P E R F O R M A N C Et h r o u g h c o l l a b o r a t i o n

FREQUENTLY ASKED QUESTIONS

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Table of Contents

GORE® VIABAHN® Endoprosthesis withPROPATEN Bioactive Surface FAQs

What is the GORE® VIABAHN® Endoprosthesis with

PROPATEN Bioactive Surface? ......................................................2

What is unique about the heparin technology of the GORE®

VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface? ........3

How does end-point covalent bonding of heparin differ

from conventional covalent bonding of heparin and ionic

bonding of heparin? ....................................................................4

How long does the heparin last? ..................................................4

What kind of heparin is used for the GORE® VIABAHN®

Endoprosthesis with PROPATEN Bioactive Surface? ......................5

Does the PROPATEN Bioactive Surface change the

microstructure of the ePTFE? ........................................................5

How many International Units (IU) of heparin are on

the surface of a GORE® VIABAHN® Endoprosthesis with

PROPATEN Bioactive Surface? ......................................................5

Does heparin elute from the surface? ...........................................5

Can I change my anticoagulation procedure while

using the GORE® VIABAHN® Endoprosthesis with

PROPATEN Bioactive Surface? ......................................................5

Can systemic heparin be reduced while using the GORE®

VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface? ......5

Can Protamine be used? ..............................................................5

Can I change my patients’ post-operative antiplatelet regime? ......5

What is HIT? ................................................................................6

How does the presence of PROPATEN Bioactive Surface

affect the risk of HIT? ...................................................................6

What treatment protocol should I follow if a GORE®

VIABAHN® Endoprosthesis with PROPATEN Bioactive

Surface patient develops HIT? ......................................................6

Can the GORE® VIABAHN® Endoprosthesis with

PROPATEN Bioactive Surface be revised if it occludes? ..................7

How is the device sterilized and can I resterilize it?.......................7

Does the PROPATEN Bioactive Surface require

any special storage requirements? ..............................................7

Will post-deployment dilation of the endoprosthesis

damage the PROPATEN Bioactive Surface? ...................................7

What is the benefit of the PROPATEN Bioactive Surface? ...............7

Who is Carmeda AB? ...................................................................7

What medical devices use Carmeda BioActive Surface

(CBAS®) technology? ...................................................................8

How does the PROPATEN Bioactive Surface on the

GORE® VIABAHN® Endoprosthesis compare to the heparin

coating on the Bx VELOCITY® Coronary Stent with HEPACOAT®? .....8

What is the indication for the GORE® VIABAHN®

Endoprosthesis with PROPATEN Bioactive Surface? ......................8

GORE® VIABAHN® Endoprosthesis FAQs

What is ePTFE? ............................................................................9

What clinical data exists for the

GORE® VIABAHN® Endoprosthesis in the SFA? ..............................9

Are there any clinical considerations when using

the GORE® VIABAHN® Endoprosthesis? ........................................9

What about in-stent restenosis? ................................................10

Is there any Level 1 clinical data for the

GORE® VIABAHN® Endoprosthesis? ............................................10

What about SFA stent fractures with the

GORE® VIABAHN® Endoprosthesis? ............................................10

What are the potential failure modes of the

GORE® VIABAHN® Endoprosthesis? ............................................11

What is the effect of the contoured proximal edge?.....................11

What is the rate of thrombosis for the

GORE® VIABAHN® Endoprosthesis? ............................................12

References ................................................................................13

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• Ultra thin wall ePTFE lining

• Unique, durable bonding film

• Polished nitinol stent

• Heparin-bonded surface

• Contoured proximal edge

• Lengths: 2.5, 5, 10, 15, 25 cm

• Diameters: 5 – 13 mm

GORE® VIABAHN® Endoprosthesis withPROPATEN Bioactive Surface FAQs

What is the GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface?

The GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface is a flexible, self-expanding endoluminal endoprosthesis consisting of an expanded polytetrafluoroethylene (ePTFE) lining with an external nitinol support extending along its entire length. The surface of the endoprosthesis is modified with covalently bonded bioactive heparin (PROPATEN Bioactive Surface).

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What is unique about the heparin technology of the GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface?

