Medical University Innsbruck, Department of Radiology, Austria.
Medical University Innsbruck, Department of Neuroradiology, Austria.
Eur J Radiol. 2021 Mar;136:109531. doi: 10.1016/j.ejrad.2021.109531. Epub 2021 Jan 11.
Pericoronary adipose tissue (PCAT) has been linked to underlying coronary artery disease (CAD) and proposed to modulate adjacent atherosclerotic plaque formation over pro-inflammatory pathways. In vitro and ex vivo studies support the bilateral communication of adipose tissue and vessel wall. We quantified PCAT and its dynamics in a low coronary risk cohort with a semi-automated software in serial coronary computed tomography angiography (CTA).
We retrospectively included patients from a tertiary care hospital who underwent serial coronary CTA with a low cardiovascular risk profile. All examinations were evaluated in a standardized approach: epicardial adipose tissue (EAT) volume and attenuation was quantified in total, in the atrioventricular (RCA, LCX) or interventricular (LAD) sulcus and within a 5 mm radius for each coronary artery (PCAT). Coronary plaques were quantified using a semi-automated software and compared for progression, stability or regression.
Of 120 patients (27% females), 59.2% showed atherosclerotic plaques. After 36 months mean follow-up, 22 (18.3%) showed plaque regression, 39 (32.5%) were stable and 49 (40.8%) were progressive. Total EAT volume decreased by -15.6 ± 37.2 mm³ in the regressive group, increased by 2.7 ± 30.6 mm³ in the stable group and by 24.3 ± 37.1 mm³ in the progressive group (p = 0.003). Per-vessel analysis showed a significant decrease of PCAT attenuation in patients with CAD regression (-3.8 ± 7.6HU) compared to the stable (1.2 ± 9.1HU) and progressive group (3.5 ± 8.2HU, p < 0.0001). Mean sulcus EAT attenuation did not show a significant change (p = 0.135).
Epicardial adipose tissue volume is mutually changing with the progression or regression of coronary artery disease. Perivascular but not epicardial attenuation levels correlate to adjacent plaque and support a direct bilateral influence.
冠状动脉周围脂肪组织（PCAT）与潜在的冠状动脉疾病（CAD）有关，并通过促炎途径被提出来调节相邻动脉粥样硬化斑块的形成。体外和离体研究支持脂肪组织和血管壁的双向通讯。我们使用半自动化软件在连续冠状动脉 CT 血管造影（CTA）中对低冠状动脉风险队列中的 PCAT 及其动态进行了量化。
我们回顾性纳入了来自三级保健医院的连续进行冠状动脉 CTA 检查且具有低心血管风险特征的患者。所有检查均采用标准化方法进行评估：全心外膜脂肪组织（EAT）体积和衰减值在总量、房室（RCA、LCX）或室间（LAD）隐窝以及每个冠状动脉的 5mm 半径内（PCAT）进行量化。使用半自动化软件对冠状动脉斑块进行量化，并对进展、稳定或消退进行比较。
在 120 名患者（27%为女性）中，59.2%存在动脉粥样硬化斑块。在 36 个月的中位随访后，22 名（18.3%）患者的斑块消退，39 名（32.5%）患者稳定，49 名（40.8%）患者进展。在消退组，EAT 总量减少了-15.6±37.2mm³，在稳定组增加了 2.7±30.6mm³，在进展组增加了 24.3±37.1mm³（p=0.003）。血管内分析显示，与稳定组（1.2±9.1HU）和进展组（3.5±8.2HU，p<0.0001）相比，CAD 消退患者的 PCAT 衰减值显著降低（-3.8±7.6HU）。平均隐窝 EAT 衰减值没有显著变化（p=0.135）。
心外膜脂肪组织体积与冠状动脉疾病的进展或消退相互变化。血管周围但不是心外膜的衰减水平与相邻斑块相关，并支持直接的双向影响。
