Myocardial infarction due to thrombotic occlusion despite anticoagulation in Kawasaki disease - a case report

Diana van Stijn1, Nikki J Schoenmaker2, R Nils Planken3

  • 1Department of Pediatric Immunology, Rheumatology and Infectious diseases, Emma Children's Hospital, Amsterdam UMC, University of Amsterdam, Meibergdreef 9, location H8-253, Amsterdam, 1105 AZ, The Netherlands. d.vanstijn@amsterdamumc.nl.

BMC Pediatrics
|February 13, 2022
PubMed

Insights

Kawasaki disease (KD) can lead to giant coronary artery aneurysms (CAAs). Even with intensive anticoagulation, thrombus growth can cause myocardial ischemia, highlighting treatment challenges in pediatric vasculitis.

Area of Science:

  • Pediatric Cardiology
  • Vascular Inflammation
  • Thrombosis Research

Background:

  • Kawasaki disease (KD) is a pediatric vasculitis affecting coronary arteries.
  • Acute inflammation can lead to coronary artery aneurysms (CAAs), increasing risks of thrombosis and myocardial ischemia.
  • Timely anti-platelet and anticoagulation therapy is crucial for preventing severe cardiac events.

Observation:

  • A 5-year-old girl with KD presented with giant CAAs and myocardial ischemia.
  • Progressive thrombus growth occurred despite 21 months of intensive anticoagulation (aspirin, acenocoumarol, clopidogrel).
  • Thrombus growth persisted after percutaneous coronary intervention (PCI) with thrombolysis and systemic thrombolysis.

Findings:

  • Anticoagulation and thrombolysis proved insufficient for acute coronary syndrome in giant CAAs.
  • Thrombus growth continued despite triple anticoagulation, likely due to low blood flow within the aneurysm.
  • Coronary artery bypass grafting (CABG) was performed, but myocardial infarction was not prevented.

Implications:

  • This case highlights the limitations of current anticoagulation and thrombolysis strategies for KD-associated giant CAAs.
  • Effective management of thrombosis in pediatric patients with giant CAAs remains a significant clinical challenge.
  • Further research into novel therapeutic approaches is warranted to prevent thrombotic occlusion and myocardial damage.
Abstract

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