• Proprietary end-point covalent bonding

• Sustained bioactivity 1

• Minimal heparin elution within the first 24 hours

The heparin molecules are covalently bonded to the surface through a proprietary end-point attachment mechanism (Carmeda® BioActive Surface (CBAS®)) which serves to anchor heparin molecules to the surface while still maintaining heparin’s intrinsic bioactive properties. The result: a surface that is intended to maintain thromboresistance over time.

A covalent end-point linkage mechanism

allows bonding of the heparin molecules to the

endoprosthesis 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).

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 endoprosthesis surface

is suppressed.

AT-T

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.AT-T

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How does end-point covalent bonding of heparin differ from conventional covalent bonding of heparin and ionic bonding of heparin?

Conventional Covalent Bonding In conventional, multiple point, covalent bonding, the anticoagulant properties of heparin are lost due to the fact that the heparin active site is not available to antithrombin.

Ionic Bonding In ionic bonding, the attractive force of negatively charged heparin and positively charged coating can be easily broken, thus allowing heparin to be released from the surface over time. Sustained thromboresistance cannot be achieved.

End-point Covalent Bonding

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. While there is no specific data for the GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface, data from other devices modified using the same proprietary end-point heparin-bonding technology gives some insight into the longevity of the heparin activity. GORE® PROPATEN® Vascular 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 weeks1. Riesenfeld has reported substantial bioactivity on Berlin Heart ventricular assist devices (same as the CBAS® technology used on the GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface) removed from patients after 855 days2. Finally, a GORE® PROPATEN® Vascular Graft explanted after occlusion of outflow vessels after 1,111 days continued to exhibit heparin activity within the original manufacturing specifications.

The negatively (-) charged heparin molecule (yellow) is

attracted to a positively (+) charged coating (orange) on the

device surface. This attractive force can be broken, allowing

heparin to release from the surface over time. Sustained

thromboresistance cannot be achieved.

The heparin molecule (yellow) is bonded (white) at

multiple points to the device surface (orange).

The heparin active site (red) is unavailable to

antithrombin. Without bioactivity, the anticoagulant

properties of heparin are lost.

End-point covalent bonding is a unique concept that allows the anticoagulant

properties of heparin to be harnessed directly on the endoprosthesis surface. The

end of each heparin molecule is bonded to the surface, allowing the heparin active

site to freely interact with anti-thrombin. Consequently, heparin is retained on the

endoprosthesis surface in a bioactive form. This results in a endoprosthesis surface

with sustained thromboresistance.

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What kind of heparin is used for the GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface?

Reduced molecular weight heparin derived from USP heparin of porcine origin is used in the construction of the PROPPATEN Bioactive Surface.

Does the PROPATEN Bioactive Surface change the microstructure of the ePTFE?

The thickness of a CBAS® coating is approximately 200 nanometers (nm)14. This is not sufficient to change the microstructure of the ePTFE.

How many International Units (IU) of heparin are on the surface of a GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface?

Heparin activity in solution is typically measured in terms of International Units (IU). Surface bound heparin, on the other hand, is normally measured in terms of picomoles of ATIII activity. A reasonable estimate of the number of IUs on the endoprosthesis surface can be obtained via theoretical calculations. Based on the mass of heparin on the surface, theoretical calculations yield an estimate of < 400 IU per endoprosthesis (8 mm x 15 cm). This is very small compared to the typical intraoperative heparin dose of ~5,000 IU.

Does heparin elute from the surface?

The GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface binds heparin to the endoprosthesis surface via a stable covalent linkage. In vitro experiments performed on the GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface have shown that less than 30 IU of heparin are released into solution during the first 24 hours after initiation of flow (data on file). Thereafter, there is minimal release of heparin and no systemic effect.

Can I change my anticoagulation procedure while using the GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface?

The physician should consider the need for intraoperative and / or postoperative anticoagulation therapy based on the pharmacological requirements and medical history of the patient. The presence of heparin on the endoprosthesis is not intended to serve as an alternative to the surgeon’s chosen intraoperative or postoperative anticoagulation regimens.

Can systemic heparin be reduced while using the GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface?

