Küng Alexander J, Dykun Iryna, Totzeck Matthias, Mincu Raluca, Michel Lars, Kill Clemens, Witzke Oliver, Buer Jan, Rassaf Tienush, Mahabadi Amir A
West German Heart and Vascular Center Essen, Department of Cardiology and Vascular Medicine, University Hospital Essen, Hufelandstr, 55, 45147 Essen, Germany.
Center for Emergency Medicine, University Hospital Essen, Essen, Germany.
Am Heart J Plus. 2025 Apr 19;54:100548. doi: 10.1016/j.ahjo.2025.100548. eCollection 2025 Jun.
Acute COVID-19 infection frequently affects the cardiovascular system and causes acute myocardial injury. Epicardial Adipose Tissue (EAT), a visceral adipose tissue surrounding the myocardium and coronary arteries, has unique paracrine and endocrine effects, modulating the heart's inflammatory environment. Systemic inflammation stimulates TNF-α and Interleukin-6 secretion from EAT, contributing to cytokine storms and intensifying systemic responses. We aimed to determine whether EAT amount differs in patients with and without acute COVID-19 infection and myocardial injury.
This study analyzed the CoV-COR registry cohort, conducted at the University Hospital Essen, including patients with symptoms suggestive of COVID-19 infection. The infection was confirmed by PCR. EAT thickness was measured by two-dimensional TTE.
A total of 296 patients (mean age 63.6 ± 17.26 years, 55.4 % male) were included. Patients with confirmed COVID-19 infection were younger, more frequently treated with antihypertensive medication, and had higher BMI and systolic blood pressures. Univariate logistic regression showed no association between EAT and myocardial injury 0.97 (0.74; 1.28, = 0.82). A trend towards an association was observed between increasing EAT thickness and COVID-19 infection 1.25 (0.99; 1.59, = 0.060). Adjusting for age and gender strengthened the association, with a 48 % (1.14; 1.93, = 0.004) increased odds of COVID-19 infection per increase in EAT thickness. Multivariable regression yielded consistent effect sizes 1.47 (1.01; 2.16, = 0.047).
EAT thickness is associated with the presence of an acute COVID-19 infection but not with a myocardial injury. Further research is needed to assess if systemic viral infection induces dynamic changes in EAT.
新型冠状病毒肺炎(COVID-19)急性感染常累及心血管系统并导致急性心肌损伤。心外膜脂肪组织(EAT)是围绕心肌和冠状动脉的内脏脂肪组织,具有独特的旁分泌和内分泌作用,可调节心脏的炎症环境。全身炎症刺激EAT分泌肿瘤坏死因子-α(TNF-α)和白细胞介素-6,导致细胞因子风暴并加剧全身反应。我们旨在确定急性COVID-19感染患者与未感染患者以及有无心肌损伤患者之间的EAT量是否存在差异。
本研究分析了在埃森大学医院进行的CoV-COR注册队列,纳入有COVID-19感染症状的患者。通过聚合酶链反应(PCR)确诊感染。通过二维经胸超声心动图(TTE)测量EAT厚度。
共纳入296例患者(平均年龄63.6±17.26岁,55.4%为男性)。确诊COVID-19感染的患者更年轻,更常接受抗高血压药物治疗,且体重指数(BMI)和收缩压更高。单因素逻辑回归显示EAT与心肌损伤之间无关联,比值比(OR)为0.97(95%置信区间[CI]:0.74;1.28,P=0.82)。观察到EAT厚度增加与COVID-19感染之间存在关联趋势,OR为1.25(95%CI:0.99;1.59,P=0.060)。校正年龄和性别后,这种关联得到加强,EAT厚度每增加,COVID-19感染的OR增加48%(95%CI:1.14;1.93,P=0.004)。多变量回归得出一致的效应量,OR为1.47(95%CI:1.01;2.16,P=0.047)。
EAT厚度与急性COVID-19感染的存在相关,但与心肌损伤无关。需要进一步研究以评估全身病毒感染是否会引起EAT的动态变化。