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Serial change of perivascular fat attenuation index after statin treatment: Insights from a coronary CT angiography follow-up study

医学 冠状动脉造影 他汀类 放射科 血管造影 心脏病学 内科学 心肌梗塞
作者
Xu Dai,Lihua Yu,Zhigang Lu,Chengxing Shen,Xinwei Tao,Jiayin Zhang
出处
期刊:International Journal of Cardiology [Elsevier BV]
卷期号:319: 144-149 被引量:101
标识
DOI:10.1016/j.ijcard.2020.06.008
摘要

Background Perivascular fat attenuation index (FAI) was thought to be an indicator of active vessel inflammation surrounding coronary plaques. However, whether this index can be reduced by statin treatment remains unknown. We aimed to investigate the serial change of lesion-specific perivascular FAI as quantified by coronary computed tomography (CCTA) after statin treatment. Methods Consecutive patients with chest pain and intermediate likelihood of coronary artery disease were referred for baseline CCTA. Patients were retrospectively included if they were treated medically and underwent follow-up CCTA at 1-year to 1.5-year interval. Lesion-specific perivascular FAI, as well as other plaque features, were measured at baseline and follow-up. Results One hundred and eight patients (mean age 67.7 ± 11.1, 76 males) were included. A significant reduction of the FAI value was found for non-calcified plaques and mixed plaques (−68.0 HU ± 8.5 HU Vs. -71.5 HU ± 8.1 HU, p < .001 and − 70.5 HU ± 8.9 HU Vs. -72.8 HU ± 9.0 HU, p = .014). However, this improvement was not observed for calcified plaques (−70.6 HU ± 9.7 HU Vs. −71.7 HU ± 9.9 HU, p = .258). For non-calcified and mixed plaques, the volumes of non-calcified as well as low attenuation component was significantly reduced whereas total plaque volume and volume of calcified component increased. For calcified plaque, total plaque volume also demonstrated remarkable increase after statin treatment Conclusions Lesion-specific perivascular FAI decreased at mid-term follow-up after statin treatment for non-calcified and mixed plaques. Perivascular FAI can be a potential imaging biomarker to monitor the anti-inflammation response to statin treatments.
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