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

脂蛋白(a)与急性心肌梗死合并射血分数保留型心力衰竭患者主要不良心血管事件的相关性

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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) (P < 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 P < 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 P < 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 P < 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, P = 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.

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