Endovascular Management of Chronic Femoropopliteal Disease

Endovascular Management of Chronic Femoropopliteal Disease

Eric M. Walser and Mahmood K. Razavi

Femoropopliteal occlusive disease is present in a significant proportion of older patients, with about 20% of men and 17% of women older than 55 living with ankle-brachial indices (ABI) under 0.9. A smaller percentage (3%-7%) present with symptoms of intermittent claudication (IC) between the ages of 60 and 70.1-5 After the age of 70, however, 25% of patients with IC clinically deteriorate, with 1% to 3.3% progressing to critical limb ischemia (CLI) and eventual amputation.6,7 Although only some patients experience worsening claudication or gangrene, many more adjust to this reduction in circulation by becoming progressively more sedentary. As such, the femoropopliteal arteries deserve respect as critical determinants in the health and mobility of our older citizens. To be sure, significant lower extremity occlusive arterial disease has ominous associations with generalized vascular disease, and the estimated 5-, 10-, and 15-year morbidity and mortality of these patients is 30%, 50%, and 70%, respectively, with 70% to 80% of deaths related to cardiovascular events (myocardial infarction, cerebrovascular accidents, and ruptured aneurysms). These figures are 2.5 times higher than that of nonclaudicants.2

The anatomy and physiology of the femoropopliteal artery is unique and poses specific challenges for both percutaneous and surgical treatments. The femoral artery is the longest artery in our body, with the fewest branches. It has thick muscular walls so that it can tolerate the variety of longitudinal and lateral compressive forces delivered to it by virtue of its fixation at the highly mobile hip and knee joints. In this milieu, catheter-based intervention often falters because this powerful artery scars, proliferates, and thromboses under the injuries inflicted by angioplasty, and it fractures and deforms metallic stents placed within its lumen.8 No wonder that multiple devices have tried and failed to tame occlusive disease in the femoropopliteal arteries.

In this chapter, the discussion of femoropopliteal occlusive disease begins with its clinical and noninvasive diagnosis. Then we describe established medical and surgical therapies. Finally, we will focus on endovascular methods, including the multitude of past failures and their evolution to more modern devices and treatments available today and in the near future.

With almost 2000 articles pertaining to femoral artery stents available in the recent medical literature,8 the importance of critical manuscript review in this subject area cannot be understated. Therefore, the reader must consider important comparative data when evaluating the various treatments for femoropopliteal arterial disease—including, but not limited to, the status of the runoff and inflow vessels, the length and degree of calcification of lesions treated, clinical versus imaging follow-up, and the presence of concomitant disease states such as diabetes, continued smoking, or renal failure.

Clinical Presentation

Peripheral arterial disease (PAD) involving the lower extremities is defined as the presence of disease causing hemodynamic compromise resulting in a resting ABI of less than 0.9. The clinical presentation of PAD can range from no symptoms to gangrene and tissue loss. PAD is a strong marker for the presence of systemic atherosclerotic disease and is therefore associated with an increased risk of major cardiovascular events (5%-7% annually).2 The most common cause of occlusive disease in the femoropopliteal segment (FPS) is atherosclerosis, with the major risk factors presented in Table 36-1 along with targets for reduction and the means for reaching those targets.

Intermittent claudication is the most common symptom related to PAD. Typical symptoms consist of muscle fatigue, ache, or cramps induced by exertion and relieved by rest (Rutherford-Becker classification II). Involvement of calves, thighs, or buttocks indicates the level of anatomic disease.

Critical limb ischemia is the most severe manifestation of PAD and refers to chronic ischemic rest pain and/or ulceration and gangrene (Rutherford-Becker classifications III and IV). This group carries the worst prognosis of all PAD patients, with an amputation-free survival of only 50% at 1 year. Approximately 25% of patients with CLI die, and another 25% require a major amputation at 1 year. The main manifestation of CLI is ischemic rest pain in the foot, which is worse at night or when the foot is in a nondependent position. Edema is another common manifestation due to prolonged dependency of the foot and/or inflammation. Ulceration and gangrene are other clinical manifestations of CLI. Gangrene typically involves the digits or the heel and may progress to affect the distal forefoot. Although ulcers above the foot can be of arterial etiology, the majority are caused by venous disease.


