Covered Stents in the Treatment of Superficial Femoral Artery Disease

VASCULAR DISEASE MANAGEMENT 2014;11(4):E76-E86

Abstract

Treatment of superficial femoral artery (SFA) disease remains challenging due to complex lesion morphologies, unique vessel characteristics, long lesion lengths and frequent chronic total occlusions. Numerous studies have been performed using various renditions of balloon angioplasty, atherectomy and stenting. The Viabahn endoprosthesis (W.L. Gore) is an attractive option for long, complex segments of SFA disease including chronic total occlusions. Use of the Viabahn endograft to create an endoluminal bypass provides an angiographically optimal primary result while potential restenosis is limited to the proximal and distal edges of the endograft resulting in a length-independent restenosis rate, an advantage not offered by any other interventional procedure. Recent enhancements to the Viabahn stent as well as better understanding of optimal device sizing and procedural technique have resulted in highly acceptable patency rates in even the most complex SFA lesions. Strategies to optimize procedural success and to treat late complications such as restenosis and/or thrombosis are reviewed.

Treatment of superficial femoral artery (SFA) occlusive disease remains one of the most challenging procedures for the peripheral vascular interventionalist. Unlike interventions, especially stenting, of other vessels such as coronary, renal, or iliac arteries, long-term patency following SFA intervention has been difficult to achieve. Although the “gold standard” remains femoropopliteal bypass surgery (particularly when venous conduit is used), many vascular surgeons advocate a conservative approach to claudication due to SFA occlusive disease, focusing on a structured exercise program, pharmacotherapy, and risk factor modification as recommended in the TASC II guidelines.¹ Avoidance of femoral-popliteal bypass using venous conduit is reasonable because many of these patients have concurrent coronary artery disease and the saphenous vein may be needed later for coronary artery bypass surgery. 

Many patients are simply managed medically and some, though relatively few, do achieve significant relief from symptoms with an exercise program. Unfortunately, most insurance companies do not offer coverage for vascular rehabilitation and as a result supervised exercise is infrequently attained. Making the situation more complicated, a large number of devices have been developed and studied for treatment of SFA disease, likely due to the generally inadequate long-term results of balloon angioplasty for all but the simplest and shortest lesions. Unfortunately, there are no “head to head” randomized trials comparing these different devices and the interventionalist is left wondering what the “best” treatment might be – novel angioplasty balloons, various atherectomy devices, a plethora of different stents, or some combination of these interventions. 

Compared to femoropopliteal bypass, the interventional data remain limited with only a handful of studies examining patency rates for much more than 1 or at most 3 years, while surgical follow-up data often extend to 10 years. This limitation is in part due to the “moving target” nature of intervention compared to surgery. While femoropopliteal bypass has been a stable procedure for decades, interventional devices constantly evolve such that by the time a study with even 1- or 2-year follow-up is completed, the device is often outdated either because a new and improved iteration has replaced the original device or because an entirely new device has come into vogue. Complicating the issue further is that many trials include entirely or mostly lesions that are simpler and shorter than the “real world” disease with which we are faced on a daily basis. For example, many trials exclude long lesions, chronic total occlusions, severely calcified stenoses, vessels with poor distal run-off, and ostial SFA disease. 

In many practices, these features are more the rule than the exception. These morphologic features, in addition to the length of the SFA and the extreme flexion (not to mention shortening/extension, torsion and compression) that occurs in the distal SFA and proximal popliteal artery, make it easy to understand why satisfactory long-term interventional results have been difficult to achieve, even with a host of different approaches. 

Although many devices have targeted various morphologic challenges, (e.g. calcification, elastic recoil, dissection, thrombus), none has addressed the challenge of long lesion length. In general, the restenosis rate is linearly related to the length of vessel treated for nearly every device available. Although most clinical trials report average lesion length of <10 cm, patients with severe diffuse disease and/or chronic total occlusion, often have lesion lengths >25 cm and sometimes much longer. 