The presence of heparin on the GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface is not intended to serve as an alternative to intraoperative or postoperative anticoagulation. The anticoagulant effect of the heparin on the endoprosthesis is limited to the device surface and does not have a systemic anticoagulant effect.

Can protamine be used?

There is no long-term effect by protamine on the bioactivity of the PROPATEN Bioactive Surface. Although protamine reverses the anticoagulant activity of heparin, its effect is transitory. Protamine can only remain bound to heparin when it is present in sustained excess quantities. Since protamine is rapidly removed from the circulation, any effect is short-lived, as protamine desorbs from the endoprosthesis surface into the blood stream.

Can I change my patients’ post-operative antiplatelet regime?

The presence of heparin on the GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface is not intended to serve as an alternative to the physician’s chosen postoperative antiplatelet regimens. The post-operative antiplatelet regimen is left at the discretion of the physician.

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What is HIT?

Heparin-Induced Thrombocytopenia (HIT) occurs in a relatively small subset of the patient population and is defined as a decrease in platelet count during or shortly following exposure to heparin3. There are two distinct types of HIT, each with very different clinical ramifications.

HIT type I is characterized by a mild and transient asymptomatic thrombocytopenia that develops within the first few days of starting heparin treatment and disappears quickly following heparin cessation4. This type of HIT is benign and is not associated with an increased risk of thrombosis.

HIT type II is characterized by rapid or delayed-onset thrombocytopenia that is associated with a risk of thrombosis5. In the following discussion, HIT type II will be referred to simply as HIT. The mechanism underlying HIT is an immune response as antibodies are formed against a heparin-platelet factor 4 (PF4) complex. The antibody-heparin-PF4 immunocomplex binds to platelets, inducing platelet activation and aggregation. Thrombocytopenia results from the clearance of activated platelets and antibody-coated platelets by the reticulo-endothelial system5, 6. Typically, patients receiving heparin for the first time experience the onset of thrombocytopenia 5 – 8 days after the administration of heparin; however, the onset can be rapid (< 1 day) in patients with antibodies from a previous exposure7, 8 or delayed up to 3 weeks after heparin therapy has stopped9-12.

How does the presence of PROPATEN Bioactive Surface affect the risk of HIT?

The GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface is contraindicated for patients with known hypersensitivity to heparin, including those patients who have had a previous incidence of HIT type II.

For patients who do not have a known hypersensitivity to heparin, the theoretical potential of any heparin bonded device to cause platelet aggregation and thrombocytopenia does exist. However, since interventions in the vascular system almost invariably involve administration of systemic heparin, it becomes difficult, if not impossible, to judge whether or not the heparin bonded device contributed to the development of HIT.

The body of clinical evidence to date for the PROPATEN Bioactive Surface does not show any relationship between the implantation of this product and HIT. In a study by Heyligers, et al13, HIT-inducing antibodies were not detected in any of the patients that received the GORE® PROPATEN® Vascular Graft even after six weeks of implantation.

The incidence of reported cases of HIT after implantation of the GORE® PROPATEN® Vascular Graft is less than 0.1% worldwide. It is not known if the graft contributed to the development of HIT in these patients.

The GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface does not elute heparin into the bloodstream and hence has no systemic effect. Based on the mass of heparin on the surface of the endoprosthesis, theoretical calculations yield an estimate of < 400 IU of heparin per endoprosthesis (8 mm x 15 cm). This is very small compared to the typical intraoperative heparin dose of ~5,000 IU.

What treatment protocol should I follow if a GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface patient develops HIT?

The incidence of HIT type II is extremely low in vascular bypass patients receiving heparin over a period of several days. If HIT type II is diagnosed, established procedures for the treatment of this condition, including immediate cessation of systemic heparin administration, should be followed. If symptoms persist, or the health of the patient appears compromised, alternative pharmaceutical or surgical procedures, including surgical bypass and / or removal of the endoprosthesis, may be considered at the discretion of the attending physician.

The incidence of reported cases of HIT after the implantation of the GORE® PROPATEN® Vascular Graft is less than 0.1%. It is not known if the graft contributed to the development of HIT.

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Can the GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface be revised if it occludes?

The GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface can be revised like the non-heparin bonded GORE® VIABAHN® Endoprosthesis. Bioactivity of the PROPATEN Bioactive Surface after a revision procedure has not been established.

How is the device sterilized and can I resterilize it?

The device is sterilized using Ethylene Oxide. The GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface should not be resterilized.

Does the PROPATEN Bioactive Surface require any special storage requirements?

The PROPATEN Bioactive Surface does have susceptibility to humidity. However, the foil pouch is both a moisture and a sterile barrier, and sufficiently protects the device from humidity. DO NOT use or store the device if the foil pouch has been compromised. The package should be stored in a cool dry place (the shelf of a cath lab is fine). The product does have an expiration date and should be used before the labeled “use by” (expiration) date marked on the box.

Will post-deployment dilation of the endoprosthesis damage the PROPATEN Bioactive Surface?

The PROPATEN Bioactive Surface is designed to withstand balloon touch up. In vitro tests show that balloon touch up with the appropriately sized balloon will not affect the activity of the heparin surface (data on file).

What is the benefit of the PROPATEN Bioactive Surface?

While there is no direct clinical evidence to indicate that the PROPATEN Bioactive Surface has an affect on the effectiveness of the GORE® VIABAHN® Endoprosthesis, the Carmeda® BioActive Surface (CBAS®), upon which PROPATEN Bioactive Surface is based, has a long clinical history. Some of the reported features and benefits of the CBAS® bioactive coating technology include: long-term bioactivity, non-leaching, reduced thrombus formation / platelet adhesion, decreased inflammatory response, and antimicrobial protection14.

Who is Carmeda AB?

Carmeda AB, a Swedish company, invented the end-point heparin bonding technology used on the GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface and other medical devices. This end-point heparin bonding technology is termed the Carmeda® BioActive Surface (CBAS®). Carmeda AB is a world leader in heparin technology with a long history of pioneering research in this field since the company was founded in 1984. In October, 2005, Carmeda AB became a wholly owned subsidiary of W. L. Gore & Associates, Inc.

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What medical devices use Carmeda® BioActive Surface (CBAS®) technology?

Carmeda AB has developed several successful partnerships with companies that manufacture medical devices such as coronary stents, oxygenator circuits, ventricular assist devices, blood gas sensors and central venous catheters. Over 200 scientific papers including numerous clinical studies have demonstrated the safety, efficacy and superiority of the CBAS® technology. The reported features and benefits of the CBAS® bioactive coating technology include: long-term bioactivity, non-leaching, reduced thrombus formation / platelet adhesion, decreased inflammatory response, and antimicrobial protection14.

The GORE® PROPATEN® Vascular Graft utilizes the same process used to create the PROPATEN Bioactive Surface. Since its 2002 market introduction in the European Union and in several countries worldwide, the GORE® PROPATEN® Vascular Graft has been used in several peripheral applications including lower extremity revascularization. Several prospective and retrospective studies undertaken thus far support the safety and efficacy of the GORE® PROPATEN® Vascular Graft15.

How does the PROPATEN Bioactive Surface on the GORE® VIABAHN® Endoprosthesis compare to the heparin coating on the Bx VELOCITY® Coronary Stent with HEPACOAT®?

Although these devices have different indications and therefore cannot be directly compared, the heparin surface on both devices utilizes the same CBAS® technology to create a permanent, bioactive heparin surface. However, there are two distinct differences between a heparin-bonded stent and a heparin-bonded stent-graft: the amount of lesion coverage provided by the coated device and the length of time that the surface is exposed to the blood stream.

Lesion coverage Placement of a coated bare stent leaves a substantial part of the diseased vessel lumen exposed. The effect of the surface-bound heparin is limited to the stent struts and not the entire stented region. However, the GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface completely lines the diseased vessel. The surface-bound heparin is present throughout the treated region.

