Some of the Heparin molecules have an antithrombin III binding region. When antithrombin binds to the Heparin active site, the Heparin impedes coagulating factors such as thrombin. After the antithrombin/thrombin is deactivated, it is then released into the bloodstream. This thrombin is then unable to attach to the stent and a thrombus is not formed. When the inactive coagulating factors are released after deactivation, the active sites on the Heparin can then react with other antithrombin molecules in the blood stream to continue to prevent clotting within the stent. However, only fifteen percent of the Heparin that coats the stent has the binding site that has a high-affinity for antithrombin III. Thus, only 15% of the Heparin molecules are responsible for the anticoagulation of the antithrombin and …show more content…
Upon reflection, it could be determined that the only different factor that would cause thrombus formation in some groups and no thrombus formation in other groups was that in some groups, high doses of Heparin were used to coat the stents. Stents that have advanced surface characteristics, such as a Heparin coating can reduce the chances of thrombosis within a stent significantly. Although the 5 pmol antithrombin III/stent Heparin-coated stent did not decrease the chance of thrombus formation within the stent, the groups that received 12 or 20 pmol antithrombin III/stent Heparin-coated stents, had a significantly lower chance of thrombus