Restenosis vs Progression of Disease

Femoropopliteal bypass offers a unique advantage compared to endovascular intervention in that disease progression within the bypassed segment of the SFA is unimportant. Following an endovascular procedure such as angioplasty, atherectomy, or stenting, there is a fairly well defined window in which recurrent disease is attributed to “restenosis,” a process that is essentially an adverse response to vessel injury. Once a patient has maintained patency past the expected window of restenosis, the development of subsequent occlusive disease can be considered progression of disease rather than a device-related episode of restenosis. In some sense, drug eluting balloons or stents may delay recurrence of disease blurring the lines between what may be considered restenosis vs progression of disease. For example, if a patient has a severe SFA stenosis treated with a drug-eluting balloon and develops recurrent disease 3 years (or 5 years) later, should that be considered restenosis or progression of disease? 

The Rationale for Covered Stents in the SFA

As shown in Table 1, balloon angioplasty often does not yield a very satisfactory primary result frequently due to elastic recoil and/or dissection. Atherectomy of various types often provided a superior angiographic primary result and, as a result, reduces the restenosis rate. The VIVA objective performance criteria, accepted by the FDA as a surrogate endpoint for new device trials, specifies the 1-year primary patency rate for SFA angioplasty as only 33%.² Atherectomy trials in the SFA have yielded considerably higher 1-year primary patency rates. For example, Zeller et al reported 1-year patency in the treatment of de novo SFA lesions of 84% using directional atherectomy.³ Drug-eluting balloons do not provide an optimal appearing primary result, but the restenosis rate seems to be reduced of drug elution. Stenting of the SFA often provided an optimal angiographic result by usually (but not always) overcoming elastic recoil and by eliminating dissections. 

Stent fractures, which have been correlated with decreased patency, remain a concern but newer stent designs such as the nitinol interwoven Supera stent (Idev Technologies, Inc.) are resolving this issue. More recently, drug-eluting SFA stents have been introduced which appear to further reduce the restenosis rate. However, despite these advances, none of these devices prevents long-term progression of disease. The Viabahn endograft (W.L. Gore) offers the unique combination of a primary result that is similar to traditional stenting, a low and length-independent restenosis rate, and permanently excludes the stented segment of the native SFA thus preventing progression of disease from impacting patency. No other interventional device offers all 3 of these advantages.

Modern-Day Viabahn

The current generation Viabahn endoprosthesis or endograft offers several improvements compared to the version available just a few years ago. The fundamental polytetrafluoroethylene (ePTFE) tube supported by a polished nitinol support frame is unchanged, but the device has been downsized to allow use of a smaller introducer sheath size. For example, a 6-mm Viabahn device currently can be delivered over a 0.018" wire through a 6 Fr sheath, whereas the older generation 6-mm Viabahn was delivered over a 0.035" wire through a 7 Fr sheath. 

Another significant enhancement has been the addition of the Carmeda BioActive Surface (W.L. Gore). This process results in heparin being permanently covalently bonded to the PTFE surface of the Viabahn endograft. This helps minimize the risk of thrombosis of the stent graft. 

Contouring of the proximal edge has been added, as well, to prevent in-folding of PTFE into the vessel lumen, particularly when the endograft is slightly oversized compared to the vessel diameter. This change was made to enhance flow dynamics and decrease the risk of proximal edge restenosis. Finally, although the longest Viabahn device currently available in the United States is 15 cm in length, a 25-cm device is already available overseas and a United States clinical trial likely will allow this longer device to be introduced in the United States in the future. 

Length-Independent Restenosis Rate

Both clinical experience and published trials (Figure 1) support the concept that the risk of restenosis following intervention, especially in the SFA, is proportional to the length of diseased segment that is treated.⁴ In sharp contrast to this axiom are the data for Viabahn. In a meta-analysis of 13 independent studies published between 2000 and 2006, the 1-year Viabahn primary patency rate was stable for studies with average lesion length varying from <10 cm to >30 cm (Figure 2).⁵ The explanation for this difference is clear: restenosis can only occur at the proximal edge and/or the distal edge of the Viabahn treated segment; this remains true whether the proximal and distal edges are separated by 5 cm or more than 30 cm as occurs when multiple Viabahn endografts are overlapped to treat a long segment of stenosis or occlusion. This finding was confirmed in the recently completed VIPER trial in which the 1-year primary patency was equivalent for lesions with length >20 cm vs lesions ≤20 cm in length.⁶ 