Exposure time Bare coronary stents rapidly re-endothelialize following implantation16. Thus, within weeks after implantation, any heparin bound to the stent struts would be masked by neointimal and endothelial cells, rendering it irrelevant. In contrast, the ePTFE lining of the GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface inhibits cellular infiltration, thus leaving the heparin exposed and bioactive. Studies of an ePTFE vascular graft with the same heparin coating have shown sustained heparin bioactivity out to at least 3 months1. Riesenfeld has reported substantial bioactivity on a CBAS®-coated Berlin Heart ventricular assist devices (same as the CBAS® technology used on the GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface) removed from patients after 855 days2. Finally, a GORE® PROPATEN® Vascular Graft explanted after occlusion of outflow vessels after 1,111 days continued to exhibit heparin activity within the original manufacturing specifications. Theoretically, as long as the endoprosthesis is free from neointimal or pseudo intimal overgrowth, the heparin is available and active.

What is the indication for the GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface?

The GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface is a flexible, self-expanding endoluminal prosthesis for endovascular grafting of peripheral arteries.

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GORE® VIABAHN® Endoprosthesis FAQs

What is ePTFE?

ePTFE is an acronym for expanded polytetrafluoroethylene. PTFE is an extremely inert, biocompatible biomaterial composed solely of carbon and fluorine. When PTFE is expanded at a high temperature and rate, ePTFE is formed with a node-fibril microstructure. This discovery was made by Bob Gore in 1969. Since the mid-1970’s, ePTFE vascular grafts have been the synthetic material of choice by vascular surgeons performing peripheral bypass operations or creating dialysis access grafts.

What clinical data exists for the GORE® VIABAHN® Endoprosthesis in the SFA?

The GORE® VIABAHN® Endoprosthesis has an impressive amount of published clinical data. There have been 17 independent studies reporting primary patency for the endoprosthesis with greater than 30 patients. For the published 1103 limbs, with an average lesion length of 16 cm, the weighted average one year primary patency is 77%.

Are there any clinical considerations when using the GORE® VIABAHN® Endoprosthesis?

Some key clinical learnings that have emerged include:

• Avoid non-compliant lesions

• Ensure adequate inflow and outflow (i.e., at least one vessel run-off)

• Correct sizing is key

• Land device at least 1 cm into healthy vessel proximally and distally to the lesion

• Every region pre-treated with PTA needs to be covered by the device

• During post dilatation, only balloon inside the region covered by the device

• Consider an antiplatelet regimen post-procedure

• Do not use the GORE® VIABAHN® Endoprosthesis with PROPATEN Bioactive Surface in patients with known hypersensitivity to heparin, including those patients who have had a previous incidence of Heparin-Induced Thrombocytopenia (HIT) type II.

Reported Patencies of GORE® VIABAHN® Endoprosthesis / GORE® HEMOBAHN® Endoprosthesis (5 – 8mm) treating the SFA in Studies of at least 30 limbs

Author Year Journal Publication / PresentationNo. of Limbs

Lesion Length

(cm)%

Occlusions

Primary Patency (years / %)

1 2 3 4

Lammer 2000 Radiology, 217:95-104 80 13.8 NR 79

Jahnke 2003 J Vasc Interv Radiol, 14:41-51 52 8.5 83 78 74 62

Bleyn 2004 Edizioni Minerva Medica, 14:87-91 67 14.3 100 82 73 68 54

Panetta 2005 Endovasc Today, August 41 30.4 90 86 77

Chopra 2006 AIM Symposium, November 13 – 16 70 20 71 93 87 72

Coats 2006 Endovasc Today, September 83 NR 47 89

Fischer 2006 J Endovasc Ther, 13:281-290 59 10.7 87 67 58 57 52

Zander 2006 SIR Meeting, April 3 31 16.6 NR 86 78 78 78

Saxon 2007 J Vasc Interv Radiol, 18:1341-1350 87 14.2 42 76 65 60 55

Alimi 2008 Eur J Vasc Endovasc Surg, 35:346-352 102 11.7 NR 74 71 71

Djelmami-Hani 2008 SCAI Meeting, March 29 – April 1 132 21 39 80

Saxon 2008 J Vasc Interv Radiol, 18:823-832 97 7 21 65

VIBRANT 2009 VIVA, September 19 – 22 72 19 60 53

Kougias 2009 Am J Surgery, 198:645-649 31 23 100 75

Farraj 2009 J Invasive Cardiol, 21:278-281 32 15.4 100 80

Rebellino 2009 Cath Cardiovasc Interv, 73:701-705 32 NR NR 82 75 75 75

McQuade 2010 J Vasc Surg, 52:584-591 50 25.6 NR 72 63 63 59

Average / Total 1103 16.1 62 77 72 67 59NR = Not Reported

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What about in-stent restenosis?

