There is a greater diversity of treatment modalities for infrainguinal vessels than for any other vascular bed. Most of the treatment options provide good acute results but are still limited in the long-term durability of the procedure. The superficial femoral artery (SFA) is perhaps the most dynamic of the arteries in the human body, because it is subjected to numerous conformational movements and forces of contraction, torsion, compression, and flexion.1 The SFA is a long vessel that is very susceptible to atherosclerosis and is frequently plagued by diffuse disease and lengthy segments of total occlusion. SFA disease is also very heterogeneous. It can be thrombotic or fibrocalcific and involve softer atherosclerotic plaque or intimal hyperplasia. Therefore, treating this vessel is complicated, and options are diverse.

Trifurcation vessels present similar challenges. The diseased segment is often long and totally occluded. Lesion composition is again heterogeneous and frequently calcific. Vessel diameters are small, and runoff can be very limited. Stent placement in trifurcation vessels may be much less of an option than in the SFA, and perforations may be much more difficult to treat. Very little data exist evaluating durability of the intervention, long-term vessel patency, and reintervention rates. Treatment options are as broad as in the SFA.

BALLOON ANGIOPLASTY AND STENTING
Balloon angioplasty alone can result in undesirable restenosis and dissections and can create challenges in treating certain long total occlusions. Self-expanding stents may provide excellent immediate angiographic results, acceptable resolution of pressure gradients, and can be fast and easy to deploy. Conversely, the long-term results are limited, can be relatively difficult to reopen after restenosis, and in some instances, the options for reintervention and surgical bypass can be limited. Covered stents can provide positive angiographic results within the stented region but can also result in edge restenosis. When restenosis occurs, stents may thrombose and require prolonged infusion of thrombolytics to resolve. The majority of patients in my practice are elderly with critical limb ischemia, and prolonged infusion of thrombolytics in this elderly population can be risky.

The initial success of infrainguinal stenting can be compromised by restenosis in the SFA and popliteal artery. Stenting in the infrainguinal vessels will often cause a permanent structural alteration of the vessel, which can, in some instances, limit or complicate reintervention options.1 Catheter-based interventions to treat in-stent restenosis are difficult and have been met with limited results. Drug-eluting stent placement in the SFA remains a hopeful strategy for the future.

Choosing a treatment option for the SFA or trifurcation vessels depends on many factors, including lesion morphology, composition, length, location, vessel size, accessibility, etc. It also depends on physician preference, comfort level, experience with particular devices, and what is available in the laboratory. I have tried almost everything on the market for treating infrainguinal vessels and have evolved to a strategy of debulking followed by CryoPlasty Therapy (Boston Scientific Corporation) with the PolarCath® Peripheral Dilatation System. In my experience, this strategy has provided good short-term results and desirable vessel patency rates over time. For de novo lesions, I have also seen examples where this combination strategy has resulted in good luminal diameter, low complication rates, good resolution of pressure gradients, and vessel patency rates of > 80% in my laboratory.

CRYOPLASTY THERAPY AND ATHERECTOMY
CryoPlasty Therapy demonstrated clinical patency rates of approximately 82.2% (74/90) at 9 months, with a 6.9% (7/102) rate of clinically significant dissections and an 8.8% (9/102) incidence of bailout stenting, in the PVD Chill Registry.2 Apoptosis is the theoretical mechanism of action for CryoPlasty Therapy and is a noninflammatory process found in human vascular pathology of proliferative restenotic lesions.3 In vitro studies of human specimen cells have shown application of extreme cold followed by a rewarming can modulate neointimal response in cells through induction of smooth muscle cell apoptosis. 4-6 Based on this theory, a large plaque burden within the vessel could prevent the freezing effect from reaching the target cells.

Advantages of atherectomy can include the ability to excise plaque and avoid barotraumas; however, lesions may require postdilatation, and intimal hyperplasia can still occur. Challenges can include the irregular flow pattern that may occur. Luminal gain may improve flow, but the rheology of flow at the end of the procedure may not always be optimal. Overly aggressive attempts to create a cylindrical lumen can result in vessel perforation or aneurysmal segments in the vessel.

