- What is the GORE PROPATEN Vascular Graft?
The GORE PROPATEN Vascular Graft is an ePTFE vascular graft that has proprietary heparin that is end-point covalently bonded to its luminal surface which imparts thromboresistant properties to the vascular graft.
The Bioactive luminal surface of a 3 mm diameter GORE PROPATEN Vascular Graft (left) remains free of thrombus, while the nonbioactive surface of a control graft (right; 3 mm diameter) is covered with thrombus. Grafts were explanted after two hours in a challenging carotid shunt canine model.- How long does the heparin last?
In order to resist thrombus build-up, it is essential that heparin is present on the surface and retains its bioactive function. Graft explants from an in vivo canine model demonstrated the continued presence of heparin on the graft surface and showed sustained heparin bioactivity over a period of 12-weeks.1 Kaufmann has reported substantial bioactivity on Berlin Heart ventricular assist devices (same as the CBAS™ technology used on the GORE PROPATEN Vascular Graft) removed from patients after 230 days.2 This speaks to the relative longevity of the bioactivity of heparin on the device surface.
- What is the clinical experience with the GORE PROPATEN Vascular Graft?
Since its market introduction in the European Union and in several countries worldwide thereafter, the GORE PROPATEN Vascular Graft has been used in several peripheral applications including lower extremity revascularization. The GORE PROPATEN Vascular Graft has been found to be safe to use with over 10,000 implants worldwide and no reports of heparin induced thrombocytopenia (HIT). Several prospective and retrospective studies undertaken thus far support the safety and efficacy of the GORE PROPATEN Vascular Graft.
- Isn’t hyperplasia the real failure mode of vascular grafts? So why do you need this heparin technology?
Hyperplasia is recognized as an important failure mode of vascular grafts. Thrombotic failure is also an important failure mode especially in the early postoperative months and it is this failure mode that is targeted with the GORE PROPATEN Vascular Graft. Grafts are at greatest risk of failure in the first few postoperative months, so targeting this part of the patency curve makes sense. There is also evidence to suggest that heparin, and specifically the GORE PROPATEN Vascular Graft end-point bonded heparin, may reduce and/or delay intimal hyperplasia.1,2,3,4 Small caliber GORE PROPATEN Vascular Grafts have been shown to significantly reduce platelet deposition and anastomotic neointimal hyperplasia and cell proliferation in both the baboon and canine animal models.1,2,
1. Lin PH, Chen C, Bush RL, Yao Q, Lumsden AB, Hanson SR. Small-caliber heparin-coated ePTFE grafts reduce platelet deposition and neointimal hyperplasia in a baboon model. Journal of Vascular Surgery 2004; 39(6):1322-1328.2. Lin PH, Bush RL, Yao Q, Lumsden AB, Chen C. Evaluation of platelet deposition and neointimal hyperplasia of heparincoated small-caliber ePTFE grafts in a canine femoral artery bypass model. Journal of Surgical Research 2004;118:45-52.3. Kocsis JF, Llanos G, Holmer E. Heparin-coated stents. Journal of Long-Term Effects of Medical Implants 2000;10(1&2):19-45.4. Chen C, Lumsden AB, Hanson SR. Local infusion of heparin reduces anastomotic neointimal hyperplasia in aortoiliac expanded polytetrafluoroethylene bypass grafts in baboons. Journal of Vascular Surgery 2000;31(2):354-363.- Have you seen any difference in anastomotic bleeding compared to other ePTFE grafts?
No significant differences in anastomotic bleeding have been observed with the GORE PROPATEN Vascular Graft as compared to other ePTFE grafts.
- What is unique about the heparin technology on the GORE PROPATEN Vascular Graft?
• Proprietary end-point covalent bonding
• Sustained bioactivity
• No elutionThe heparin molecules are covalently bonded to the luminal surface through a proprietary end-point attachment mechanism (Carmeda ® BioActive Surface (CBAS™)) which serves to anchor heparin molecules to the luminal surface while still maintaining heparin’s intrinsic bioactive properties. The result: a thromboresistant graft surface that retains its bioactive properties over time.
A covalent end-point linkage mechanism allows bonding of the heparin molecules to the graft lumen while retaining heparin’s anticoagulant activity. The active site of a heparin molecule enables antithrombin (AT) to bind, thus increasing the efficiency of AT to subsequently bind to thrombin (T).
When thrombin (T) binds to antithrombin (AT) an AT-T complex is formed. The neutralized thrombin loses its ability to catalyze the conversion of fibrinogen to fibrin. Consequently, fibrin (a major component of thrombus) deposition on the graft luminal surface is suppressed.
The neutral AT-T complex detaches from the heparin molecule thus leaving the heparin bioactive site available to again bind antithrombin. The resulting catalytic cycle enables the thromboresistant process to perpetuate.