The ePTFE lining of the GORE® VIABAHN® Endoprosthesis limits in-stent restenosis, and because of this, patency is independent of lesion length. For the studies presented in the table above, a plot of the 1 year primary patency versus lesion length (17 studies, 1103 limbs) shows that patency is indeed independent of lesion length.

Is there any Level 1 clinical data for the GORE® VIABAHN® Endoprosthesis?

There are 2 published studies that present Level 1 clinical data for the GORE® VIABAHN® Endoprosthesis.

From 1998 – 1999, the GORE® VIABAHN® Endoprosthesis was evaluated in a randomized, multicenter trial, and published in the Journal of Vascular and Interventional Radiology in 200828. The purpose of the study was to compare the safety and effectiveness of the GORE® VIABAHN® Endoprosthesis to percutaneous transluminal angioplasty (PTA) in patients with chronic lower limb ischemia or chronic lifestyle altering claudication due to superficial femoral artery (SFA) atherosclerotic disease. A total of 241 patients or 244 cases (limbs) were treated in the study. Each site was permitted up to two training cases. A total of 47 training cases were performed; 197 cases were randomized with 100 assigned to PTA and 97 to the GORE® VIABAHN® Device. The GORE® VIABAHN® Endoprosthesis showed 25% better 12-month redefined primary patency than PTA: 65% vs. 40%. Patency in this study was defined as target vessel, not target lesion, patency (PSVR < 2.0 via DUS at 12 months).

A second study was published in the Journal of Vascular Surgery by McQuade et al33 in 2010. In this randomized, single center study, the GORE® VIABAHN® Endoprosthesis was compared to prosthetic fem-pop surgical bypass in treating superficial femoral artery occlusive disease. Fifty limbs were enrolled into each study arm with ankle-brachial indices and color duplex flow sonography imaging performed at 3, 6, 9, 12, 18, 24, 36, and 48 months. The primary patency rate for the stent graft group at 12, 24, 36, and 48 months was 72%, 63%, 63%, and 59%, respectively, while the primary patency for the surgical bypass group was 76%, 63%, 63%, and 58%, respectively,The average treatment length was 25.6 cm for the GORE® VIABAHN® Endoprosthesis.

What about SFA stent fractures with the GORE® VIABAHN® Endoprosthesis?

The device has excellent flexibility and is well-suited for the SFA. There is a very low incidence (<0.01%) of reported stent fractures in the SFA.

1 Ye

ar P

rim

ary

Pate

ncy

Average Lesion Length Treated (cm)

0 5 10

0%

20%

40%

60%

80%

100%

15 20 25 30 35

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What are the potential failure modes of the GORE® VIABAHN® Endoprosthesis?

Although primary patency at 1 year is excellent (77%), the literature does report some failure modes and how they can be mitigated. Examples include:

What is the effect of the contoured proximal edge?

The contoured proximal edge is a manufacturing change that was implemented to improve repeatability in processing, and leads to improved apposition of the device to the vessel wall. The conformable fit of the stent-graft may improve flow dynamics at the proximal edge of the stent.

Failure Mode Mitigators

Edge Restenosis Don’t balloon outside the device; properly oversize the device (5 – 20%)

Progression of Disease Cover all of the diseased vessel; distal and proximal landing zones should be in healthy vessel

Thrombosis Complete post-dilatation; appropriate antiplatelet therapy; regular patient follow-up

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What is the rate of thrombosis for the GORE® VIABAHN® Endoprosthesis?

There are two thrombosis events to consider: acute and late.

Acute Thrombosis (< 30 days of procedure). As reported in the literature, the GORE® VIABAHN® Endoprosthesis has an acute thrombosis rate of 2 – 5%17, 19, 34, 35. This is similar to the 3 – 4% acute thrombosis rates of bare nitinol stents36, 37. Thus, this acute thrombosis rate is likely procedure related rather than related to any inherent thrombogenicity of the device.