Because of this advantage in long lesions and long chronic occlusions, it is often difficult to compare Viabahn trials with other device trials that typically study shorter lesions with fewer total occlusions. For example, the VIPER trial of Viabahn evaluated vessels with average lesion length of 19 cm with 56% of those vessels exhibiting chronic total occlusions. Similarly, the VIASTAR trial⁷ of Viabahn stenting included lesions with average lesion length of 19 cm with 79% chronic total occlusions. In comparison, the randomized arm of the Zilver PTX trial⁸ included vessels with average lesion length of 6.3 cm with only 27.4% total occlusions. Even the single-arm registry of Zilver PTX enrolled patients with average lesion length of only 10 cm with 38.3% total occlusions. Cross-trial comparisons are always statistically problematic, but when the lesions studied are so dramatically different, any comparison loses its effectiveness. 

Viabahn Results in Complex SFA Disease

The Viabahn endograft is supported by an extensive body of literature dating back to Lammer’s initial publication in 2000.⁹ At that time, the device was known as the Hemobahn. In 2010, McQuade et al published a randomized comparison of Viabahn vs PTFE femoropopliteal bypass surgery demonstrating virtually identical results for the two procedures.¹⁰ Despite a lesion length for the Viabahn patients of 25.6 cm, the primary and secondary patency rates at 1, 2, 3, and 4 years were virtually identical. Remarkably, this study utilized the older version of Viabahn that did not include heparin bonding or the contoured proximal edge. 

The two most relevant “modern day” Viabahn studies are VIPER and VIASTAR. VIPER was a single-arm study of 119 patients (Table 2) with long SFA lesions (mean length 19 cm) including 56% chronic total occlusions.¹¹Moderate to severe calcification was common, as well (61%). Despite the long lesion length and unfavorable lesion characteristics, primary patency at 1 year was 74% with secondary patency of 92% based on duplex ultrasound follow-up (Figure 3). Several key lessons were learned from VIPER (Table 3). 

Smaller diameter endografts (5 mm, n=23) fared as well as 6 mm endografts (n=85) with primary patency of 79% for the smaller endografts compared to 70% for the larger endografts. As noted earlier, primary patency for lesions of >20 cm length (72%, n=51) was comparable to shorter lesions of ≤20 cm length (patency 75%, n=68). Perhaps the most critical finding of the study was that patency rate was adversely affected when the endografts were oversized by more than 20% compared to the true vessel diameter (Figure 4). Whereas 1-year primary patency was 91% when the Viabahn stent was properly sized, the patency rate declined to 70% when the endograft was oversized by >20%. 

The VIASTAR study was a physician-initiated, prospective, randomized, multicenter trial comparing the Viabahn endografts to bare metal stents (BMS) in the treatment of complex SFA\ disease (Table 4). Lesion length was long in both groups (17 cm to 19 cm) and chronic total occlusions were present in 70% of BMS patients and 79% of Viabahn patients. 

At 1 year, the primary patency rate was 78% for Viabahn stents but only 54% for BMS patients (P=.009). As expected, this difference was accentuated for longer lesions. For lesions >20 cm in length, primary patency was 73% for Viabahn stented patients but only 33% for BMS patients (P=.004). 

Viabahn Stenting in Clinical Practice

In clinical practice, SFA disease often exceeds the severity and complexity of lesions studied in clinical trials. We reviewed our use of the Viabahn endografts in SFA disease between September 2007 and December 2010. Adequate follow-up data were available for 42 of 45 patients treated. Average patient age was 72.1±11.3 years and 48% of patients were male. The population included 38% diabetics, 43% with a history of smoking, 76% with coronary artery disease, 86% with hyperlipidemia, and 95% with hypertension. No patients were excluded for lesion length, chronic total occlusion, ostial disease, or any other reason. Duplex ultrasound follow-up studies were obtained at 4 month to 6 month intervals as per practice protocol. 

