Endovascular therapy is often an appropriate method for treating symptomatic femoropopliteal artery (FPA) occlusive disease, but few comparative data are available to aid in the determination of the best strategy for an individual patient. Various patient and lesion characteristics can adversely impact long-term patency after an FPA intervention.1-3 For example, with most endovascular techniques, patency clearly decreases with increasing lesion length and complexity. Patency after angioplasty is worse when occlusions, rather than stenoses, are treated or when densely calcified lesions, rather than lesions with no calcification, are addressed.

The recognition of such facts led to the TASC classification system and the current recommendation that endovascular therapy is most appropriate for lesions that are shorter than 15 cm in length.1 However, because results vary according to treatment modality and change as new and improved devices become available, broad generalizations, such as those in the TASC document, may be inaccurate or outdated and difficult to use as a decisionmaking tool for a specific patient. For example, stent graft treatment is likely an exception to the “rule” that patency after endovascular therapy diminishes with increasing lesion length. Most studies, including the recently completed VIPER trial, have shown that patency with stent grafts is essentially independent of lesion length.4-6

LACK OF DATA IN CURRENT PRACTICE

Unfortunately, many aspects of the techniques needed to achieve the best long-term results with a given treatment have yet to be thoroughly studied; instead, “consensus" tends to rule the day. For instance, in the early days of angioplasty, balloons were routinely oversized by 10% or more, relative to the vessel being treated. This was done partly to account for the parallax and magnification created by “cut-film” angiography, but it was also thought that the vessels should be overdilated by 5% to 10% to create a larger vessel lumen and overcome negative remodeling that might occur over time. Today, however, most interventionists try to match the balloon size to the vessel size with the aim of promoting better patency. They assume that this approach minimizes barotrauma to the vessel wall, even though there is no proof that this “kinder and gentler” method of angioplasty has clinical benefits.

Another example of a consensus-based practice is the use of longer balloons so that balloon length is matched with lesion length. Prolonged balloon inflations (2–4 minutes) are now commonly performed. These approaches are based on an assumption that better results will be achieved—with greater luminal gain and fewer dissections—if less damage occurs during dilation of the viscoelastic arterial wall. It is often stated that long balloons and prolonged inflations decrease dissections and obviate the need for stents in some cases. But are there any data that substantiate this claim? Although I use these techniques routinely and believe they are helpful, as far as I know, the possible benefits of matching the balloon diameter with the vessel size, employing longer balloons, and using prolonged inflation have not been established by means of quantitative analysis.

Quantitative data on the optimal stent diameter for a specific vessel luminal size are also lacking. Interventionists routinely try to oversize self-expanding nitinol stents in the FPA by 1 or 2 mm, but is this really the optimal approach? In fact, there is a more basic issue: Are we accurately estimating the luminal diameter of the vessel we are treating? Because few of us routinely use quantitative techniques to measure vessels, many of us could be substantially and commonly overestimating the size of vessels and thus choosing stents that are too large.

Although we know that nitinol stents are relatively forgiving and that oversizing them does not lead to immediate technical failure, can we be certain that marked oversizing does not cause long-term vessel irritation and in-stent restenosis? Is it not possible that the chronic outward force of a too-large nitinol stent increases vessel injury and that the resultant inflammation promotes intimal hyperplasia and in-stent restenosis? Studies in animals have suggested that such a process can occur.7 Therefore, exactly how to determine the device size that is most appropriate for treating a given vessel is an example of a poorly investigated aspect of endovascular treatment of FPA lesions with implantable devices. In order to achieve optimal outcomes with FPA stenting, however, the specific effect of device-to-vessel sizing on longterm patency must be understood.

OUR RESEARCH AND OBSERVATIONS

Our group has been evaluating the failure modes of FPA stent grafts for several years. Our results with the first-generation GORE® VIABAHN® Endoprosthesis (W. L. Gore & Associates, Flagstaff, AZ), which did not have a heparin coating, indicated that patency with 5-mm devices was inferior to that of 6- and 7-mm devices;6 therefore, we temporarily stopped using 5-mm stent grafts. However, the diminished patency with 5-mm devices may have been caused by several factors other than absolute device size.

Perhaps the treated vessels were too small or diseased; that is, maybe stent grafts simply fail more often when the vessel lumen is < 4 or 4.5 mm in size. Or, did we tend to oversize devices more frequently when treating smaller or diseased vessels, which led to a greater device-vessel lumen mismatch at the landing zones or ends of the device? In avoiding use of 5-mm devices, we undoubtedly did oversize in some cases by placing 6-mm devices into small vessels, and this clearly caused some early occlusions (Figure 1). Our reviews of these various possibilities led to the idea that a more careful approach to vessel and device sizing might be important in achieving optimal outcomes.

