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临床变量的价值及纵向超声评估颈动脉斑块在单纯急性冠状动脉综合征后主要不良心血管事件预测中的潜力

The Value of Clinical Variables and the Potential of Longitudinal Ultrasound Carotid Plaque Assessment in Major Adverse Cardiovascular Event Prediction After Uncomplicated Acute Coronary Syndrome.

作者信息

Bershtein Leonid L, Sumin Alexey N, Kutina Anna V, Lunina Marina D, Evdokimov Dmitrii S, Nayden Tatyana V, Gumerova Viktoriya E, Kochanov Igor N, Ivanov Arkadii A, Boldueva Svetlana A, Evdokimova Ekaterina D, Zbyshevskaya Elizaveta V, Evtushenko Alina E, Piltakyan Vartan K, Sayganov Sergey A

机构信息

Department of Internal Medicine & Cardiology, Northwestern State Medical University named after I.I. Mechnikov, 191015 St. Petersburg, Russia.

Laboratory of Comorbidity in Cardiovascular Disease, Federal State Budgetary Institution 'Research Institute for Complex Issues of Cardiovascular Disease', 650002 Kemerovo, Russia.

出版信息

Life (Basel). 2025 Mar 9;15(3):431. doi: 10.3390/life15030431.

DOI:10.3390/life15030431
PMID:40141776
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11943730/
Abstract

Due to the routine use of endovascular revascularization and improved medical therapy, the majority of acute coronary syndrome (ACS) cases now have an uncomplicated course. However, in spite of the currently accepted secondary prevention standards, the residual risk of remote major adverse cardiovascular events (MACEs) after ACS remains high. Ultrasound carotid/subclavian atherosclerotic plaque assessment may represent an alternative approach to estimate the MACE risk after ACS and to control the quality of secondary prevention. : To find the most important clinical predictors of MACEs in contemporary patients with predominantly uncomplicated ACS treated according to the Guidelines, and to study the potential of the longitudinal assessment of quantitative and qualitative ultrasound carotid/subclavian atherosclerotic plaque characteristics for MACE prediction after ACS. Patients with ACS, obstructive coronary artery disease (CAD) confirmed by coronary angiography, and carotid/subclavian atherosclerotic plaque (AP) who underwent interventional treatment were prospectively enrolled. The exclusion criteria were as follows: death or significant bleeding at the time of index hospitalization; left ventricular ejection fraction (EF) <30%; and statin intolerance. The clinical variables potentially affecting cardiovascular prognosis after ACS as well as the quantitative and qualitative AP characteristics at baseline and 6 months after the index hospitalization were studied as potential MACE predictors. : A total of 411 primary patients with predominantly uncomplicated ACS were included; AP was detected in 343 of them (83%). The follow-up period duration was 450 [269; 634] days. MACEs occurred in 38 patients (11.8%): seven-cardiac death, twenty-five-unstable angina/acute myocardial infarction, and six-acute ischemic stroke. In multivariate regression analyses, the most important baseline predictors of MACEs were diabetes (HR 2.22, 95% CI 1.08-4.57); the decrease in EF by every 5% from 60% (HR 1.22, 95% CI 1.03-1.46); the Charlson comorbidity index (HR 1.24, 95% CI 1.05-1.48); the non-prescription of beta-blockers at discharge (HR 3.24, 95% CI 1.32-7.97); and a baseline standardized AP gray scale median (GSM) < 81 (HR 2.06, 95% CI 1.02-4.19). Among the predictors assessed at 6 months, after adjustment for other variables, only ≥ 3 uncorrected risk factors and standardized AP GSM < 81 (cut-off value) at 6 months were significant (HR 3.11, 95% CI 1.17-8.25 and HR 3.77, 95% CI 1.43-9.92, respectively) (for all HRs above, all -values < 0.05; HR and 95% CI values varied minimally across regression models). The baseline quantitative carotid/subclavian AP characteristics and their 6-month longitudinal changes were not associated with MACEs. All predictors retained significance after the internal validation of the models, and models based on the baseline predictors also demonstrated good calibration; the latter were used to create MACE risk calculators. : In typical contemporary patients with uncomplicated interventionally treated ACS, diabetes, decreased EF, Charlson comorbidity index, non-prescription of beta-blockers at discharge, and three or more uncontrolled risk factors after 6 months were the most important clinical predictors of MACEs. We also demonstrated that a lower value of AP GSM reflecting the plaque vulnerability, measured at baseline and after 6 months, was associated with an increased MACE risk; this effect was independent of clinical predictors and risk factor control. According to our knowledge, this is the first demonstration of the independent role of longitudinal carotid/subclavian AP GSM assessment in MACE prediction after ACS.

