重程度之间存在密切关系,而心外膜脂肪量预示着普通人群的AF。肥胖和2型糖尿病患者心外膜脂肪组织的扩张也可能会影响左心室,保留射血分数(HFpEF)会损害其扩张性并导致心力衰竭。肥胖或2型糖尿病伴AF的患者经常患有HFpEF,但如果呼吸困难归因于体重增加或心律失常,则可能会漏诊。肥胖,糖尿病或房颤的预期治疗反应可能受其对心外膜炎症以及潜在的心房和心室肌病的影响。减肥手术和二甲双胍可减少心外膜脂肪量并改善房颤,而胰岛素可促进脂肪形成和心脏纤维化,其使用会增加房颤的风险。AF的心率控制策略可能会削弱运动耐力,因为对于因心脏纤维化和HFpEF而不能耐受体量负荷的患者,它们会占用更多的时间进行心室充盈。
更新日期:2019-09-24
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