Related Experiment Video
Updated: Dec 30, 2025

Ferric Chloride-induced Murine Thrombosis Models
Published on: September 5, 2016
Dual-pathway inhibition for secondary and tertiary antithrombotic prevention in cardiovascular disease
Davide Capodanno1, Deepak L Bhatt2, John W Eikelboom3
1Division of Cardiology, C.A.S.T., P.O. 'G. Rodolico', Azienda Ospedaliero-Universitaria 'Policlinico-Vittorio Emanuele', University of Catania, Catania, Italy.
Insights
Balancing bleeding and ischaemia risks in cardiovascular disease patients is challenging. Dual-pathway inhibition, combining antiplatelet and anticoagulant drugs, offers a novel strategy to prevent atherothrombotic events.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Thrombosis Research
Background:
- Antiplatelet therapies have improved cardiovascular disease (CVD) outcomes but leave residual ischaemic risk.
- Balancing ischaemia and bleeding risks remains a significant clinical challenge.
- Novel strategies are needed to enhance atherothrombotic event prevention beyond platelet inhibition.
Purpose of the Study:
- To review the pharmacological rationale and clinical development of dual-pathway inhibition strategies.
- To explore combining antiplatelet agents with non-vitamin K antagonist oral anticoagulants (NOACs).
- To assess the potential for preventing atherothrombotic events in various CVD manifestations.
Main Methods:
- Review of emerging pharmacological data on dual-pathway inhibition.
- Analysis of clinical trial data for combined antiplatelet and anticoagulant therapies.
- Examination of mechanisms targeting both platelet aggregation and fibrin formation.
Main Results:
- NOACs attenuate fibrin formation by inhibiting factor Xa or thrombin.
- Dual-pathway inhibition strategies are being developed to address residual ischaemic risk.
- These strategies aim for improved prevention of atherothrombotic events with acceptable bleeding risk.
Conclusions:
- Dual-pathway inhibition represents a promising approach for managing atherothrombotic risk in CVD.
- Combining antiplatelet therapy with anticoagulation (e.g., NOACs) warrants further investigation.
- This strategy may offer enhanced protection against ischaemic events in coronary, cerebrovascular, and peripheral artery disease.
Abstract:
Advances in antiplatelet therapies for patients with cardiovascular disease have improved patient outcomes over time, but the challenge of balancing the risks of ischaemia and bleeding remains substantial. Moreover, many patients with cardiovascular disease have a residual risk of ischaemic events despite receiving antiplatelet therapy. Therefore, novel strategies are needed to prevent clinical events through mechanisms beyond platelet inhibition and with an acceptable associated risk of bleeding. The advent of non-vitamin K antagonist oral anticoagulants, which attenuate fibrin formation by selective inhibition of factor Xa or thrombin, has renewed the interest in dual-pathway inhibition strategies that combine an antiplatelet agent with an anticoagulant drug. In this Review, we highlight the emerging pharmacological rationale and clinical development of dual-pathway inhibition strategies for the prevention of atherothrombotic events in patients with different manifestations of cardiovascular disease, such as coronary artery disease, cerebrovascular disease and peripheral artery disease.
Related Concept Videos
Venous Thrombosis III: Interprofessional Care
Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
Anticoagulant Drugs: Low-Molecular-Weight Heparins
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Coronary Artery Disease V: Interprofessional Care
Peripheral Artery Disease III: Interprofessional Care

