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急性心肌梗死临床模型中早期缺血性生物标志物的释放动力学。

Release kinetics of early ischaemic biomarkers in a clinical model of acute myocardial infarction.

机构信息

Department of Cardiology, Kerckhoff Heart and Thorax Center, , Bad Nauheim, Germany.

出版信息

Heart. 2014 Apr;100(8):652-7. doi: 10.1136/heartjnl-2013-305253. Epub 2014 Jan 31.

DOI:10.1136/heartjnl-2013-305253
PMID:24488609
Abstract

OBJECTIVE

To determine the release kinetics of different biomarkers with potential as novel early ischaemic biomarkers in patients with acute coronary syndrome (ACS); it is difficult to establish the detailed release kinetics in patients with acute myocardial infarction (AMI).

METHODS

We analysed the release kinetics of soluble fms-like tyrosine kinase (sFlt-1), ischaemia modified albumin (IMA), and heart-type fatty acid binding protein (hFABP) in patients with hypertrophic obstructive cardiomyopathy who were undergoing transcoronary ablation of septal hypertrophy (TASH), a procedure mimicking AMI. Consecutive patients (n=21) undergoing TASH were included. Blood samples were collected before TASH and 15, 30, 45, 60, 75, 90, and 105 min and 2, 4, 8, and 24 h after TASH. sFlt-1 and hFABP were quantified in serum, and IMA was quantified in plasma using immunoassays.

RESULTS

sFLT-1 and hFABP increased significantly 15 min after induction of AMI vs baseline as follows: sFlt-1, 3657.5 ng/L (IQR 2302.3-4475.0) vs 76.0 ng/L (IQR 71.2-88.8) (p<0.001); hFABP, 9.0 ng/mL (IQR 7.0-15.4) vs 4.6 ng/mL (IQR 3.4-7.1) (p<0.001). sFlt-1 demonstrated a continuous decrease after the 15th min. hFABP showed a continuous increase until the 8th hour with a decline afterwards. The IMA concentrations increased significantly 30 min after induction of AMI vs baseline, with values of 26.0 U/mL (IQR 21.8-38.6) vs 15.6 U/mL (IQR 10.1-24.7) (p=0.02), and then decreased after 75 min.

CONCLUSIONS

sFlt-1 and hFABP increased very early after induction of myocardial ischaemia, showing different release kinetics. The additional information provided by these findings is helpful for developing their potential combined use with cardiac troponins in patients with suspected AMI.

摘要

目的

确定不同生物标志物在急性冠状动脉综合征(ACS)患者中作为新型早期缺血生物标志物的释放动力学;在急性心肌梗死(AMI)患者中建立详细的释放动力学较为困难。

方法

我们分析了接受经冠状窦消融间隔肥厚术(TASH)的肥厚型梗阻性心肌病患者的可溶性 fms 样酪氨酸激酶(sFlt-1)、缺血修饰白蛋白(IMA)和心脏型脂肪酸结合蛋白(hFABP)的释放动力学,该手术模拟了 AMI。纳入了连续接受 TASH 的患者(n=21)。在 TASH 前和 TASH 后 15、30、45、60、75、90 和 105 分钟以及 2、4、8 和 24 小时采集血样。使用免疫分析法检测血清中的 sFlt-1 和 hFABP,以及血浆中的 IMA。

结果

与基线相比,AMI 诱导后 15 分钟 sFLT-1 和 hFABP 显著增加,结果如下:sFlt-1,3657.5 ng/L(IQR 2302.3-4475.0)vs 76.0 ng/L(IQR 71.2-88.8)(p<0.001);hFABP,9.0 ng/mL(IQR 7.0-15.4)vs 4.6 ng/mL(IQR 3.4-7.1)(p<0.001)。sFlt-1 在第 15 分钟后呈持续下降趋势。hFABP 在 8 小时内持续增加,随后下降。IMA 浓度在 AMI 诱导后 30 分钟与基线相比显著升高,为 26.0 U/mL(IQR 21.8-38.6)vs 15.6 U/mL(IQR 10.1-24.7)(p=0.02),75 分钟后下降。

结论

sFlt-1 和 hFABP 在心肌缺血诱导后很早即升高,呈现不同的释放动力学。这些发现提供的额外信息有助于开发它们与可疑 AMI 患者的心肌肌钙蛋白联合使用的潜力。

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