Zhang Tianhao, Zhang Hongkai, Gao Xuelian, Peng Pingan, Chen Tianlong, Zhang Xiaoming, Yang Jingyao, Zheng Yang, Peng Yulu, Ma Xiaonan, Shi Dongmei, Wang Zhijian, Xu Lei, Zhou Yujie, Du Yu
Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, 100029, China.
Department of Radiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, 100029, China.
Diabetol Metab Syndr. 2025 Feb 25;17(1):71. doi: 10.1186/s13098-025-01645-4.
Pericoronary adipose tissue (PCAT) attenuation, as assessed by coronary computed tomography angiography (CCTA), has been identified as a marker of pericoronary inflammation and a predictor of future adverse atherosclerotic events. However, the impact of changes in PCAT attenuation, as evaluated by consecutive CCTAs, on plaque progression in high-risk atherosclerotic patients with improved modifiable cardiovascular risk factors (mCRFs) remains unclear.
Consecutive patients with type 2 diabetes mellitus (T2DM) who had improved mCRFs and underwent serial, clinically indicated CCTA examinations (time interval ≥ 12 months) at our center between July 2019 and July 2022 were screened. Eligible participants had at least one study plaque, defined as a plaque without significant anatomic stenosis, located in one of the major coronary arteries, which had not been intervened upon or caused adverse events between serial CCTA scans. Percent atheroma volume (PAV) and PCAT attenuation were measured for each study plaque at baseline and follow-up using CCTA plaque analysis software. Changes in PAV (δPAV = follow-up PAV - baseline PAV) were compared based on changes in PCAT attenuation [δPCAT attenuation] (> 0 or ≤ 0). Multivariate linear regression models were used to evaluate the relationship between δPCAT attenuation and δPAV.
A total of 98 T2DM patients (mean age: 59.9 years; 75.3% men; 152 plaques) had mCRFs that reached therapeutic targets at follow-up CCTA. However, overall PAV progressed from baseline in all patients [(41.68 ± 12.47)% vs. (43.71 ± 12.24)%, p = 0.035], accompanied by an increase in coronary inflammation (i.e., PCAT attenuation) during a median follow-up of 13.5 months (interquartile range [IQR]: 12.2, 17.5 months).Compared to patients with δPCAT attenuation ≤ 0, those with δPCAT attenuation > 0 had a significantly greater increase in overall PAV from baseline [(4.09 ± 12.09)% vs. (-0.82 ± 10.74)%, p = 0.011], calcified PAV [1.57% (IQR: 0.13%, 3.84%) vs. 0.38% (IQR: -0.26%, 2.58%), p = 0.008], and a numerical but non-significant increase in non-calcified PAV [(1.29 ± 11.75)% vs. (-1.87 ± 10.47)%, p = 0.089]. Multivariate linear regression models demonstrated that increased PCAT attenuation was significantly associated with the progression of overall PAV (β = 0.339, 95% CI: 0.129-0.549), non-calcified PAV (β = 0.237, 95% CI: 0.019-0.455), and calcified PAV (β = 0.109, 95% CI: 0.019-0.200), independent of age, sex, cardiovascular risk factors, medications, and baseline PCAT attenuation and PAV (all p < 0.05). The effect of elevated PCAT attenuation on overall plaque progression was consistent across subgroups (all p for interaction > 0.05).
In this longitudinal CCTA cohort of T2DM patients with improved mCRFs, increased pericoronary inflammation was associated with the progression of atherosclerotic plaque, particularly non-calcified plaque.
通过冠状动脉计算机断层扫描血管造影（CCTA）评估的冠状动脉周围脂肪组织（PCAT）衰减已被确定为冠状动脉周围炎症的标志物和未来不良动脉粥样硬化事件的预测指标。然而，连续CCTA评估的PCAT衰减变化对具有改善的可改变心血管危险因素（mCRF）的高危动脉粥样硬化患者斑块进展的影响仍不清楚。
筛选2019年7月至2022年7月在我们中心连续接受临床指示的CCTA检查（时间间隔≥12个月）且mCRF得到改善的2型糖尿病（T2DM）患者。符合条件的参与者至少有一个研究斑块，定义为位于主要冠状动脉之一且无明显解剖狭窄的斑块，在连续CCTA扫描之间未进行干预或未引起不良事件。使用CCTA斑块分析软件在基线和随访时测量每个研究斑块的粥样硬化体积百分比（PAV）和PCAT衰减。根据PCAT衰减的变化[δPCAT衰减]（>0或≤0）比较PAV的变化（δPAV =随访PAV - 基线PAV）。使用多变量线性回归模型评估δPCAT衰减与δPAV之间的关系。
共有98例T2DM患者（平均年龄：59.9岁；75.3%为男性；152个斑块）在随访CCTA时mCRF达到治疗目标。然而，所有患者的总体PAV从基线开始进展[（41.68±12.47）%对（43.71±12.24）%，p = 0.035]，在中位随访13.5个月（四分位间距[IQR]：12.2，17.5个月）期间冠状动脉炎症增加（即PCAT衰减）。与δPCAT衰减≤0的患者相比，δPCAT衰减>0的患者总体PAV从基线开始的增加显著更大[（4.09±12.09）%对（-0.82±10.74）%，p = 0.011]，钙化PAV[1.57%（IQR：0.13%，3.84%）对0.38%（IQR：-0.26%，2.58%），p = 0.008]，非钙化PAV有数值增加但无统计学意义[（1.29±11.75）%对（-1.87±10.47）%，p = 0.089]。多变量线性回归模型表明，PCAT衰减增加与总体PAV（β = 0.339，95%CI：0.129 - 0.549）、非钙化PAV（β = 0.237，95%CI：0.019 - 0.455）和钙化PAV（β = 0.109，95%CI：0.019 - 0.200）的进展显著相关，独立于年龄、性别、心血管危险因素、药物以及基线PCAT衰减和PAV（所有p < 0.05）。PCAT衰减升高对总体斑块进展的影响在各亚组中一致（所有交互作用p > 0.05）。
在这个mCRF得到改善的T2DM患者纵向CCTA队列中，冠状动脉周围炎症增加与动脉粥样硬化斑块进展相关，尤其是非钙化斑块。
