Hemostatic biomarkers and antithrombotic strategy in percutaneous left atrial interventions: State-of-the-art review

Errol W Aarnink1, Marina F M Huijboom1, Willem L Bor2

  • 1Department of Cardiology, St. Antonius Hospital, Nieuwegein, the Netherlands; Department of Cardiology, Amsterdam University Medical Center, Amsterdam, the Netherlands.

Thrombosis Research
|May 31, 2022
PubMed

Insights

Percutaneously closing heart defects with devices can cause blood clots. Coagulation activation, not platelet issues, appears key, suggesting anticoagulation may be better than antiplatelets for managing these risks.

Area of Science:

  • Cardiovascular Medicine
  • Interventional Cardiology
  • Biomarker Research

Background:

  • Percutaneous closure of atrial septal defects, patent foramen ovale, and left atrial appendage is common.
  • Thromboembolic events are significant complications following these procedures.
  • Optimal post-procedural antithrombotic management remains under investigation.

Purpose of the Study:

  • To investigate the mechanisms of left atrial device-related thrombus and thromboembolic complications.
  • To evaluate the temporal changes in coagulation and platelet activation post-procedure.
  • To identify potential biomarkers for predicting device-related complications.

Main Methods:

  • Monitoring of coagulation activation biomarkers after percutaneous device placement.
  • Assessment of platelet reactivity following interventions.
  • Analysis of endothelial activation and fibrinolysis markers.

Main Results:

  • Biomarkers of coagulation activation were elevated post-procedure, peaking at one month and normalizing by three months.
  • Platelet reactivity did not show a significant post-procedural increase.
  • Elevated coagulation activation suggests a potential role for anticoagulation therapy.

Conclusions:

  • Current antiplatelet-based regimens may not be optimal for preventing device-related thrombus.
  • Anticoagulation therapy might be a more suitable strategy.
  • Biomarkers of endothelial activation, fibrinolysis, and platelet reactivity could guide personalized antithrombotic strategies.

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