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半乳糖凝集素-3反映冠心病患者的全身性动脉粥样硬化。

Galectin-3 Reflects Systemic Atherosclerosis in Patients with Coronary Artery Disease.

作者信息

Onea Horea-Laurentiu, Homorodean Calin, Lazar Florin-Leontin, Negrea Mihai Octavian, Calin Teodora, Bitea Ioan Cornel, Teodoru Minodora, Nechita Vlad Ionut, Olteanu Ariela Ligia, Olinic Dan-Mircea

机构信息

4th Department of Internal Medicine Medical Clinic No.1, Iuliu Hatieganu University of Medicine and Pharmacy, 400006 Cluj-Napoca, Romania.

Department of Cardiology, County Clinical Emergency Hospital Sibiu, 550245 Sibiu, Romania.

出版信息

Medicina (Kaunas). 2025 Jul 30;61(8):1388. doi: 10.3390/medicina61081388.

DOI:10.3390/medicina61081388
PMID:40870433
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12388253/
Abstract

: Galectin-3 (Gal-3), a pro-inflammatory cytokine, has been implicated in atherosclerosis and adverse cardiovascular outcomes. While its role in coronary artery disease (CAD) is increasingly recognized, its association with systemic atherosclerosis remains underexplored. Objective: To investigate serum Gal-3 levels in patients with CAD and evaluate correlations between CAD severity and extra-coronary atherosclerotic involvement (carotid, femoral, and radial territories). : We prospectively enrolled 56 patients with CAD undergoing coronary angiography (42.8% with acute-ACS; 57.2% with chronic coronary syndromes-CCS). Gal-3 levels were measured within 24 h of admission. Atherosclerosis severity was assessed angiographically and through vascular ultrasound of the carotid, femoral, and radial arteries. Patients were stratified by median Gal-3 levels, and clinical follow-up was performed at 1 and 3 months. Gal-3 levels were significantly higher in CAD vs. controls (20.7 vs. 10.1 ng/mL; < 0.00001) and in ACS vs. CCS (22.18. vs. 17.93 ng/mL; = 0.019). Gal-3 correlated positively with culprit lesion diameter stenosis (DS) (R = 0.30; = 0.023) and maximum severity of additional treated lesions (R = 0.62; = 0.006). Gal-3 also correlated positively with carotid plaque thickness (R = 0.32; = 0.016), while patients with Gal-3 levels above the median showed increased median values for femoral plaque thickness (32.4 vs. 26.45 mm, = 0.046). No correlation was found with radial artery calcification. Gal-3 showed moderate discrimination for ACS (AUC = 0.685; cut-off 20.18 ng/mL). On multivariate analysis age, DS, and ACS presentation were independent predictors of Gal-3 above 19.07 ng/mL. Gal-3 levels are elevated in ACS and correlate with atherosclerotic burden, particularly in coronary, carotid, and femoral territories. These findings support Gal-3 as a potential marker of lesion severity and systemic vascular involvement, highlighting its possible role in risk stratification and the monitoring of atherosclerotic disease progression. This study provides integrated insights into the impact of Gal-3 across multiple vascular beds by assessing them concurrently within the same patient cohort.

摘要

半乳糖凝集素-3(Gal-3)是一种促炎细胞因子,与动脉粥样硬化和不良心血管结局有关。虽然其在冠状动脉疾病(CAD)中的作用日益受到认可,但其与全身性动脉粥样硬化的关联仍未得到充分研究。目的:研究CAD患者的血清Gal-水平,并评估CAD严重程度与冠状动脉外动脉粥样硬化累及情况(颈动脉、股动脉和桡动脉区域)之间的相关性。我们前瞻性纳入了56例接受冠状动脉造影的CAD患者(42.8%为急性ACS;57.2%为慢性冠状动脉综合征-CCS)。在入院24小时内测量Gal-3水平。通过血管造影以及颈动脉、股动脉和桡动脉的血管超声评估动脉粥样硬化严重程度。根据Gal-3水平中位数对患者进行分层,并在1个月和3个月时进行临床随访。与对照组相比,CAD患者的Gal-3水平显著更高(分别为20.7 ng/mL和10.1 ng/mL;P<0.00001),与CCS相比,ACS患者的Gal-3水平也更高(分别为22.18 ng/mL和17.93 ng/mL;P = 0.019)。Gal-3与罪犯病变直径狭窄(DS)呈正相关(R = 0.30;P = 0.023),与其他治疗病变的最大严重程度也呈正相关(R = 0.62;P = 0.006)。Gal-3还与颈动脉斑块厚度呈正相关(R = 0.32;P = 0.016),Gal-3水平高于中位数的患者股动脉斑块厚度的中位数增加(分别为32.4 mm和26.45 mm,P = 0.046)。未发现与桡动脉钙化存在相关性。Gal-3对ACS具有中度鉴别能力(AUC = 0.685;临界值为20.18 ng/mL)。多因素分析显示,年龄、DS和ACS表现是Gal-3水平高于19.07 ng/mL的独立预测因素。ACS患者的Gal-3水平升高,且与动脉粥样硬化负担相关,尤其是在冠状动脉、颈动脉和股动脉区域。这些发现支持Gal-3作为病变严重程度和全身性血管累及的潜在标志物,突出了其在风险分层和动脉粥样硬化疾病进展监测中的可能作用。本研究通过在同一患者队列中同时评估多个血管床,对Gal-3的影响提供了综合见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0895/12388253/a8885d0f3ea8/medicina-61-01388-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0895/12388253/d7c4392a66cd/medicina-61-01388-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0895/12388253/c0c1afce29c9/medicina-61-01388-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0895/12388253/a8885d0f3ea8/medicina-61-01388-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0895/12388253/d7c4392a66cd/medicina-61-01388-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0895/12388253/c0c1afce29c9/medicina-61-01388-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0895/12388253/a8885d0f3ea8/medicina-61-01388-g003.jpg

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