中性粒细胞百分比与白蛋白比率与慢性完全闭塞成功经皮冠状动脉介入治疗后不良临床结果之间的相关性：一项队列研究

摘要(中文译文)

慢性完全闭塞（CTO）经皮冠状动脉介入治疗（PCI）的结局已有改善，但残余心血管风险仍然持续存在。中性粒细胞百分比与白蛋白比值（NPAR）是炎症与营养状态的综合标志物，尚未在成功血运重建的CTO患者中进行研究。我们探讨了NPAR是否与该人群的长期不良结局独立相关。本单中心回顾性队列研究连续纳入1513例接受成功CTO PCI的患者。NPAR按（中性粒细胞百分比×100）/白蛋白（g/dL）计算。主要终点为全因死亡，次要终点为心血管死亡和心血管事件（心血管死亡、非致死性心肌梗死、非致死性卒中）。采用多变量Cox回归和限制性立方样条（RCS）评估NPAR与临床结局之间的关联。使用时间依赖性受试者工作特征（ROC）曲线评价NPAR预测全因死亡的能力。在中位随访810天期间，发生83例（5.5%）全因死亡、53例（3.5%）心血管死亡和73例（4.8%）心血管事件。经多变量校正后，NPAR每增加1个标准差与全因死亡风险升高50%相关（HR 1.50，95% CI 1.23-1.83，P<0.001），与心血管死亡风险升高59%相关（HR 1.59，95% CI 1.23-2.05，P<0.001），与心血管事件风险升高42%相关（HR 1.42，95% CI 1.13-1.79，P=0.003）。RCS分析显示NPAR与全因死亡（非线性P=0.971）、心血管死亡（非线性P=0.150）和主要心血管事件（非线性P=0.152）之间呈线性关联。时间依赖性ROC分析表明，将NPAR加入由年龄、多支血管病变和LVEF组成的基础模型后，可显著改善对1年、2年和3年全因死亡的区分能力（ΔAUC分别为0.092、0.076和0.058；均P<0.0001）。由最大约登指数得出的最佳NPAR截断值在三个时间点均保持稳定（分别为15.71、16.18和15.37），灵敏度为71.8%至72.6%，特异度为73.2%至75.7%。在接受成功CTO PCI的患者中，NPAR升高与长期死亡率和主要心血管事件增加独立且线性相关。这一简单、客观的生物标志物可能有助于完善干预后风险分层，并识别需要强化二级预防的高危个体。

Abstract

Chronic total occlusion (CTO) percutaneous coronary intervention (PCI) has improved outcomes, yet residual cardiovascular risk persists. The neutrophil percentage-to-albumin ratio (NPAR), an integrated marker of inflammation and nutritional status, has not been examined in successfully revascularized CTO patients. We investigated whether NPAR is independently associated with long-term adverse outcomes in this population. This single-center retrospective cohort study included 1513 consecutive patients who underwent successful CTO PCI. NPAR was calculated as (neutrophil percentage × 100)/albumin (g/dL). The primary endpoint was all-cause mortality, secondary endpoints were cardiovascular mortality and cardiovascular events (cardiovascular death, non-fatal myocardial infarction, non-fatal stroke). Multivariable Cox regression and restricted cubic splines (RCS) assessed the association between NPAR and clinical outcomes. Time-dependent Receiver operating characteristics (ROC) curves were used to evaluate the ability for NPAR to predict all-cause mortality. During a median follow-up of 810 days, 83 (5.5%) all-cause deaths, 53 (3.5%) cardiovascular deaths, and 73 (4.8%) cardiovascular events occurred. After multivariable adjustment, each 1-standard deviation increase in NPAR was associated with a 50% higher risk of all-cause mortality (HR 1.50, 95% CI 1.23-1.83, P<0.001), a 59% higher risk of cardiovascular mortality (HR 1.59, 95% CI 1.23-2.05, P<0.001), and a 42% higher risk of cardiovascular events (HR 1.42, 95% CI 1.13-1.79, P = 0.003). RCS analysis revealed a linear association between NPAR and all-cause mortality (P for non-linearity = 0.971), cardiovascular mortality (P for non-linearity = 0.150), and major cardiovascular events (P for non-linearity = 0.152). Time-dependent ROC analyses demonstrated that adding NPAR to a basic model comprising age, multi-vessel disease, and LVEF significantly improved discrimination for all-cause mortality at 1, 2, and 3 years (ΔAUC 0.092, 0.076, and 0.058, respectively; all P < 0.0001). The optimal NPAR cut-off values derived from the maximum Youden index were stable across all three time points (15.71, 16.18, and 15.37, respectively), yielding sensitivities of 71.8% to 72.6% and specificities of 73.2% to 75.7%. In patients undergoing successful CTO PCI, elevated NPAR is independently and linearly associated with increased long-term mortality and major cardiovascular events. This simple, objective biomarker may refine post-intervention risk stratification and identify high-risk individuals warranting intensified secondary prevention.

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