Chronic total occlusions were common (67%) and a lumen re-entry device was utilized in 43% of procedures. One-third of patients were being treated for severe stent restenosis or occlusion. Although lesion length was not measured, the average length of Viabahn endografts deployed was 34.9±9.7 cm. Angiograms from a typical procedure before and after Viabahn stenting are shown in Figure 5. Mean length of follow-up was just over 2 years. Primary patency was 71.8% with secondary patency of 90.5% at 27.8±9.5 months. Baseline and follow-up Ankle Brachial Index (ABI) was available in 25 patients showing improvement in ABI from 0.52±0.16 to 0.83±0.22 (P<.0001). 

Management of Edge Restenosis and Viabahn Thrombosis

Although restenosis rates for Viabahn are low, it is important to follow patients closely, especially during the first year, with duplex ultrasound to monitor for proximal or distal edge restenosis. As shown in the VIBRANT trial, these edge restenoses are often asymptomatic and frequently do not compromise the ABI significantly due to the focal nature of the stenosis.¹² However, it is important to treat edge restenosis to prevent the development of slow flow and resulting thrombosis of the endografts. There is some variability among operators, but most will treat an edge restenosis that is associated with a peak systolic velocity of greater than 250 cm/sec to 300 cm/sec. Although there are no clinical trials to guide treatment of edge restenosis, many experienced users treat this problem with balloon angioplasty (sometimes with a cutting or scoring balloon) followed by placement of an overlapped short (5 cm) Viabahn stent. 

Viabahn thrombosis is uncommon but can be effectively treated in a variety of ways. Thrombosis is infrequently associated with critical limb ischemia even when distal collaterals are covered. However, in patients with an inadequate profunda femoris or who are unable to recruit more distal collaterals, Viabahn thrombosis may result in acute limb ischemia, which should prompt either percutaneous or surgical emergent revascularization. 

Stent occlusion resulting in acute limb ischemia may occur after BMS as well as after endograft procedures. Although many physicians are particularly concerned about the risk of this complication with Viabahn endografts, in the VIBRANT trial stent occlusion presenting as rest pain occurred more frequently in patients treated with BMS than in patients treated with Viabahn stents. Although thrombosis resulting in acute limb ischemia must be treated urgently, most patients with thrombosis present electively with recurrent claudication. These less acute patients with Viabahn thrombosis can be successfully treated even several months after the thrombotic event. 

Various approaches in the treatment of Viabahn thrombosis have been utilized, including simple catheter-directed thrombolysis, AngioJet (Bayer HealthCare) with PowerPulse Spray technique and EKOS (BTG) ultrasound-assisted thrombolysis. We have found the EKOS technique to be effective and efficient, although more rapid revascularization may be required for patients presenting with acute limb ischemia. In the EKOS technique, the thrombosed Viabahn endograft is crossed with a 0.035" hydrophilic guide wire and the EKOS catheter is placed with its distal tip extending just past the distal edge of the Viabahn and the proximal aspect of the ultrasound element and the catheter sideholes positioned proximal to the leading edge of the Viabahn. 

Based on the length of the stented segment, an EKOS catheter with an appropriate treatment zone length, typically 24, 30, or 40 cm, is placed. We typically infuse tPA at a dose of 1 mg/hr for up to 12 hr and then reduce the dose of tPA to 0.5 mg/hr. A low-dose heparin drip is infused through the introducer sheath during the infusion. The patient is returned to the catheterization lab a minimum of 8 hours but no more than 24 hours later. The EKOS catheter is removed and angiography is performed. In our experience, we have not observed residual thrombus or evidence of any distal thromboembolism. At that point, the culprit lesion (or lesions) can be easily treated as simple edge restenosis. 

