化学趋化因子配体 18 预测疑似冠心病胸痛住院患者的全因死亡率

IF 1.9 Q3 PERIPHERAL VASCULAR DISEASE
Dennis W.T. Nilsen , Reidun Aarsetoey , Volker Poenitz , Thor Ueland , Pål Aukrust , Annika E. Michelsen , Trygve Brugger-Andersen , Harry Staines , Heidi Grundt
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引用次数: 0

摘要

导言:趋化因子介导白细胞的招募和活化。趋化因子配体 18(CCL18)主要由单核细胞/巨噬细胞和树突状细胞表达。它在慢性炎症性疾病中、动脉粥样硬化斑块局部(尤其是稳定性降低的部位)以及急性冠状动脉综合征患者全身均有高表达。方法研究对象包括 871 名连续胸痛患者,其中 386 人根据肌钙蛋白-T(TnT)水平诊断为急性心肌梗死(AMI)。采用归一化连续 loge/SD 值对生物标记物进行逐步 Cox 回归模型拟合,并将 2 年内的心脏死亡率以及 2 年和 7 年内的总死亡率作为因变量。随访2年后,138名患者(15.8%)死亡,其中86人死于心脏疾病。单变量分析显示,CCL18与总死亡之间存在显著的正相关[HR 1.55 (95% 1.30-1.83), p < 0.001],与心脏死亡之间也存在显著的正相关[HR 1.32 (95% 1.06-1.64), p = 0.013]。调整后的相关性不显著。随访 7 年后,有 332 名(38.1%)患者死亡。CCL18与全因死亡率[HR 1.14 (95% CI, 1.01-1.29), p = 0.030]独立相关,但与心肌梗死(n = 203)或中风(n = 55)无关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Chemokine ligand 18 predicts all-cause mortality in patients hospitalized with chest pain of suspected coronary origin

Introduction

Chemokines mediate recruitment and activation of leucocytes. Chemokine ligand 18 (CCL18) is mainly expressed by monocytes/macrophages and dendritic cells. It is highly expressed in chronic inflammatory diseases, and locally in atherosclerotic plaques, particularly at sites of reduced stability, and systemically in acute coronary syndrome patients. Reports on its prognostic utility in the latter condition, including myocardial infarction (MI), are scarce.

Aim

To assess the utility of CCL18 as a prognostic marker of recurrent cardiovascular events in patients hospitalized with chest pain of suspected coronary origin.

Methods

The population consisted of 871 consecutive chest-pain patients, of whom 386 were diagnosed with acute myocardial infarction (AMI) based on Troponin-T (TnT) levels >50 ng/L. Stepwise Cox regression models, applying normalized continuous loge/SD values, were fitted for the biomarkers with cardiac mortality within 2 years and total mortality within 2 and 7 years as the dependent variables.

Results

Plasma samples from 849 patients were available. By 2 years follow-up, 138 (15.8%) patients had died, of which 86 were cardiac deaths. Univariate analysis showed a positive, significant association between CCL18 and total death [HR 1.55 (95% 1.30–1.83), p < 0.001], and for cardiac death [HR 1.32 (95% 1.06–1.64), p = 0.013]. Associations after adjustment were non-significant. By 7 years follow-up, 332 (38.1%) patients had died. CLL18 was independently associated with all-cause mortality [HR 1.14 (95% CI, 1.01–1.29), p = 0.030], but not with MI (n = 203) or stroke (n = 55).

Conclusion

CCL18 independently predicts long-term all-cause mortality but had no independent prognostic bearing on short-term cardiac death and CVD events.

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