Optimal Strategy in Lower Extremity Peripheral Percutaneous Interventions: An Interventionalist’s Perspective
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author affiliations:
From the Midwest Cardiovascular Research Foundation, Davenport, Iowa.
Disclosure: Supported by the Nicolas and Gail Shammas Research Fund at the Midwest Cardiovascular Research Foundation (MCRF). MCRF has received research grants from ev3 and Foxhollow.
Manuscript submitted December 4, 2008 and accepted January 9, 2009.
Address for correspondence: Nicolas W. Shammas, MS, MD, Cardiovascular Medicine PC, 1236 E. Rusholme, Davenport, IA 52803 E-mail: shammas@mchsi.com
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Abstract
Peripheral artery disease (PAD) is a global problem, affecting 12–14% of the general population. Its prevalence increases with age. Peripheral percutaneous interventions (PPI) have sharply increased over the past decade to treat symptomatic PAD. PPI is effective in reducing claudication symptoms and in improving limb salvage in patients with critical limb ischemia. However, PPI is limited by a high rate of repeat revascularization, particularly in the infrainguinal vessels, and by significant distal embolization in a certain subset of high-risk patients. We discuss a strategy addressing the triad of mechanical, biological and procedural factors that need to be optimized for immediate and long-term success in patients undergoing PPI. It is our opinion that a successful strategy for optimal outcomes after PPI is to reduce acute recoil and negative remodeling, inhibit smooth muscle cell proliferation and protect the distal tibial vessels while keeping the procedure safe for both operators and patients.
Introduction
Peripheral arterial disease (PAD) is a widely prevalent problem in the United States.1 A sharp increase in peripheral percutaneous interventions (PPI) over the past decade has been recently reported.2 This is likely to be partly related to the marked improvement in percutaneous procedural techniques allowing the endovascular specialist to tackle complex and difficult lesions. Although the “tool box” to treat symptomatic PAD has expanded, many unanswered questions have surfaced about the relative effectiveness, safety and application of these devices. Unquestionably, evidence-based PPI is currently several years behind percutaneous coronary interventions. There is as yet no clear consensus on the best approach to treat certain lesion subsets to optimize short- and long-term outcomes.
We describe a strategy to treat PAD based on the following three principles (Figure 1):
1. Reducing acute recoil and negative remodeling, and therefore limiting the need for primary or provisional stenting;
2. Suppressing smooth muscle cell proliferation following vascular injury;
3. Protecting the infrapopliteal vessels to preserve distal flow.
Following is a discussion of each of these principles.
Reducing vessel recoil and negative remodeling and improving vessel compliance
There are many advantages to reducing immediate recoil in PPI. Acute recoil and dissection following superficial femoral artery (SFA) balloon angioplasty leads to suboptimal angiographic results requiring provisional stenting in up to 50% of patients.3 Stenting to avoid acute recoil, however, has its limitations. Current stents continue to have a high rate of fractures that have been linked to an increase in restenosis rates.4,5 Restenosis, with or without stent fractures, presents a challenging treatment problem for the interventionalist. Thrombus is typically found within occluded restenotic lesions and carries a high rate of embolization during treatment.6 Also, balloon angioplasty (PTA) of in-stent thrombotic/restenotic lesions often leads to additional stenting because of suboptimal results. In addition, stents may limit future surgical targets for peripheral bypass, preventing a viable revascularization alternative to patients. Furthermore, it is possible that the effectiveness of upcoming new therapeutic modalities, such as drug-eluting stents or local infusion of antiproliferative drugs, may be negatively influenced by preexisting nitinol or stainless steel stents within a vessel. Finally, despite the reported improvement in restenosis with stenting, the rate of restenosis has remained as high as 37% in the stented patients at 1-year follow up,7 highlighting the overall challenge in treating SFA lesions.
Although primary stenting of the SFA has been shown to have a small but statistically significant advantage over PTA in reducing restenosis, its effectiveness was limited by a similar reintervention rate in both groups at 1 year.7 Also, the added symptomatic improvement with stenting above PTA does not appear until after 6 months to 1 year post treatment,7 which could be explained by the later negative remodeling in the PTA group rather than a reduction of smooth muscle cell proliferation by the stent.8 We hypothesize that if acute recoil and negative remodeling can be reduced using non-stenting interventional modalities, the need for stenting could be significantly reduced.
Preliminary data from a randomized trial of PTA versus atherectomy3 have shown that SilverHawk atherectomy (ev3, Inc., Plymouth, Minnesota) reduces recoil and the rate of stenting during PPI. Cryoplasty also might reduce vessel recoil and dissection, and lead to less stenting.9 This hypothesis is currently being tested in the ongoing POLAR randomized trial. Finally, it remains unclear whether changing vessel compliance in severely calcified vessels can lead to a reduction in dissection and stenting rates.
Reducing smooth muscle cell proliferation
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