Viabahn for Treatment of Stent Restenosis

Although the use of Viabahn endografts is not FDA approved for treatment of bare metal stent restenosis, it is often utilized for this purpose. Several trials have been attempted including the SALVAGE trial, which unfortunately was terminated prematurely.¹³ In SALVAGE, Viabahn stenting was preceded by debulking of the restenotic tissue with excimer laser. Only 27 of the planned 100 patients were enrolled. The trial yielded satisfactory short-term results but suboptimal primary patency rate of 48% at 12 months, although the target lesion revascularization rate was only 17.4%. 

More recently, the RELINE trial randomized 83 patients with BMS restenosis to treatment with balloon angioplasty (PTA) vs treatment with Viabahn endografts.¹⁴ The 12-month patency data were highly favorable with primary patency of 74.8% in the Viabahn group compared to 28% patency in the angioplasty patients (P<.001).  

Conclusion

Complex SFA occlusive disease remains a challenge for interventionalists. A wide variety of treatment options are available and there are little head-to-head data to permit evidence-based decisions regarding the optimal approach. However, utilizing the Viabahn stent to construct an endoluminal bypass is an attractive option for long SFA lesions including chronic total occlusions. Viabahn restenosis has been well documented to be length-independent due to limitation of restenosis to the proximal and distal edges. Restenosis is typically a focal process at the edge of the Viabahn and is simpler to treat than diffuse in-stent restenosis observed frequently with nitinol BMS. Furthermore, as in surgical bypass, the native SFA is excluded such that the patient is protected from long-term progression of SFA disease. 

Advances in Viabahn design including smaller device profile, contouring of the proximal edge, and heparin bonding to reduce the risk of thrombosis have all contributed to steady improvement in device performance and clinical outcomes. Recent studies such as VIPER have delineated the importance of proper device sizing and have demonstrated that proper sizing translates to superior patency. Appropriate monitoring for and treatment of edge restenosis, especially during the first year after device placement is important to decrease the risk of Viabahn thrombosis. However, in the rare case of thrombosis, thrombolysis may be easily achieved and patency effectively restored. Although there are many available treatment options, Viabahn should be considered a front-line treatment for complex SFA disease. Based on recent data from RELINE, it appears that Viabahn is a superior option for treatment of bare metal stent restenosis compared to balloon angioplasty.

Top 10: Key Technique Points for Successful Viabahn Stenting

1. Always stent “normal to normal” and cover any vessel segment that has been treated with angioplasty, atherectomy, or other therapy regardless of how “normal” it looks.
2. Do not worry about covering collaterals in the distal superficial femoral artery (SFA).
3. If stenting back to the proximal SFA, it is best to stent back to the SFA origin.
4. Use ipsilateral angulated view to align the Viabahn stent with the SFA origin.
5. Do not stent vessels <4.5 mm in diameter.
6. Do not oversize Viabahn by more than 20% of true diameter; a properly sized 5 mm Viabahn will have better patency than an oversized 6 mm device.
7. Continue dual antiplatelet therapy for a minimum of 6 months and preferably indefinitely if not clinically contraindicated. 
8. Postdilate with balloon angioplasty but do not allow the balloon to extend past the edge of the Viabahn stent to avoid risk of edge dissection and subsequent restenosis.
9. Perform duplex ultrasound surveillance every 4 months for 1 year, then every 6 months to monitor for edge restenosis; treat edge restenosis if peak systolic velocity >300 cm/sec regardless of symptoms or Ankle Brachial Index.
10. Consider “telescoping” from 5 mm Viabahn distally to larger 6 mm Viabahn proximally; always overlap Viabahn stents by 1 cm to 2 cm. 

Disclosure: The author has completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The author reports consultancy, honoraria, and reimbursements from W.L. Gore and honoraria from EKOS Corporation. 

[Additional disclosures were reported October 2, 2014. Dr. Weinstock reports past stock ownership in Idev Technologies.]

Manuscript submitted September 2, 2013; provisional acceptance given September 30, 2013; final version accepted October 16, 2013. 

Address for correspondence: Barry S. Weinstock, MD, Florida Heart & Vascular Associates, 511 Medical Plaza Dr. Ste. 101, Leesburg, FL 34748, United States. Email: bweinstock@me.com

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