Targeting therapy to the fibrin-mediated pathophysiology of acute coronary syndrome

Harvey White1

  • 1Green Lane Cardiovascular Service, Auckland City Hospital, New Zealand HarveyW@adhb.govt.nz.

Insights

Dual antiplatelet therapy is standard for acute coronary syndrome (ACS). This review explores the role of fibrin and anticoagulation in managing ACS, aiming to reduce residual cardiovascular event risk.

Area of Science:

  • Cardiology
  • Hematology
  • Thrombosis Research

Background:

  • Acute coronary syndrome (ACS) involves plaque disruption and thrombus formation.
  • Current treatments focus on dual antiplatelet therapy (DAPT) but leave residual risk.
  • Fibrin formation is a key factor in thrombogenesis during ACS.

Purpose of the Study:

  • To review the role of the coagulation cascade in ACS pathophysiology.
  • To provide a rationale for incorporating anticoagulation into ACS management.
  • To discuss novel oral anticoagulants (NOACs) for secondary ACS prevention.

Main Methods:

  • Literature review of studies on coagulation, thrombosis, and ACS.
  • Analysis of evidence supporting anticoagulation in ACS.
  • Examination of current research on NOACs combined with DAPT.

Main Results:

  • Plaque disruption activates both primary and secondary hemostasis.
  • Fibrin contributes significantly to thrombus burden and residual risk in ACS.
  • Anticoagulation presents a potential strategy to mitigate this residual risk.

Conclusions:

  • The coagulation cascade plays a critical role in ACS.
  • Anticoagulation therapy is a promising adjunct to DAPT for secondary ACS prevention.
  • Further research into NOACs in ACS is warranted to improve patient outcomes.

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