Late Thrombosis (> 30 days of procedure). If a GORE® VIABAHN® Endoprosthesis fails, it may present itself as a thrombosed endoprosthesis. Often this is secondary to another failure mode (edge stenosis or disease progression) and a result of low blood flow through the endoprosthesis. The occluded endoprosthesis can be revised, and the adjacent disease treated using an additional endoprosthesis. The long-term patency of the GORE® VIABAHN® Endoprosthesis at 5 years in a selected patient population was recently reported to be 62% (primary patency) and 90% (secondary patency) by Fischer, et al 23. This secondary patency demonstrates the durability and patency of the endoprosthesis after revision.

Occluded GORE® VIABAHN® Device

(arrow indicates proximal edge of device)

After lysis, edge stenosis apparent PTA of the edge stenosis

Images courtesy of Richard Saxon

References1. Begovac PC, Thomson RC, Fisher JL, Hughson A, Gällhagen A. Improvements in GORE-TEX® Vascular Graft performance by Carmeda® bioactive surface heparin

immobilization. European Journal of Vascular and Endovascular Surgery 2003;25(5):432-437.

2. Riesenfeld J, Ries D, Hetzer R. Analysis of the heparin coating of an EXCOR® Ventricular Assist Device after 855 days in a patient. Abstract presented at the 32nd Society for Biomaterials Annual Meeting. April 18-21, 2007. Chicago, IL. Abstract 180.

3. Warkentin TE. An overview of the heparin-induced thrombocytopenia syndrome. Seminars in Thrombosis & Hemostasis 2004;30(3):273-283.

4. Franchini M. Heparin-induced thrombocytopenia: an update. Thrombosis Journal 2005;3(1):14-18.

5. Jang IK, Hursting MJ. When heparins promote thrombosis: review of heparin-induced thrombocytopenia. Circulation 2005;111(20):2671-2683.

6. Chong BH. Heparin-induced thrombocytopenia. Journal of Thrombosis & Haemostasis 2003;1(7):1471-1478.

7. Lubenow N, Kempf R, Eichner A, Eichler P, Carlsson LE, Greinacher A. Heparin-induced thrombocytopenia: temporal pattern of thrombocytopenia in relation to initial use or reexposure to heparin. Chest 2002;122(1):37-42.

8. Warkentin TE, Kelton JG. Temporal aspects of heparin-induced thrombocytopenia. New England Journal of Medicine 2001;344(17):1286-1292.

9. Jackson MR, Neilson WJ, Lary M, Baay P, Web K, Clagett GP. Delayed-onset heparin-induced thrombocytopenia and thrombosis after intraoperative heparin anticoagulation-four case reports. Vascular & Endovascular Surgery 2006;40(1):67-70.

10. Rice L, Attisha WK, Drexler A, Francis JL. Delayed-onset heparin-induced thrombocytopenia. Annals of Internal Medicine 2002;136(3):210-215.

11. Smythe MA, Stephens JL, Mattson JC. Delayed-onset heparin-induced thrombocytopenia. Annals of Emergency Medicine 2005;45(4):417-419.

12. Warkentin TE, Kelton JG. Delayed-onset heparin-induced thrombocytopenia and thrombosis. Annals of Internal Medicine 2001;135(7):502-506.

13. Heyligers JMM, Lisman T, Verhagen HJM, Weeterings C, de Groot PhG, Moll FL. A heparin-bonded vascular graft generates no systemic effect on markers of haemostasis activation or detectable HIT-inducing antibodies in humans. In: Heyligers JMM, ed. Novel Strategies To Improve the Patency of Vascular Prostheses. 2006;7:95-108.

14. Carmeda AB. 2000. CBASTM Compendium. Upplands Väsby, Sweden. Rev 2.

15. Bosiers M, Deloose K, Verbist J, et al. Heparin-bonded expanded polytetrafluoroethylene vascular graft for femoropopliteal and femorocrural bypass grafting: 1-year results. Journal of Vascular Surgery 2006;43(2):313-319.

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