Pietro G Lacaita, Susanne Schoegl, Fabian Barbieri, Gerlig Widmann, Julia Held, David Haschka, Guenter Weiss, Andrea Klauser, Gudrun M Feuchtner
{"title":"血清尿酸对冠状动脉粥样硬化斑块表型的影响:缺失的环节?","authors":"Pietro G Lacaita, Susanne Schoegl, Fabian Barbieri, Gerlig Widmann, Julia Held, David Haschka, Guenter Weiss, Andrea Klauser, Gudrun M Feuchtner","doi":"10.1016/j.numecd.2024.103828","DOIUrl":null,"url":null,"abstract":"<p><strong>Background and aims: </strong>The interaction of serum uric acid (SUA) with atherogenesis is incompletely understood. Aim of our study was to investigate the association of SUA levels with coronary plaque composition including high-risk-plaque (HRP) features by coronary computed tomography angiography (CTA) and for the prediction of major adverse cardiac events (MACE).</p><p><strong>Methods and results: </strong>1242 patients (age 66.17 ± 11.03; 56 % males) referred to coronary CTA were included. SUA>6.5 mg/dl was defined as hyperuricemia. CTA-image analysis included: Coronary stenosis severity (CADRADS), plaque burden (SIS/G-score weighted for non-calcifying plaque), plaques types (1 = calcifying; 2 = mixed (predominantly calcifying); 3 = mixed (predominantly noncalcifying), 4 = noncalcifying.\"High-risk-plaque\"(HRP)-features were quantified: Low-attenuation plaque (LAP) density, Spotty calcification, Napkin-Ring Sign (NRS), Remodeling Index. Coronary Artery Calcium Score (CAC) was measured. Primary outcome was MACE. HRP-features were more prevalent in patients with hyperuricemia (p = 0.005, p = 0.0002, p = 0.0004). SUA level was associated with LAP<30HU (HR:1.23; p = 0.04). Plaque burden and CAC-score were higher in the hyperuricemia group (G-score:p = 0.022 and CAC:p = 0.027). After a mean follow-up of mean 8,32 years, MACE rate was 2.9 %. There was no difference in the MACE rate between subjects with elevated SUA and normals (HR 1.221:95%CI:0.817-2.563; p = 0.597). Low-attenuation-plaque density/LAP<30HU was the strongest prognosticator for MACE (p = 0.033 and p = 0.013); stenosis severity, plaque types and G-score were also predictive, but not SUA, CAC and the other conventional cardiovascular risk factors (except smoking).</p><p><strong>Conclusion: </strong>SUA is associated with HRP-features and coronary plaque burden. Low attenuation plaque is the strongest predictor of MACE, but not SUA level and other major CVRF. CTA imaging biomarkers may improve CV-risk stratification in patients with hyperuricemia.</p>","PeriodicalId":49722,"journal":{"name":"Nutrition Metabolism and Cardiovascular Diseases","volume":" ","pages":"103828"},"PeriodicalIF":3.3000,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The influence of serum uric acid on coronary atherosclerosis plaque phenotypes by computed tomography angiography: The missing link?\",\"authors\":\"Pietro G Lacaita, Susanne Schoegl, Fabian Barbieri, Gerlig Widmann, Julia Held, David Haschka, Guenter Weiss, Andrea Klauser, Gudrun M Feuchtner\",\"doi\":\"10.1016/j.numecd.2024.103828\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background and aims: </strong>The interaction of serum uric acid (SUA) with atherogenesis is incompletely understood. Aim of our study was to investigate the association of SUA levels with coronary plaque composition including high-risk-plaque (HRP) features by coronary computed tomography angiography (CTA) and for the prediction of major adverse cardiac events (MACE).</p><p><strong>Methods and results: </strong>1242 patients (age 66.17 ± 11.03; 56 % males) referred to coronary CTA were included. SUA>6.5 mg/dl was defined as hyperuricemia. CTA-image analysis included: Coronary stenosis severity (CADRADS), plaque burden (SIS/G-score weighted for non-calcifying plaque), plaques types (1 = calcifying; 2 = mixed (predominantly calcifying); 3 = mixed (predominantly noncalcifying), 4 = noncalcifying.