摘要

由于血管内血运重建的常规应用和医学治疗的改进,现在大多数急性冠状动脉综合征(ACS)病例病程平稳。然而,尽管有目前公认的二级预防标准,ACS后远期主要不良心血管事件(MACE)的残余风险仍然很高。超声评估颈动脉/锁骨下动脉粥样硬化斑块可能是一种评估ACS后MACE风险和控制二级预防质量的替代方法。:寻找当代主要为病情平稳的ACS患者中MACE的最重要临床预测因素,并研究纵向评估颈动脉/锁骨下动脉粥样硬化斑块的定量和定性特征对ACS后MACE预测的潜力。前瞻性纳入接受介入治疗的ACS患者、经冠状动脉造影证实的阻塞性冠状动脉疾病(CAD)患者以及有颈动脉/锁骨下动脉粥样硬化斑块(AP)的患者。排除标准如下:索引住院时死亡或严重出血;左心室射血分数(EF)<30%;以及他汀类药物不耐受。研究ACS后可能影响心血管预后的临床变量以及索引住院后基线和6个月时AP的定量和定性特征,作为潜在的MACE预测因素。:共纳入411例主要为病情平稳的ACS初治患者;其中343例(83%)检测到AP。随访期为450[269;634]天。38例患者(11.8%)发生MACE:7例心源性死亡,25例不稳定型心绞痛/急性心肌梗死,6例急性缺血性卒中。在多因素回归分析中,MACE的最重要基线预测因素为糖尿病(HR 2.22,95%CI 1.08 - 4.57);EF从60%每降低5%(HR 1.22,95%CI 1.03 - 1.46);Charlson合并症指数(HR 1.24,95%CI 1.05 - 1.48);出院时未开具β受体阻滞剂(HR 3.24,95%CI 1.32 - 7.97);以及基线标准化AP灰阶中位数(GSM)<81(HR 2.06,95%CI 1.02 - 4.19)。在6个月时评估的预测因素中,在调整其他变量后,只有≥3个未校正的危险因素和6个月时标准化AP GSM<81(临界值)具有统计学意义(HR分别为3.11,95%CI 1.17 - 8.25和HR 3.77,95%CI 1.43 - 9.92)(对于上述所有HR,所有P值<0.05;HR和95%CI值在各回归模型中变化极小)。基线颈动脉/锁骨下动脉AP的定量特征及其6个月的纵向变化与MACE无关。模型内部验证后所有预测因素均保持显著性,基于基线预测因素的模型也显示出良好的校准;后者用于创建MACE风险计算器。:在典型的当代接受介入治疗的病情平稳的ACS患者中,糖尿病、EF降低、Charlson合并症指数、出院时未开具β受体阻滞剂以及6个月后三个或更多未控制的危险因素是MACE的最重要临床预测因素。我们还证明,反映斑块易损性的较低AP GSM值,在基线和6个月时测量,与MACE风险增加相关;这种效应独立于临床预测因素和危险因素控制。据我们所知,这是首次证明纵向颈动脉/锁骨下动脉AP GSM评估在ACS后MACE预测中的独立作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2702/11943730/47d4eb39d8ed/life-15-00431-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2702/11943730/6c0216f057d5/life-15-00431-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2702/11943730/47d4eb39d8ed/life-15-00431-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2702/11943730/6c0216f057d5/life-15-00431-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2702/11943730/47d4eb39d8ed/life-15-00431-g002.jpg

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