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Original article
Release kinetics of early ischaemic biomarkers in a clinical model of acute myocardial infarction
  1. Christoph Liebetrau1,2,
  2. Holger M Nef3,
  3. Oliver Dörr3,
  4. Luise Gaede1,2,
  5. Jedrzej Hoffmann1,2,
  6. Astrid Hahnel1,2,
  7. Andreas Rolf1,2,
  8. Christian Troidl1,2,
  9. Karl J Lackner4,
  10. Till Keller5,6,
  11. Christian W Hamm1,2,3,
  12. Helge Möllmann1,2
  1. 1Department of Cardiology, Kerckhoff Heart and Thorax Center, Bad Nauheim, Germany
  2. 2DZHK (German Centre for Cardiovascular Research), Bad Nauheim, Germany
  3. 3Division of Cardiology, Department of Internal Medicine I, Justus Liebig University Giessen, Giessen, Germany
  4. 4University Medical Center, Johannes Gutenberg University, Institute for Clinical Chemistry and Laboratory Medicine, Mainz, Germany
  5. 5Division of Cardiology, Department of Medicine III, Goethe University Frankfurt, Frankfurt am Main, Germany
  6. 6DZHK (German Centre for Cardiovascular Research), Frankfurt am Main, Germany
  1. Correspondence to Dr Christoph Liebetrau, Department of Cardiology, Kerckhoff Heart and Thorax Center, Benekestr. 2-8, Bad Nauheim 61231, Germany; c.liebetrau{at}kerckhoff-klinik.de

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.

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