Epicardial Adipose Tissue Thickness is Higher in Right Ventricular Outflow Tract Tachycardia

IF 0.8 Q4 CARDIAC & CARDIOVASCULAR SYSTEMS
Ferdi Kahraman, S. Kanat, T. Peker, Sema Can, M. Demir
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Abstract

ABSTRACT Introduction: Idiopathic ventricular arrhythmias, which occur in the absence of structural heart disease, are commonly originating from the outflow tract, and 80% of the them arise from the right ventricle. Epicardial adipose tissue (EAT), which originates from the splanchnopleuric mesoderm, has been shown to be an important source of inflammatory mediators and plays an important role in cardiac autonomic function by epicardial ganglionated plexuses. EAT may potentially contribute to the pathophysiology of idiopathic right ventricular outflow tract (RVOT) tachycardia by different mechanisms. In this study, we aimed to investigate the relationship between EAT thickness and RVOT tachycardia. Methods: This study included 55 patients (32 male, 23 female) with RVOT tachycardia and 60 control subjects (38 male, 22 female). Patients who had more than three consecutive ventricular beats over 100 bpm with specific morphological features on the electrocardiogram (ECG) were diagnosed with RVOT tachycardia. EAT thickness was measured by transthoracic echocardiography. Results: EAT thickness was significantly higher in the RVOT tachycardia group (p <0.05). Ejection fraction (EF), and the thickness of the posterior wall of the left ventricle and of the interventricular septum were significantly lower, and left ventricular end-diastolic diameter, left ventricular end-systolic diameter, and left atrial diameter were significantly higher in patients who had RVOT tachycardia compared to normal subjects (p <0.05). Conclusion: Patients who were diagnosed with RVOT tachycardia had increased EAT thickness compared to normal subjects. The underlying mechanism of the condition could be mechanical, metabolic, infiltrative, or autonomic effects of the EAT.
右心室流出道心动过速时心外膜脂肪组织厚度增高
摘要简介:特发性室性心律失常是在无结构性心脏病的情况下发生的,通常起源于流出道,其中80%起源于右心室。心外膜脂肪组织(EAT)起源于内脏胸膜中胚层,是炎症介质的重要来源,并通过心外膜神经节神经丛在心脏自主神经功能中发挥重要作用。EAT可能通过不同的机制潜在地促进特发性右心室流出道(RVOT)心动过速的病理生理。在这项研究中,我们旨在探讨EAT厚度与RVOT心动过速的关系。方法:本研究纳入55例RVOT型心动过速患者(男32例,女23例)和60例对照组(男38例,女22例)。连续3次以上心室搏动超过100bpm并伴有特定心电图形态特征的患者可诊断为RVOT型心动过速。经胸超声心动图测量EAT厚度。结果:RVOT心动过速组EAT厚度显著增高(p <0.05)。RVOT心动过速患者的射血分数(EF)、左心室后壁厚度、室间隔厚度均显著低于正常组,左室舒张末期内径、左室收缩末期内径、左房内径均显著高于正常组(p <0.05)。结论:与正常受试者相比,诊断为RVOT心动过速的患者EAT厚度增加。这种情况的潜在机制可能是EAT的机械性、代谢性、浸润性或自主作用。
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