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无已知冠状动脉疾病患者非钙化低衰减冠状动脉斑块负荷的决定因素:一项冠状动脉CT血管造影研究

Determinants of Non-calcified Low-Attenuation Coronary Plaque Burden in Patients Without Known Coronary Artery Disease: A Coronary CT Angiography Study.

作者信息

Yamaura Hiroki, Otsuka Kenichiro, Ishikawa Hirotoshi, Shirasawa Kuniyuki, Fukuda Daiju, Kasayuki Noriaki

机构信息

Department of Cardiovascular Medicine, Kashibaseiki Hospital, Kashiba, Japan.

Department of Cardiovascular Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan.

出版信息

Front Cardiovasc Med. 2022 Apr 7;9:824470. doi: 10.3389/fcvm.2022.824470. eCollection 2022.

DOI:10.3389/fcvm.2022.824470
PMID:35463764
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9021435/
Abstract

BACKGROUND

Although epicardial adipose tissue (EAT) is associated with coronary artery disease (CAD), it is unclear whether EAT volume (EAV) can be used to diagnose high-risk coronary plaque burden associated with coronary events. This study aimed to investigate (1) the prognostic impact of low-attenuation non-calcified coronary plaque (LAP) burden on patient level analysis, and (2) the association of EAV with LAP volume in patients without known CAD undergoing coronary computed tomography angiography (CCTA).

MATERIALS AND METHODS

This retrospective study consisted of 376 patients (male, 57%; mean age, 65.2 ± 13 years) without known CAD undergoing CCTA. Percent LAP volume (%LAP, <30 HU) was calculated as the LAP volume divided by the vessel volume. EAT was defined as adipose tissue with a CT attenuation value ranging from -250 to -30 HU within the pericardial sac. The primary endpoint was a composite event of death, non-fatal myocardial infarction, and unstable angina and worsening symptoms requiring unplanned coronary revascularization >3 months after CCTA. The determinants of %LAP (Q4) were analyzed using a multivariable logistic regression model.

RESULTS

During the follow-up period (mean, 2.2 ± 0.9 years), the primary endpoint was observed in 17 patients (4.5%). The independent predictors of the primary endpoint were %LAP (Q4) (hazard ratio [HR], 3.05; 95% confidence interval [CI], 1.09-8.54; = 0.033] in the Cox proportional hazard model adjusted by CAD-RADS category. Cox proportional hazard ratio analysis demonstrated that %LAP (Q4) was a predictor of the primary endpoint, independnet of CAD severity, Suita score, EAV, or CACS. The independent determinants of %LAP (Q4) were CACS ≥218.3 ( < 0.0001) and EAV ≥125.3 ml ( < 0.0001). The addition of EAV to CACS significantly improved the area under the curve (AUC) to identify %LAP (Q4) than CACS alone (AUC, EAV + CACS . CACS alone: 0.728 . 0.637; = 0.013).

CONCLUSIONS

CCTA-based assessment of EAV, CACS, and LAP could help improve personalized cardiac risk management by administering patient-suited therapy.

摘要

背景

虽然心外膜脂肪组织(EAT)与冠状动脉疾病(CAD)相关,但尚不清楚EAT体积(EAV)是否可用于诊断与冠状动脉事件相关的高危冠状动脉斑块负荷。本研究旨在调查:(1)低衰减非钙化冠状动脉斑块(LAP)负荷在患者水平分析中的预后影响;(2)在接受冠状动脉计算机断层扫描血管造影(CCTA)且无已知CAD的患者中,EAV与LAP体积之间的关联。

材料与方法

这项回顾性研究纳入了376例无已知CAD且接受CCTA的患者(男性占57%;平均年龄65.2±13岁)。LAP体积百分比(%LAP,<30 HU)计算为LAP体积除以血管体积。EAT定义为心包腔内CT衰减值在-250至-30 HU之间的脂肪组织。主要终点是CCTA后>3个月时死亡、非致命性心肌梗死、不稳定型心绞痛以及需要非计划冠状动脉血运重建的症状恶化的复合事件。使用多变量逻辑回归模型分析%LAP(Q4)的决定因素。

结果

在随访期(平均2.2±0.9年)内,17例患者(4.5%)出现主要终点事件。在根据CAD-RADS分类进行调整的Cox比例风险模型中,主要终点的独立预测因素为%LAP(Q4)(风险比[HR],3.05;95%置信区间[CI],1.09 - 8.54;P = 0.033)。Cox比例风险比分析表明,%LAP(Q4)是主要终点的预测因素,独立于CAD严重程度、Suita评分、EAV或冠状动脉钙化积分(CACS)。%LAP(Q4)的独立决定因素为CACS≥218.3(P < 0.0001)和EAV≥125.3 ml(P < 0.0001)。与单独使用CACS相比,将EAV加入CACS可显著提高识别%LAP(Q4)的曲线下面积(AUC)(AUC,EAV + CACS:0.728;单独使用CACS:0.637;P = 0.013)。

结论

基于CCTA评估EAV、CACS和LAP,通过给予适合患者的治疗,有助于改善个性化心脏风险管理。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b22/9021435/28d8470cdc20/fcvm-09-824470-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b22/9021435/f4b0d2d60052/fcvm-09-824470-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b22/9021435/bf0e3e8c33f4/fcvm-09-824470-g0002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b22/9021435/28d8470cdc20/fcvm-09-824470-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b22/9021435/f4b0d2d60052/fcvm-09-824470-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b22/9021435/bf0e3e8c33f4/fcvm-09-824470-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b22/9021435/7b517a1c310b/fcvm-09-824470-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b22/9021435/28d8470cdc20/fcvm-09-824470-g0004.jpg

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