Pericoronary fat attenuation index and its relationship with markers of inflammation and extracellular matrix remodeling in patients with acute coronary syndrome and vulnerable plaque
Aim. To study the relationship between the pericoronary fat attenuation index (FAI), markers of inflammation and extracellular matrix remodeling, and vulnerable plaque criteria according to computed tomography coronary angiography (CTCA) in patients with acute coronary syndrome (ACS).Material and...
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| Main Authors: | , , , , |
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| Format: | Article |
| Language: | Russian |
| Published: |
«SILICEA-POLIGRAF» LLC
2025-05-01
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| Series: | Кардиоваскулярная терапия и профилактика |
| Subjects: | |
| Online Access: | https://cardiovascular.elpub.ru/jour/article/view/4369 |
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| Summary: | Aim. To study the relationship between the pericoronary fat attenuation index (FAI), markers of inflammation and extracellular matrix remodeling, and vulnerable plaque criteria according to computed tomography coronary angiography (CTCA) in patients with acute coronary syndrome (ACS).Material and methods. This study, carried out within the prospective single-center clinical trial Combi-LLT (NCT05624658), included 72 patients aged 57 (50;67) years. Of these, 68,1% were men, admitted with the clinical performance of ACS. All underwent percutaneous coronary intervention of the infarct-related artery. All patients had plaques with <50% stenosis. After 1 month, we performed CTCA to detect vulnerable plaques, as well as assess FAI, lipid profile, levels of inflammation biomarkers, and extracellular matrix remodeling as follows: neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), monocyte-to-high-density lipoprotein ratio (MHR), matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinases 1 (TIMP-1), galectin-3 (Gal-3), neutrophil gelatinase-associated lipocalin (NGAL). The follow-up period was 12 months.Results. Myocardial infarction (MI) was diagnosed in 56 patients (78%), including ST-elevation MI in 33 (46%) and non-ST-elevation MI in 23 (32%), while the remaining patients had unstable angina. Vulnerable plaque criteria according to CTCA were identified in 42 patients (58%). FAI in the left anterior descending (LAD) artery with plaques with a low-density area was higher (median -76 and -98 HU, respectively, p=0,038). In the presence of punctate calcifications, FAI in the LAD was also higher (median -67 and -90 HU, respectively, p=0,045). The threshold level of FAI for the vulnerable plaque using the punctate calcification criterion was -73,5 HU (area under the curve (AUC) =0,80 (95% confidence interval: 0,587-1,0, p=0,05), sensitivity 75%, specificity 80%). The threshold level of FAI for the low-density area was -92 HU (AUC =0,73 (95% confidence interval: 0,537-0,916, p=0,038)). Sensitivity and specificity were 79 and 60%, respectively. After 12 months, there was a decrease in FAI in the LAD from -77 (-85;-72) HU to -84 (-98;-71) HU (p=0,014). However, in patients with ST-elevation MI it remained higher compared to patients with unstable angina (p=0,002). In patients with achieved target low-density lipoprotein cholesterol level, FAI in the right coronary artery significantly decreased as follows: -70 (-82;-62) HU vs -78 (-90;-60) HU (p=0,022). The above-mentioned biomarkers were higher among individuals with FAI≥-70,1 HU compared to FAI<-70,1 HU as follows: NLR — 2,3 (2,1;3,2) and 1,9 (1,5;2,3), respectively (p=0,015); PLR — 133 (98;185,4) and 106,4 (83,3;128,9) (p=0,026), MMP-9 — 36 (25,87;44,2) and 25,9 (17,84;34,85) (p=0,026), Gal-3 — 5,65 (3,03;6,87) and 3,05 (2,03;8,68) (p=0,035).Conclusion. FAI in patients after ACS has a significant relationship with vulnerable plaques in the non-infarct-related artery, lipid profile parameters, as well as inflammation and matrix remodeling markers. The obtained data may be useful in stratifying cardiovascular risks and identifying new targeted preventive strategies. |
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| ISSN: | 1728-8800 2619-0125 |