Stefanie Jehn, Anja Roggel, Iryna Dykun, Bastian Balcer, Fadi Al-Rashid, Matthias Totzeck, Joachim Risse, Clemens Kill, Tienush Rassaf, Amir A Mahabadi
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As part of the initial workup, we performed bedside echocardiography for quantification of EAT thickness by a dedicated study physician, blinded to all patient characteristics. Treating physicians remained unaware of the results of the EAT assessment. The primary endpoint was defined as the presence of obstructive CAD, as detected in subsequent invasive coronary angiography. Patients reaching the primary endpoint had significantly more EAT than patients without obstructive CAD (7.90 ± 2.56 mm vs. 3.96 ± 1.91 mm, <i>P</i> < 0.0001). In a multivariable regression analysis, a 1 mm increase in EAT thickness was associated with a nearby two-fold increased odds of the presence of obstructive CAD [1.87 (1.64-2.12), <i>P</i> < 0.0001]. 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引用次数: 1
摘要
目的:我们验证了心外膜脂肪组织(EAT)量化可以提高急诊科急性胸痛患者对阻塞性冠状动脉疾病(CAD)存在的预测。方法和结果:在这项前瞻性观察队列研究中,我们纳入了657例连续患者(平均年龄58.06±18.04岁,53%男性),于2018年12月至2020年8月期间因提示急性冠状动脉综合征的急性胸痛就诊于急诊科。排除st段抬高型心肌梗死、血流动力学不稳定或已知CAD的患者。作为初始检查的一部分,我们在不了解所有患者特征的情况下,由专门的研究医生进行床边超声心动图,以量化EAT的厚度。治疗医生仍然不知道EAT评估的结果。主要终点被定义为存在阻塞性CAD,在随后的有创冠状动脉造影中检测到。达到主要终点的患者的EAT明显多于非阻塞性CAD患者(7.90±2.56 mm vs. 3.96±1.91 mm, P < 0.0001)。在一项多变量回归分析中,EAT厚度每增加1毫米,阻塞性CAD存在的几率增加近两倍[1.87 (1.64-2.12),P < 0.0001]。将EAT加入到GRACE评分、心脏生物标志物和传统危险因素的多变量模型中,受试者工作特征曲线下面积显著提高(0.759-0.901,P < 0.0001)。结论:心外膜脂肪组织对急诊科急性胸痛患者阻塞性CAD的存在有强烈且独立的预测作用。我们的研究结果表明,EAT的评估可以改善急性胸痛患者的诊断算法。
Epicardial adipose tissue and obstructive coronary artery disease in acute chest pain: the EPIC-ACS study.
Aims: We tested the hypothesis that epicardial adipose tissue (EAT) quantification improves the prediction of the presence of obstructive coronary artery disease (CAD) in patients presenting with acute chest pain to the emergency department.
Methods and results: Within this prospective observational cohort study, we included 657 consecutive patients (mean age 58.06 ± 18.04 years, 53% male) presenting to the emergency department with acute chest pain suggestive of acute coronary syndrome between December 2018 and August 2020. Patients with ST-elevation myocardial infarction, haemodynamic instability, or known CAD were excluded. As part of the initial workup, we performed bedside echocardiography for quantification of EAT thickness by a dedicated study physician, blinded to all patient characteristics. Treating physicians remained unaware of the results of the EAT assessment. The primary endpoint was defined as the presence of obstructive CAD, as detected in subsequent invasive coronary angiography. Patients reaching the primary endpoint had significantly more EAT than patients without obstructive CAD (7.90 ± 2.56 mm vs. 3.96 ± 1.91 mm, P < 0.0001). In a multivariable regression analysis, a 1 mm increase in EAT thickness was associated with a nearby two-fold increased odds of the presence of obstructive CAD [1.87 (1.64-2.12), P < 0.0001]. Adding EAT to a multivariable model of the GRACE score, cardiac biomarkers and traditional risk factors significantly improved the area under the receiver operating characteristic curve (0.759-0.901, P < 0.0001).
Conclusion: Epicardial adipose tissue strongly and independently predicts the presence of obstructive CAD in patients presenting with acute chest pain to the emergency department. Our results suggest that the assessment of EAT may improve diagnostic algorithms of patients with acute chest pain.