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Updated: Mar 29, 2026

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
Kinetics of coagulation in ST-elevation myocardial infarction following successful primary percutaneous coronary
Paul F A Teunissen1, Ruben Tijssen1, Maurits L van Montfoort2
1Department of Cardiology, VU University Medical Center, Amsterdam, The Netherlands.
Insights
Coagulation markers change rapidly after ST-elevated myocardial infarction (STEMI) treated with PCI. However, these early changes do not predict long-term cardiac outcomes like ejection fraction or infarct size.
Area of Science:
- Cardiology
- Hematology
- Biochemistry
Background:
- ST-elevated myocardial infarction (STEMI) is often caused by atherosclerotic plaque rupture and thrombus formation.
- Kinetics of coagulation markers post-STEMI in patients receiving current guideline-based treatment are not well understood.
- This study investigates coagulation marker dynamics in percutaneous coronary intervention (PCI)-treated STEMI patients.
Purpose of the Study:
- To examine the kinetic profiles of key coagulation markers in STEMI patients undergoing PCI.
- To assess the relationship between early coagulation marker levels and cardiac outcomes determined by cardiac magnetic resonance (CMR).
Main Methods:
- Prospective study of 60 PCI-treated STEMI patients.
- Coagulation markers (ADAMTS13, VWF, fibrinogen, D-dimer, α2AP, PAP, F1+2, PT, aPTT, anti-Xa) measured at baseline (90 days post-PCI) and at 1, 4, and 7 days post-PCI.
- Cardiac magnetic resonance (CMR) assessed LVEF, infarct size, and microvascular injury (MVI) at 4-6 and 90 days post-PCI.
Main Results:
- Immediately post-PCI, ADAMTS13, fibrinogen, and α2AP levels decreased, while VWF activity, antigen, and propeptide levels increased compared to baseline.
- No significant correlations were found between individual or combined coagulation markers and LVEF, infarct size, or MVI at specified time points.
Conclusions:
- Coagulation parameters exhibit dynamic changes in the early phase following STEMI.
- These early coagulation marker dynamics do not serve as predictors for CMR-defined left ventricular ejection fraction, infarct size, or microvascular injury.
Introduction:
ST-elevated myocardial infarction (STEMI) is most frequently caused by coronary occlusion due to formation of an intracoronary thrombus in reaction to rupture of atherosclerotic plaques. Little is known about kinetics of coagulation markers after STEMI in patients treated according to current guidelines. We aimed to investigate kinetics of important coagulation markers in percutaneous coronary intervention (PCI)-treated STEMI patients.
Materials And Methods:
60 consecutive PCI-treated STEMI patients were prospectively included. Blood samples were collected immediately after as well as 1, 4 and 7 days following PCI. Samples collected 90 days after PCI served as baseline values. ADAMTS13 activity, VWF (von Willebrand factor) activity, VWF antigen, VWF propeptide, fibrinogen antigen, D-dimer, alpha2-antiplasmin (α2AP), plasmin-alpha2-antiplasmin complex (PAP), prothrombin fragment F1+2 (F1+2), prothrombin time (PT), activated partial thromboplastin time (aPTT), and anti-factor Xa (anti-Xa) were measured. Cardiac magnetic resonance (CMR) was performed at 4-6 and 90 days after PCI in 49 patients and left ventricular ejection fraction (LVEF), infarct size and microvascular injury (MVI) were determined.
Results:
Immediately after PCI, ADAMTS13 activity, fibrinogen antigen and α2AP levels were significantly decreased and VWF activity, VWF antigen and VWF propeptide levels were significantly elevated, compared to baseline. Individual coagulation markers and different combinations thereof were not related to LVEF or infarct size at 90 days, or the occurrence of MVI at 4-6 days after PCI.
Conclusion:
Coagulation parameters show a very dynamic profile in the early days after STEMI. However, individual coagulation parameters or combinations thereof do not predict CMR-defined LVEF, infarct size or MVI.
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