急性冠状动脉综合征的危险分层:全身免疫-炎症指数作为预后指标。

IF 4.4 Q1 Medicine
Elena Emilia Babes, Andrei-Flavius Radu, Noemi Adaus Cretu, Gabriela Bungau, Camelia Cristina Diaconu, Delia Mirela Tit, Victor Vlad Babes
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引用次数: 0

摘要

背景/目的:炎症在急性冠状动脉综合征(ACS)中起关键作用。综合免疫和炎症标志物的全身免疫炎症指数(SII)可作为一种有价值的预后工具。本研究旨在评估SII作为ACS患者死亡率和主要心血管和大脑不良事件(MACCE)的短期预测指标的效用。方法:对2023年收治的964例ACS患者进行回顾性分析。SII由入院血液学参数计算。主要和次要结局分别为30天死亡率和MACCE。结果:SII水平在ACS亚型间差异显著(p < 0.001), st段抬高型心肌梗死(STEMI)最高,不稳定型心绞痛最低。SII在死亡患者(2003.79±1601.17)明显高于幸存者(722.04±837.25,p < 0.001),并且仍然是死亡率的独立预测因子(OR = 1.038, p < 0.001)。同样,MACCE患者SII升高(1717±1611.32),而非MACCE患者SII升高(664.68±713.11,p < 0.001),并且在多变量分析中仍然具有预测性(OR = 1.080, p < 0.001)。MACCE的预测准确度为中等(AUC = 0.762),与GRACE 2联合使用后有所提高,特别是特异性(p = 0.07)。在STEMI中,SII具有极好的准确性(AUC = 0.874),优于中性粒细胞淋巴细胞比和c反应蛋白。STEMI患者SII在24小时上升,48小时下降,MACCE患者SII下降较慢。结论:SII被证明是一种具有成本效益的反映炎症、免疫和血栓形成的生物标志物。SII升高可预测ACS患者的短期MACCE和死亡率,与GRACE 2联合使用可改善预后。持续升高可能是持续炎症和MACCE风险增加的信号。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Risk Stratification in Acute Coronary Syndromes: The Systemic Immune-Inflammation Index as Prognostic Marker.

Risk Stratification in Acute Coronary Syndromes: The Systemic Immune-Inflammation Index as Prognostic Marker.

Risk Stratification in Acute Coronary Syndromes: The Systemic Immune-Inflammation Index as Prognostic Marker.

Risk Stratification in Acute Coronary Syndromes: The Systemic Immune-Inflammation Index as Prognostic Marker.

Background/objectives: Inflammation plays a key role in acute coronary syndromes (ACS). The systemic immune-inflammation index (SII), which integrates immune and inflammatory markers, may serve as a valuable prognostic tool. This study aimed to evaluate the utility of SII as a short-term predictor of mortality and major adverse cardiovascular and cerebral events (MACCE) in ACS patients.

Methods: A retrospective analysis was conducted on 964 ACS patients admitted in 2023. SII was calculated from admission hematological parameters. Primary and secondary outcomes were 30-day mortality and MACCE, respectively.

Results: SII levels differed significantly across ACS subtypes (p < 0.001), highest in ST-segment elevation myocardial infarction (STEMI) and lowest in unstable angina. SII was markedly higher in deceased patients (2003.79 ± 1601.17) vs. survivors (722.04 ± 837.25; p < 0.001) and remained an independent predictor of mortality (OR = 1.038, p < 0.001). Similarly, SII was elevated in MACCE cases (1717 ± 1611.32) vs. non-MACCE (664.68 ± 713.11; p < 0.001) and remained predictive in multivariate analysis (OR = 1.080, p < 0.001). Predictive accuracy for MACCE was moderate (AUC = 0.762), improved when combined with GRACE 2, especially in specificity (p = 0.07). In STEMI, SII had excellent accuracy (AUC = 0.874), outperforming neutrophil-lymphocyte ratio and C-reactive protein. SII rose at 24 h and declined at 48 h in STEMI, with a slower decline in MACCE patients.

Conclusions: SII proved to be a cost-effective biomarker reflecting inflammation, immunity, and thrombosis. Elevated SII predicted short-term MACCE and mortality in ACS, with improved prognostic power when combined with GRACE 2. Persistent elevation may signal ongoing inflammation and increased MACCE risk.

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