VIPER DATA

It is now clear that correctly sizing stent grafts relative to the proximal and distal landing zones is a critical issue when using these devices to treat FPA occlusive disease. The multicenter VIPER study (n = 119 limbs/patients) was a prospective, nonrandomized, single-arm, postmarketing evaluation of the heparin-coated GORE® VIABAHN® Device (5–8 mm). Although the results of this investigation have not yet been published, some preliminary data have been reported.8,9 Most of the patients in the study had TASC C or D lesions, with a mean lesion length of approximately 19 cm. The overall primary patency rate at 1 year was 73%—a rate that is substantially higher than that in the earlier VIBRANT trial (a trial in which GORE® VIABAHN® Devices without a heparin coating or contoured edge were used, and no 5-mm devices were implanted because they were not yet available).10 In the VIPER trial, neither device diameter, vessel size, nor lesion length appeared to have an effect on patency outcomes.

Data from the VIPER investigation do indicate, however, that patency was better in patients in whom the stent grafts were appropriately sized (ie, in accordance with the manufacturer's instructions for use) than in those in whom the device used was too large for the vessel treated. The 1-year primary patency rate for stent grafts that were oversized by < 20% at the proximal landing zone was 88%, whereas for devices that were oversized by more than 20% was 70%; this difference is significant.

The mechanisms by which a mismatch between device size and vessel luminal size might lead to stent graft failure remain unknown, although there are several possible explanations. For example, the mismatch may cause an infolding of the device that eventually results in acute occlusion or thrombosis. It is more likely that the mismatch produces turbulent flow and chronic vessel irritation at the end of the device, which in turn promotes the most common form of stent graft failure: the development of intimal hyperplasia or edge stenosis at the ends of the device.

SUGGESTIONS FOR QUANTITATIVE VESSEL SIZING AND FUTURE RESEARCH

In the VIPER trial, in which only experienced interventionists participated, mismatches between device size and vessel size were found to be relatively common. This indicates that many of the sizing methods currently used during endovascular FPA interventions may not be providing information that is accurate enough. It seems to me that the best way to address this problem is to make much greater use of quantitative vessel analysis. I think that vessel evaluations employing quantitative angiography, endovascular ultrasonography, or both, should be considered in almost all patients with FPA disease who undergo endovascular therapy.

Quantitative analysis using calibration devices, such as wires and catheters with markers at known intervals, should become routine. When results are equivocal, endovascular ultrasonography should be contemplated. Such methods will produce much more accurate luminal measurements. The “eye-balling” technique for estimating vessel diameter is simply not sufficiently precise, especially in cases in which extensive disease has reduced the vessel lumen diameter available for device placement. Moreover, even when vessels are measured using the software built into many angiographic systems, the results can be erroneous if calibration against a known reference length is not performed (Figure 1).

Measuring vessels can add additional rigor and time to an endovascular procedure, but the results of the VIPER trial leave little doubt that, at least for stent graft implantation, careful quantitative analysis can contribute to excellent outcomes. Trials evaluating the importance of device-to-vessel mismatch for other treatment modalities are needed. Until those studies are performed, I think that we are obligated to slow down a bit and try to be more accurate in estimating vessel size during any FPA intervention, even if this approach has the potential to improve patency and other outcomes only minimally. The cost of a wire with 1-cm markers and the 10 minutes that careful vessel sizing may add to a procedure are insignificant compared with the expenditure of resources, cost, and amount of patient distress associated with any reintervention. Peripheral interventionists, get out your measuring sticks!

Richard R. Saxon, MD, FSIR, is Director of Research, San Diego Cardiac and Vascular Institute, North County Radiology Medical Group in Oceanside, California. He has disclosed that he is a consultant to and receives research support from W. L. Gore & Associates. Dr. Saxon may be reached at (750) 940-4055, rsaxonmd@ northcountyrad.com.

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  4. Saxon RR, Dake MD, Volgelzang RL, et al. Randomized, multicenter study comparing expanded polytetrafluoroethylene- covered endoprosthesis placement with percutaneous transluminal angioplasty in the treatment of superficial femoral artery occlusive disease. J Vasc Interv Radiol. 2008;19:823-832.
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  7. Zhao HQ, Nikanorov A, Virmani R, et al. Late stent expansion and neointimal proliferation of oversized nitinol stents in peripheral arteries. Cardiovasc Intervent Radiol. 2009;32:720-726.
  8. VIVA 2011: VIPER 1-year results in long SFA lesions. Endovascular Today website. http://www.bmctoday.net/ evtoday/2011/10/article.asp?f=viva-2011-viper-1-year-results-in-long-sfa-lesions. Published October 18, 2011. Accessed June 10, 2012.
  9. Zoler ML. Heparin-coated stent graft gave high SFA patency. Vasc Specialist. 2012;8:14.
  10. Interim 1-year VIBRANT results presented for Gore Viabahn in SFA treatment. Endovascular Today website. http:// bmctoday.net/evtoday/2009/10/article.asp?f=eNews102909_05.htm. Published October 22, 2009. Accessed December 1, 2011.