From the Department of Cardiology, Kerckhoff Heart and Thorax Center, Bad Nauheim, Germany (C.L., J.H., L.G., J.B., H.B., L.P., P.T., C.T., A.B., A.R., S.V., C.W.H., H.M.); DZHK (German Centre for Cardiovascular Research), partner site Rheine-Main, Bad Nauheim, Germany (C.L., J.H., L.G., J.B., H.B., L.P., P.T., C.T., A.B., A.R., S.V., C.W.H., H.M.); and Department of Internal Medicine I, Division of Cardiology, University of Giessen, Giessen, Germany (C.L., O.D., C.W.H., H.N.).
Circ Res. 2015 Feb 27;116(5):867-75. doi: 10.1161/CIRCRESAHA.116.304653. Epub 2014 Dec 16.
Inflammation in the setting of acute myocardial infarction (MI) has been linked to risk stratification; however, the release kinetics of inflammatory biomarkers in patients with acute MI has been difficult to establish.
The aim of this study was to determine the kinetics of changes in the levels of several biomarkers specifically linked to inflammation after transcoronary ablation of septal hypertrophy, a procedure that mimics acute MI.
We analyzed release kinetics of C-reactive protein, high-sensitivity C-reactive protein, interleukin-6, soluble CD40 ligand, and peripheral blood leukocyte subsets in patients (n=21) undergoing transcoronary ablation of septal hypertrophy. Blood samples were collected before transcoronary ablation of septal hypertrophy and at various times after transcoronary ablation of septal hypertrophy. Serum levels of C-reactive protein were increased at 24 hours (1.0 mg/dL [interquartile range [IQR], 0.7-1.75] versus 0.2 mg/dL [IQR, 0.1-1.05] at baseline [BL]; P<0.001), whereas high-sensitivity C-reactive protein increased as early as 8 hours (2.68 mg/L [IQR, 1.23-11.80] versus 2.17 mg/L [IQR, 1.15-5.06] at BL; P=0.002). Interleukin-6 was significantly increased at 45 minutes (2.59 pg/mL [IQR, 1.69-5.0] versus 1.5 pg/mL [IQR, 1.5-2.21] at BL; P=0.002), and soluble CD40 ligand was significantly decreased at 60 minutes (801.6 pg/mL [IQR, 675.0-1653.5] versus 1750.0 pg/mL [IQR, 1151.0-2783.0] at BL; P=0.016). Elevated counts of polymorphonuclear neutrophils were detectable at 15 minutes, with a significant increase at 2 hours (6415 cells/μL [IQR, 5288-7827] versus 4697 cells/μL [IQR, 2892-5620] at BL; P=0.004). Significant monocytosis was observed at 24 hours (729 cells/μL [IQR, 584-1344] versus 523 cells/μL [IQR, 369-701] at BL; P=0.015).
Interleukin-6 and neutrophil granulocytes showed a continuous rise at all prespecified time points after induction of MI. Our results provide valuable additional evidence of the diagnostic value of inflammatory biomarkers in the setting of early acute MI.
急性心肌梗死（MI）时的炎症与危险分层相关；然而，急性 MI 患者的炎症生物标志物的释放动力学一直难以确定。
本研究旨在确定经冠状动脉消融治疗室间隔肥厚（模拟急性 MI）后几种特定与炎症相关的生物标志物水平变化的动力学。
我们分析了 21 例接受经冠状动脉消融治疗室间隔肥厚的患者的 C 反应蛋白、高敏 C 反应蛋白、白细胞介素 6、可溶性 CD40 配体和外周血白细胞亚群的释放动力学。在经冠状动脉消融治疗室间隔肥厚之前和之后的不同时间采集血样。C 反应蛋白血清水平在 24 小时升高（1.0mg/dL[四分位距[IQR]，0.7-1.75]vs. 基线时的 0.2mg/dL[IQR，0.1-1.05]；P<0.001），而高敏 C 反应蛋白早在 8 小时就增加（2.68mg/L[IQR，1.23-11.80]vs. 基线时的 2.17mg/L[IQR，1.15-5.06]；P=0.002）。白细胞介素 6 在 45 分钟时显著升高（2.59pg/mL[IQR，1.69-5.0]vs. 基线时的 1.5pg/mL[IQR，1.5-2.21]；P=0.002），可溶性 CD40 配体在 60 分钟时显著降低（801.6pg/mL[IQR，675.0-1653.5]vs. 基线时的 1750.0pg/mL[IQR，1151.0-2783.0]；P=0.016）。多形核中性粒细胞的计数在 15 分钟时即可检测到升高，在 2 小时时显著增加（6415 个/μL[IQR，5288-7827]vs. 基线时的 4697 个/μL[IQR，2892-5620]；P=0.004）。单核细胞增多症在 24 小时时显著（729 个/μL[IQR，584-1344]vs. 基线时的 523 个/μL[IQR，369-701]；P=0.015）。
白细胞介素 6 和中性粒细胞在诱导急性 MI 后的所有预设时间点均呈持续上升。我们的结果为早期急性 MI 中炎症生物标志物的诊断价值提供了有价值的额外证据。
