The following animations provide a visual demonstration of how ReoPro works in the vascular system.

Animation: "In PCI, ReoPro prevents thrombus formation"

Section 1

Length of Video Animation (no audio): 34 seconds

Overview:

  1. When administered prior to PCI, ReoPro prevents thrombus formation during the procedure.
  2. ReoPro binds to GP IIb/IIIa receptors.

This sequence illustrates how ReoPro, when given prior to percutaneous coronary intervention (PCI), prevents thrombus formation, following the vessel damage caused by coronary interventions.

Initially, blood can be seen flowing through a heavily atherosclerosed vessel. ReoPro has been administered (represented as a teal green cloud entering the vessel) and can be seen flowing past the plaque. It now begins to bind to GP IIb/IIIa receptors.

Ten minutes after the administration of ReoPro, a balloon is inserted into the plaque-filled vessel. Balloon inflation flattens the plaque and opens up the partially occluded vessel. However, it also disrupts the plaque, causing the formation of deep cracks in its surfaces, which results in the exposure of collagen to the flowing blood, and the release of other platelet activators into the bloodstream. We can also see that small sections of thrombus have broken away from the plaque as a result of the intervention. Inactive platelets traversing the damaged plaque come into contact with the exposed collagen and become activated.

Section 2

Length of Video Animation (no audio): 24 seconds

Overview

  1. Mechanical disruption of the endothelium activates platelets and causes the exposure of their GP IIb/IIIa receptors.
  2. ReoPro binds to GP IIb/IIIa receptors, preventing the binding of fibrinogen and thus preventing thrombus formation.
  3. ReoPro enables interventions to proceed smoothly - with a significantly diminished risk of thrombus formation - and thus minimizes the risk of ischemic complications.

This animation begins with a view of activated platelets at the molecular level. Due to the disruption caused by intervention, the coagulation cascade has been initiated resulting in a chain of reactions including the production of fibrinogen. Fibrinogen is a ligand, which binds to GP IIb/IIIa receptors on activated platelets, enabling them to aggregate. When platelets are not activated, the platelets and fibrinogen circulate freely in the blood together. As the platelets become activated by mechanical disruption of the endothelium, their GP IIb/IIIa receptors are exposed. Fibrinogen molecules (blue) can be seen surrounding the platelets and binding to some of the GP IIb/IIIa receptors.

ReoPro molecules can be seen surrounding the platelets. ReoPro is a non-competitive GP IIb/IIIa inhibitor that binds directly to GP IIb/IIIa receptors and prevents the binding of fibrinogen. It thus prevents thrombus formation.

Panning out to a cellular view, it can be noted that ReoPro molecules are occupying most of the GP IIb/IIIa receptor sites on the activated platelets. Only a few receptor–fibrinogen complexes can be seen. As a result, platelet aggregation is significantly curtailed and free-floating fibrinogen molecules are visible. The activated platelets - with ReoPro bound to their surface receptors - can be seen traveling freely through the vessel.

Panning out further to view the whole vessel, notice that a stent has been inserted at the site of the injury. Due to the administration of ReoPro, blood is flowing freely through the stent and past the injured plaque.

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