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急性心肌梗死合并射血分数保留的心力衰竭患者中脂蛋白(a)与主要不良心血管事件的相关性。

The correlation between lipoprotein(a) and major adverse cardiovascular events in patients with acute myocardial infarction combined with heart failure with preserved ejection fraction.

作者信息

Zhang Xiaodong, Niu Nan, Yu Shengqin, Zhang Xinxin, Zhang Yanli, Chen Xuefu, Zhang Wenmiao, Yang Song, Zhang Ning, Xia Yunlong, Liu Ying

机构信息

Department of Cardiology, The First Affiliated Hospital of Dalian Medical University, Dalian, China.

Department of Cardiology, The Second Affiliated Hospital of Dalian Medical University, Dalian, China.

出版信息

Front Cardiovasc Med. 2025 Jun 9;12:1515916. doi: 10.3389/fcvm.2025.1515916. eCollection 2025.

DOI:10.3389/fcvm.2025.1515916
PMID:40552189
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12183255/
Abstract

AIMS

This study aimed to confirm the correlation between lipoprotein(a) [Lp(a)] and major adverse cardiovascular events (MACE) in patients with acute myocardial infarction (AMI) combined with heart failure with preserved ejection fraction (HFpEF).

METHODS

This retrospective study was conducted at the First Affiliated Hospital of Dalian Medical University and included 399 patients who were diagnosed with AMI combined with HFpEF and who were hospitalised and underwent percutaneous coronary intervention (PCI) treatment between January 1, 2018, and January 1, 2023. Based on Lp(a) levels, patients were divided into three tertiles: T1 (≤356 mg/L), T2 [356 mg/L < Lp(a) ≤ 487 mg/L], and T3 (>487 mg/L). The study employed univariate and multivariate Cox regression analysis, subgroup analysis, and receiver operating characteristic (ROC) curve analysis to evaluate the correlation between Lp(a) and MACE.

RESULTS

Compared to the non-MACE group, the MACE group had higher levels of Lp(a) ( < 0.001). Tertile-based analysis of Lp(a) levels showed that as Lp(a) increased, the incidence of MACE, rehospitalization due to worsening HF, non-fatal recurrent MI, and unplanned repeat revascularization all increased significantly (all  < 0.05). During an average follow-up period of 30.5 months, multivariate Cox regression analysis confirmed that Lp(a) consistently remained an independent predictor of MACE across unadjusted, partially adjusted, and fully adjusted models (all  < 0.05). Further component analysis indicated that Lp(a) was significantly associated with cardiac death, rehospitalization due to worsening HF, and non-fatal recurrent MI, with the highest risk observed in the T3 group. Subgroup analysis further demonstrated that the association between elevated Lp(a) and MACE remained statistically significant across various strata (all  < 0.05). ROC curve analysis revealed that the area under the curve (AUC) for Lp(a) in predicting MACE was 0.662 (95% CI: 0.607-0.718), which was higher than that of systolic blood pressure (AUC = 0.560) and fasting plasma glucose (AUC = 0.543), but not significantly different from age (AUC = 0.610,  = 0.211).

CONCLUSIONS

In patients with AMI combined with HFpEF, elevated Lp(a) levels were significantly associated with an increased risk of MACE, and this association remained consistent across multiple subgroups.

摘要

目的

本研究旨在证实急性心肌梗死(AMI)合并射血分数保留的心力衰竭(HFpEF)患者中脂蛋白(a)[Lp(a)]与主要不良心血管事件(MACE)之间的相关性。

方法

本回顾性研究在大连医科大学附属第一医院进行,纳入了399例诊断为AMI合并HFpEF且于2018年1月1日至2023年1月1日期间住院并接受经皮冠状动脉介入治疗(PCI)的患者。根据Lp(a)水平,将患者分为三个三分位数组:T1(≤356mg/L)、T2[356mg/L<Lp(a)≤487mg/L]和T3(>487mg/L)。本研究采用单因素和多因素Cox回归分析、亚组分析以及受试者工作特征(ROC)曲线分析来评估Lp(a)与MACE之间的相关性。

结果

与非MACE组相比,MACE组的Lp(a)水平更高(<0.001)。基于三分位数的Lp(a)水平分析表明,随着Lp(a)升高,MACE、因HF恶化再次住院、非致命性复发性心肌梗死以及计划外重复血运重建的发生率均显著增加(均<0.05)。在平均30.5个月的随访期内,多因素Cox回归分析证实,在未调整、部分调整和完全调整模型中,Lp(a)始终是MACE的独立预测因子(均<0.05)。进一步的成分分析表明,Lp(a)与心源性死亡、因HF恶化再次住院以及非致命性复发性心肌梗死显著相关,T3组的风险最高。亚组分析进一步表明,Lp(a)升高与MACE之间的关联在各个亚组中均具有统计学意义(均<0.05)。ROC曲线分析显示,Lp(a)预测MACE的曲线下面积(AUC)为0.662(95%CI:0.607 - 0.718),高于收缩压(AUC = 0.560)和空腹血糖(AUC = 0.543),但与年龄无显著差异(AUC = 0.610, = 0.211)。

结论

在AMI合并HFpEF患者中,Lp(a)水平升高与MACE风险增加显著相关,且这种关联在多个亚组中保持一致。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/043b/12183255/ac2d0543c0e3/fcvm-12-1515916-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/043b/12183255/1bc5da1cb529/fcvm-12-1515916-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/043b/12183255/2304b222d2fc/fcvm-12-1515916-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/043b/12183255/ac2d0543c0e3/fcvm-12-1515916-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/043b/12183255/1bc5da1cb529/fcvm-12-1515916-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/043b/12183255/2304b222d2fc/fcvm-12-1515916-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/043b/12183255/ac2d0543c0e3/fcvm-12-1515916-g003.jpg

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