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Updated: May 14, 2026

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model
Published on: June 4, 2021
Targeting therapy to the fibrin-mediated pathophysiology of acute coronary syndrome
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.
Abstract:
Acute coronary syndrome (ACS) encompasses a spectrum of diseases, ranging from ST-elevation myocardial infarction to non-ST-elevation myocardial infarction and unstable angina. A key initiating event in the pathology of ACS is atheromatous plaque disruption, in which the exposure of thrombogenic material triggers simultaneous activation of primary and secondary hemostatic pathways. Targeting platelet-mediated thrombus formation with dual antiplatelet therapy comprising acetylsalicylic acid and a P2Y12 antagonist is the current mainstay for management of ACS. However, a significant proportion of patients remain at risk of cardiovascular events. Fibrin is an important contributor to thrombogenesis and may account for the residual event rates. This review examines evidence for the role of the coagulation cascade in thrombus formation in ACS, which provides a rationale for the use of anticoagulation therapy. The current status of research with novel oral anticoagulants in combination with dual antiplatelet therapy for the secondary prevention of ACS is also discussed.
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