In my own practice, stand-alone debulking has produced good short-term results in infrainguinal patients, but I have seen limited long-term patency. Ultimately, debulking followed by drug-coated balloon angioplasty may prove effective, but this is years away from commercial availability in the United States. In the interim, I have employed a strategy of debulking followed by postdilatation with the PolarCath Peripheral Dilatation System as a currently available surrogate, with the hope that the addition of CryoPlasty Therapy may provide some additional impact with respect to restenotic lesions. I try to avoid stenting in the infrainguinal vessels, and debulking followed by CryoPlasty Therapy has been shown to be a useful and attractive alternative for some of my patients.

The combination strategy of atherectomy and CryoPlasty Therapy can potentially create a useful synergy. In theory, postdilating debulked lesions with the PolarCath Peripheral Dilatation System may allow any potential biological effect of stand-alone CryoPlasty Therapy to bring the freezing surface closer to the target cells. CryoPlasty Therapy may have benefit if “smoothing” the irregular internal lumen that may be left by directional atherectomy can create an improved rheology of flow and/or increase acute luminal gain by stretching the vessel.

In my experience, debulking followed by CryoPlasty Therapy has demonstrated desirable results for long total occlusions as compared to stand-alone CryoPlasty Therapy or atherectomy alone. The dualtherapy approach has allowed me to stop debulking sooner and create a larger lumen.

Treating critical limb ischemia rarely involves simple focal lesions. In my experience, debulking before CryoPlasty Therapy has demonstrated limited dissections, desirable acute luminal gain, infrequent elastic recoil, which in theory may have some relation to the proximity of the freezing surface to the vessel wall. I have seen excellent end-angiographic results and velocity of flow when using the combined therapy approach. In my experience, the combined technologies have synergy.

Aggressive restenosis is a difficult freight train to stop. In my experience, CryoPlasty Therapy does not stop restenosis once it begins, but restenosis has seemed to occur less often, and I have used this therapy as first-line treatment in the initial intervention. CryoPlasty Therapy has been an excellent postdilatation strategy after debulking in my experience.

CONCLUSION
I have employed the combined method of atherectomy and CryoPlasty Therapy in practical application, and it has been demonstrated to be cost-effective in my experience. To me, debulking before CryoPlasty Therapy makes intuitive sense. It is a technically straightforward alternative that has, in my experience, shown low complication rates and infrequent need to leave an implant.

Although my experience provides initial evidence that may support a dual-therapy approach to complex vascular lesions, further study is warranted, and no data currently exist to measure the true effectiveness of this methodology. We are currently involved in a retrospective evaluation of several hundred cases with several operators to gather outcome data for this strategy both above and below the knee and plan to pursue a prospective multisite evaluation. These types of studies will be required to better define the role of this therapy relative to the other modalities that are currently available for treating femoropopliteal and infrapopliteal disease.

Louis A. Lopez, MD, is an interventional cardiologist with St. Joseph's Hospital in Fort Wayne, Indiana. Dr. Lopez. He has disclosed that he is a paid consultant to Boston Scientific Corporation. Dr. Lopez has received no financial compensation for participation in this supplement. Dr. Lopez may be reached at lal10000@aol.com

  1. Rogers JH, Laird JR. Overview of new technologies for lower extremity revascularization. Circulation. 2007;116:2072-2085
  2. Laird J, Jaff MR, Biamino G, et al. Cryoplasty for the treatment of femoropopliteal arterial disease: results of a prospective, multicenter registry. J Vasc Interv Radiol. 2005;16:1067-1073.
  3. Isner JM, Kearney M, Bortman S, et al. Apoptosis in human atherosclerosis and restenosis. Circulation. 1995;91:2703-2711.
  4. Tatsutani KN, Joye JD, Virmani R, et al. In vitro evaluation of vascular endothelial and smooth muscle cell survival and apoptosis in response to hypothermia and freezing. Cryo Letters. 2005;26:55-64.
  5. Yiu W, Cheng SWK, Sumpio BE. Direct comparison of endothelial cell and smooth muscle cell response to supercooling and rewarming. J Vasc Surg 2007;46:557-64.
  6. Yiu W, Cheng SWK, Sumpio BE. Vascular smooth muscle cell apoptosis induced by “supercooling” and rewarming. J Vasc Interv Radiol. 2006;17:1971-1977.