\\\"High-risk-plaque\\\"(HRP)-features were quantified: Low-attenuation plaque (LAP) density, Spotty calcification, Napkin-Ring Sign (NRS), Remodeling Index. Coronary Artery Calcium Score (CAC) was measured. Primary outcome was MACE. HRP-features were more prevalent in patients with hyperuricemia (p = 0.005, p = 0.0002, p = 0.0004). SUA level was associated with LAP<30HU (HR:1.23; p = 0.04). Plaque burden and CAC-score were higher in the hyperuricemia group (G-score:p = 0.022 and CAC:p = 0.027). After a mean follow-up of mean 8,32 years, MACE rate was 2.9 %. There was no difference in the MACE rate between subjects with elevated SUA and normals (HR 1.221:95%CI:0.817-2.563; p = 0.597). Low-attenuation-plaque density/LAP<30HU was the strongest prognosticator for MACE (p = 0.033 and p = 0.013); stenosis severity, plaque types and G-score were also predictive, but not SUA, CAC and the other conventional cardiovascular risk factors (except smoking).</p><p><strong>Conclusion: </strong>SUA is associated with HRP-features and coronary plaque burden. Low attenuation plaque is the strongest predictor of MACE, but not SUA level and other major CVRF. 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引用次数: 0
摘要
背景和目的:血清尿酸(SUA)与动脉粥样硬化的相互作用尚不完全清楚。我们的研究目的是通过冠状动脉计算机断层血管造影(CTA)研究SUA水平与冠状动脉斑块组成(包括高风险斑块(HRP)特征)的关系,以及对主要心脏不良事件(MACE)的预测。方法与结果:1242例患者(年龄66.17±11.03;(56%男性)被纳入冠状动脉CTA。SUA 6.5 mg/dl定义为高尿酸血症。cta图像分析包括:冠状动脉狭窄严重程度(CADRADS)、斑块负担(SIS/ g评分加权为非钙化斑块)、斑块类型(1 =钙化;2 =混合型(以钙化为主);“高风险斑块”(HRP)特征被量化:低衰减斑块(LAP)密度、点状钙化、餐巾环征(NRS)、重塑指数。测量冠状动脉钙化评分(CAC)。主要终点为MACE。高尿酸血症患者的酶标特征更为普遍(p = 0.005, p = 0.0002, p = 0.0004)。结论:SUA与心率特征和冠状动脉斑块负荷相关。低衰减斑块是MACE最强的预测因子,而不是SUA水平和其他主要CVRF。CTA成像生物标志物可能改善高尿酸血症患者的cv风险分层。
The influence of serum uric acid on coronary atherosclerosis plaque phenotypes by computed tomography angiography: The missing link?
Background and aims: The interaction of serum uric acid (SUA) with atherogenesis is incompletely understood. Aim of our study was to investigate the association of SUA levels with coronary plaque composition including high-risk-plaque (HRP) features by coronary computed tomography angiography (CTA) and for the prediction of major adverse cardiac events (MACE).
Methods and results: 1242 patients (age 66.17 ± 11.03; 56 % males) referred to coronary CTA were included. SUA>6.5 mg/dl was defined as hyperuricemia. CTA-image analysis included: Coronary stenosis severity (CADRADS), plaque burden (SIS/G-score weighted for non-calcifying plaque), plaques types (1 = calcifying; 2 = mixed (predominantly calcifying); 3 = mixed (predominantly noncalcifying), 4 = noncalcifying."High-risk-plaque"(HRP)-features were quantified: Low-attenuation plaque (LAP) density, Spotty calcification, Napkin-Ring Sign (NRS), Remodeling Index. Coronary Artery Calcium Score (CAC) was measured. Primary outcome was MACE. HRP-features were more prevalent in patients with hyperuricemia (p = 0.005, p = 0.0002, p = 0.0004). SUA level was associated with LAP<30HU (HR:1.23; p = 0.04). Plaque burden and CAC-score were higher in the hyperuricemia group (G-score:p = 0.022 and CAC:p = 0.027). After a mean follow-up of mean 8,32 years, MACE rate was 2.9 %. There was no difference in the MACE rate between subjects with elevated SUA and normals (HR 1.221:95%CI:0.817-2.563; p = 0.597). Low-attenuation-plaque density/LAP<30HU was the strongest prognosticator for MACE (p = 0.033 and p = 0.013); stenosis severity, plaque types and G-score were also predictive, but not SUA, CAC and the other conventional cardiovascular risk factors (except smoking).
Conclusion: SUA is associated with HRP-features and coronary plaque burden. Low attenuation plaque is the strongest predictor of MACE, but not SUA level and other major CVRF. CTA imaging biomarkers may improve CV-risk stratification in patients with hyperuricemia.
期刊介绍:
Nutrition, Metabolism & Cardiovascular Diseases is a forum designed to focus on the powerful interplay between nutritional and metabolic alterations, and cardiovascular disorders. It aims to be a highly qualified tool to help refine strategies against the nutrition-related epidemics of metabolic and cardiovascular diseases. By presenting original clinical and experimental findings, it introduces readers and authors into a rapidly developing area of clinical and preventive medicine, including also vascular biology. Of particular concern are the origins, the mechanisms and the means to prevent and control diabetes, atherosclerosis, hypertension, and other nutrition-related diseases.