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Pick up to three peptides to see how their mechanisms, studied uses and evidence levels differ. Rows where the entries disagree are marked with a blue edge.
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Comparison
Bivalirudin
Cardiovascular & blood
Evidence level
Strong evidence
Approval status
Approved drug
Mechanism of action
- 1.Binds the active site and exosite I of thrombin, blocking fibrin formation.
- 2.Inhibits both free and clot-bound thrombin, unlike heparin.
- 3.Its effect is reversible because thrombin slowly cleaves the peptide, so clotting recovers within about an hour of stopping.
- 4.Does not require antithrombin, so it works when antithrombin is low.
- 5.No risk of heparin-induced thrombocytopenia or the associated antibodies.
Studied for
- Anticoagulation during percutaneous coronary intervention
- Patients with heparin-induced thrombocytopenia
- Acute coronary syndrome managed invasively
- Comparisons against heparin plus glycoprotein IIb/IIIa inhibitors
Reported effects
- Similar or lower rates of major bleeding than heparin plus a glycoprotein IIb/IIIa inhibitor in PCI trials
- Comparable ischaemic outcomes at 30 days
- Rapid loss of anticoagulant effect after stopping the infusion
- A higher rate of stent thrombosis in one large trial when bailout glycoprotein inhibitors were withheld
Side effects
- Bleeding, including major and access-site bleeding
- Hypotension
- Back pain
- Nausea
- Rare allergic reactions
- Stent thrombosis if anticoagulation is inadequate
Research protocol
Research context only - a hospital anticoagulant. In the PCI trials the regimen was a 0.75 mg per kilogram intravenous bolus followed by an infusion of 1.75 mg per kilogram per hour for the duration of the procedure; trials measured major bleeding and major adverse cardiac events at 30 days and one year.
Research context only
Evidence justification
Several large randomised trials in PCI, including REPLACE-2, HORIZONS-AMI and VALIDATE-SWEDEHEART, with bleeding and ischaemic endpoints.