Objective: This study aimed to investigate the linear association between lipoprotein(a) [Lp(a)] levels and all-cause and cardiovascular mortality in patients with acute coronary syndrome (ACS).

Methods: This retrospective cohort study included 578 patients with ACS who were hospitalized at Henan Provincial People's Hospital between January 2020 and January 2024. Patients were categorized into two groups: lower Lp(a) group (≤ 300 mg/L) and higher Lp(a) group (> 300 mg/L). Kaplan-Meier survival analysis, Cox regression models, subgroup and sensitivity analyses were used to evaluate the association between Lp(a) and all-cause and cardiovascular mortality. Restricted cubic spline (RCS) analysis was conducted to explore nonlinear associations.

Results: During a median follow-up of 27.5 months, a total of 124 all-cause deaths occurred (21.5%), of which 79 cases (13.7%) were classified as cardiovascular deaths. Compared to the lower Lp(a) group, the higher Lp(a) group exhibited a significantly increased risk of all-cause and cardiovascular mortality across all models. In the fully adjusted model (Model 3), the hazard ratio (HR) for all-cause mortality was 1.719 (95% confidence interval [CI]: 1.197-2.470, P = 0.003), while the HR for cardiovascular mortality was 2.505 (95% CI: 1.529-4.102, P < 0.001). In an additional analysis using a 500 mg/L cut-off, patients with Lp(a) > 500 mg/L had a significantly higher risk of cardiovascular mortality (HR = 2.209, P = 0.001), while the association with all-cause mortality (P = 0.284) was not statistically significant in the fully adjusted model. When Lp(a) was analyzed as a continuous variable, each 90 mg/L increase in Lp(a) was associated with a 5% higher risk of all-cause mortality (HR = 1.052, 95% CI: 1.003-1.104, P = 0.038), and each 45 mg/L increase was associated with a 5% higher risk of cardiovascular mortality (HR = 1.054, 95% CI: 1.026-1.084, P < 0.001). For log10-transformed Lp(a), the HR was 1.954 (95% CI: 1.252-3.050, P = 0.003) for all-cause mortality and 3.913 (95% CI: 2.108-7.265, P < 0.001) for cardiovascular mortality. Similarly, for standardized Lp(a) (Z-score), the HR was 1.178 (95% CI: 1.009-1.375, P = 0.038) for all-cause mortality and 1.408 (95% CI: 1.179-1.681, P < 0.001) for cardiovascular mortality. Most subgroup analyses showed that elevated Lp(a) levels were significantly associated with an increased risk of all-cause and cardiovascular mortality (P < 0.05). Sensitivity analyses confirmed the robustness of the findings, with significant associations persisting after excluding patients with early mortality or without stent implantation. Kaplan-Meier analysis showed that both all-cause and cardiovascular survival rates were significantly lower in the high Lp(a) group compared to the low Lp(a) group (P < 0.001 for both). RCS analyses revealed a linear positive association between Lp(a) levels and both all-cause and cardiovascular mortality.

Conclusions: Higher Lp(a) levels were independently and linearly associated with an increased risk of all-cause and cardiovascular mortality in ACS patients.

Keywords: acute coronary syndrome; all-cause mortality; cardiovascular mortality; lipoprotein(a); restricted cubic spline.

Copyright © 2025 Qin and Zhang.

目标：

本研究旨在探讨脂蛋白(a) [Lp(a)]水平与急性冠状动脉综合征（ACS）患者全因死亡率和心血管死亡率之间的线性关联。

方法：

这项回顾性队列研究包括了2020年1月至2024年1月期间在河南省人民医院住院的578名ACS患者。根据Lp(a)水平，将患者分为两组：较低Lp(a)组（≤300 mg/L）和较高Lp(a)组（> 300 mg/L）。使用Kaplan-Meier生存分析、Cox回归模型、亚组和敏感性分析来评估Lp(a)与全因死亡率和心血管死亡率之间的关联。采用限制三次样条（RCS）分析来探索非线性关联。

结果：

在中位随访27.5个月期间，共有124例患者发生全因死亡（占21.5%），其中79例（占13.7%）被归类为心血管死亡。与较低Lp(a)组相比，在所有模型中较高Lp(a)组的全因和心血管死亡风险显著增加。在完全调整后的模型（Model 3）中，全因死亡的风险比（HR）为1.719（95%置信区间[CI]：1.197-2.470, P = 0.003），而心血管死亡的HR为2.505（95% CI: 1.529-4.102，P 500 mg/L患者的全因死亡风险没有统计学意义（P = 0.284），而心血管死亡风险显著增加（HR = 2.209，P = 0.001）。将Lp(a)作为连续变量进行分析时，每增加90 mg/L的Lp(a)，全因死亡风险增加5%（HR = 1.052，95% CI：1.003-1.104，P = 0.038），每增加45 mg/L，心血管死亡风险增加5%（HR = 1.054，95% CI: 1.026-1.084，P 结论：

在ACS患者中，较高的Lp(a)水平独立且线性地与全因死亡率和心血管死亡率增加的风险相关联。

关键词：

急性冠状动脉综合征；全因死亡率；心血管死亡率；脂蛋白(a)；限制三次样条。