Interim 1-Year VIBRANT Results Presented for Gore Viabahn in SFA Treatment

October 22, 2009—In the late-breaking trials session at the Vascular Interventional Advances meeting in Las Vegas, Nevada, Gary M. Ansel, MD, presented 1-year interim results from the VIBRANT (Viabahn Versus Bare-Nitinol Stent) study of the Gore Viabahn endoprosthesis (WL Gore & Associates, Inc., Flagstaff, AZ) in the treatment of long-lesion (≥ 8 cm) superficial femoral artery (SFA) occlusive disease.

According to Dr. Ansel, VIBRANT is a multicenter, real-world trial of the highest femoropopliteal disease burden ever performed. VIBRANT is studying real-world femoropopliteal lesions and real-world device use, such as allowing stent overlaps. It will report longer-term results, clinical application of various duplex velocities, and evaluate potential predictors of patency. Michael R. Jaff, DO, is directing the core lab control at the Vascular Ultrasound Core Laboratory in Boston. Patrick Geraghty, MD, Mark Mewissen, MD, and Dr. Ansel are the coprincipal investigators of VIBRANT. The 3-year VIBRANT study hypothesizes that the use of Gore Viabahn endoprosthesis will result in greater mid- and long-term patency (≥ 2 years) of the treated arterial lesion compared to the use of bare-nitinol stents in treating chronic SFA long lesion with ≥ 8 cm stenoses and occlusions.

The study enrolled 148 patients who were randomized to treatment with the Gore Viabahn endoprosthesis in the test group (n = 72) and to treatment with a bare-nitinol stent in the control group (n = 76). Follow-up was available for 120 patients (81%). Primary endpoints are 3-year primary patency (duplex PSV ratio < 2.0 per core lab determination) and safety determined by 30-day composite of major complications.

Dr. Ansel noted that the US Food and Drug Administration approved the Viabahn for SFA indication on June 14, 2005. The device tested does not include include the bioactive heparin surface or contoured-edge designs. The control group devices were commercially available bare-nitinol stent as determined by institutional standard of care when treating SFA occlusive disease and were not devices approved for SFA use.

Secondary endpoints include primary assisted patency, secondary patency, technical success, target vessel revascularization, target lesion revascularization, clinical success, change in ankle brachial from baseline, alternate peak systolic velocity (PSV) ratios of 2.5 and 3.0 (core lab adjudicated), and stent fracture on plain x-ray (core lab adjudicated).

In 30-day safety outcomes, the two groups were statistically equal. There was overall only one procedure-related issue, which was in the Viabahn group. This was a single access-site complication. In both the Viabahn group and the control group, there were no other access- or treatment-site complications and no death, myocardial infarction, acute renal insufficiency, or study-limb amputation.

Complex and diffuse lesion characteristics of patients in the Viabahn group versus patients in the control group included treated occlusions (59.7% vs 56.6%; P = .74) target lesion length (mean: 19 ± 8 cm vs 18 ± 7 cm; median [range]: 20 cm [8 – 40 cm] vs 16 cm [8 – 36 cm], lesion calcification (none to mild: 37.5% vs 57.9%, moderate to severe: 62.5% vs 42.1%; P =.01), and tibial runoff (one vessel: 15.3% vs 22.4%, two vessel: 50% vs 32.9%, and three vessel: 34.7% vs 44.7%; P = .1).

The 1-year interim efficacy outcomes of Viabahn group versus the control group include technical success (97% vs 97%; P = 1.00), primary patency, defined as PSV ratio = 2.5 (53% vs 58%; P = .58), freedom from target lesion revascularization (73% vs 69%; P = .69), assisted primary patency (84% vs 91%; P = .41), and secondary patency (93% vs 98%; P = .19).

Overall investigator-defined device occlusion was reported in nine patients in the Viabahn endoprosthesis group compared to six patients in the bare-nitinol stent group (P = .18). These instances included acute limb ischemia (2 vs 4; P = .14), chronic limb ischemia (7 vs 2; P = .14), intervention < 24 hours (1 vs 4; P =.09), and intervention > 24 hours (7 vs 1; P = .04).

In terms of clinical success, the quality-of-life questionnaires demonstrated significant improvement in intermittent claudication and SF-36 physical summary scores at 1 year and no significant difference between treatment groups.

Regarding patterns of restenosis, focal-edge stenosis comprised 87% of failures in the Viabahn group (50%, isolated proximal edge; 30%, both proximal and distal edges; 6% isolated distal edge; 14%, undetermined). In-stent stenosis comprised 93% of bare-nitinol stent failures.

Dr. Ansel explained that the clinical implications of restenosis patterns involve calculation of flow-dynamics that assume 80% focal (5 mm) versus diffuse (10 cm) restenosis pattern. The pressure drop in diffuse, in-stent stenosis is an order of magnitude higher than a focal edge stenosis. The flow-rate through diffuse, in-stent stenosis is reduced by 50% as compared to flow through an edge stenosis.

In the Gore Viabahn group, there was one stent fracture with Grade 1 severity in the 47 patients available at follow-up compared to 16 stent fractures in the 52 bare-nitinol stent patients available at follow-up (2% vs 30.8%; P < .01). The bare-nitinol stent fractures included seven with Grade 1 severity, seven with Grade 2 severity, three with Grade 3 severity, and two with Grade 4 severity.

Bare-nitinol stents experienced significantly higher fracture rates. The two groups had equal outcomes of 5.9% in stent fractures of lengths < 15 cm. However, in lengths > 15 cm, there was a 0% stent fracture rate in the Gore Viabahn group compared to 42.9% in the bare-nitinol stent group. In long lesions (> 15 cm), the bare-nitinol fractured stents were associated with a 17% lower patency rate and 25% higher target lesion revascularization rate compared to unfractured stents (P = .4 and .17, respectively). There were fractures in 11 of 37 (30%) tubular stents and in six of 17 (35%) helical stents.

In summarizing the presentation, Dr. Ansel stated that the study's interim results demonstrate that treating claudicants with long diffuse disease is clinically safe and effective at 1 year. Also, they showed that the Viabahn endograft restenosed at edge but bare-metal stents restenosed diffusely. The Viabahn's and bare-nitinol stents' primary patencies have been suboptimal, whereas primary-assisted and secondary patencies are good even in diffuse lesions but strategies need to be refined. Viabahn fractures were found to be a rare event whereas bare-nitinol stents, even those with a helical design, appear to have high fracture rates in long lesions, and these are associated with vessel restenosis. The investigators are finding that surveillance appears to be important at achieving high assisted and secondary patency to over 80% at 1 year. Finally, longer-term follow-up continues, and the primary endpoint will be completed by 2011, Dr. Ansel reported.

Looking toward the future, the VIPER (Gore Viabahn Endoprosthesis With Heparin Bioactive Surface in the Treatment of SFA Obstructive Disease) trial has already commenced for the next-generation Viabahn, which incorporates a heparin bioactive surface, and a contoured end that may potentially improve flow dynamics on the proximal end. Dr. Ansel concluded that these results suggest that there is not an optimal bare-metal solution for treating long SFA disease and that new stent designs may need to be developed for the treatment of longer lesions.