Patients with IC give a history of leg muscle pain that is relieved by rest. The differential diagnosis of IC includes arthritis of the hip, knee, and ankle joints; spinal stenosis; nerve root compression; Baker cyst; and venous claudication. The clinical features of IC that differentiate it from other conditions include quick relief of symptoms by rest and lack of dependence on patient or extremity position. Frequently, musculoskeletal pain or pain due to spinal stenosis is worse in the morning before any significant muscular exertion, whereas claudication virtually never affects patients before they get out of bed.

Key components of the physical examination in patients with PAD include palpation of extremity pulses and evaluation of the extremities for color, temperature, chronic hair loss, nail changes, and skin ulcerations. Those patients with a history and/or physical findings suggestive of PAD should proceed to objective testing, including the ABI.

As mentioned earlier, an ABI of less than 0.9 is a highly sensitive measure for the presence of obstructive lesions in the arterial supply to the leg. Thus, measurement of the ABI is a good screening tool for the presence of PAD. A formal noninvasive test of the lower extremity should also include segmental limb systolic pressure measurement and segmental plethysmography or pulse-volume recordings. Measurement of toe pressures and toe-brachial index would be desirable in the presence of CLI and noncompressible arteries that may occur with conditions such as diabetes and renal failure. The toe pressure is usually 30 mmHg below the ankle pressure, and hence an abnormal toe-brachial index is defined as less than 0.7. Doppler velocity waveform analysis is also a useful tool that is frequently done as part of a formal noninvasive vascular study. Triphasic arterial waveforms become biphasic, then flat (monophasic) as arterial flow diminishes.

Computed tomographic angiography (CTA) and magnetic resonance angiography (MRA) are moderately sensitive and specific for arterial occlusive disease in the large and medium-sized vessels. Most practitioners reserve costly cross-sectional imaging for those patients with symptoms warranting intervention and segmental limb pressures indicative of potentially correctable arterial disease. A more detailed discussion of CTA and MRA is presented elsewhere in this book.

The diagnosis of CLI cannot be made based on clinical presentation alone and should be confirmed by ABI, toe systolic pressure, or transcutaneous oxygen tension. Patients with CLI typically have ankle and toe systolic pressures of less than 50 mmHg and 30 mmHg, respectively. The presence of ulceration or rest pain alone does not confirm the diagnosis of CLI. The differential diagnosis of ischemic ulceration includes traumatic, neuropathic, or venous ulcerations. A combination of these causes is not uncommon, especially in diabetic patients. The differential diagnosis of ischemic rest pain includes diabetic neuropathy, nerve root compression, complex regional pain syndrome (previously known as reflex sympathetic dystrophy), and miscellaneous conditions such as various inflammatory conditions affecting the foot or digits and peripheral neuropathy caused by vitamin B12 deficiency or some chemotherapeutic agents.


Treatment planning for patients with femoropopliteal disease should consider the epidemiology and natural history of the disease, as well as the risks and benefits of the proposed therapy. The treatment of patients with IC and CLI will hence be considered separately owing to their disparate natural histories and risk/benefit ratio of therapy. The overall goals of therapy for both groups, however, remain the relief of symptoms, limb preservation, and reduction of cardiovascular morbidity and mortality. As such, risk factor modification should be an integral part of therapy in any patient with PAD.

Medical Management

As discussed earlier, many factors contribute to the development and progression of atherosclerosis (see Table 36-1). Attempts should be made to address all modifiable risk factors. Surprisingly, medical therapies have not been instituted or optimized in a large proportion of patients referred for lower extremity revascularization. This represents an opportunity and an obligation for the interventionalist to evaluate and institute appropriate therapies for various risk factors.

Along with efforts to modify a patient’s risk factors, a program of structured exercise is the recommended initial step in the treatment of IC. Patients with CLI, however, bypass this step and generally proceed directly to revascularization owing to their advanced occlusive disease and walking impairment. Supervised exercise conducted for 3 months or longer increases treadmill performance and lessens the severity of claudication,9 but there are three major limitations to exercise programs. First, unfortunately, exercise is contraindicated in 9% to 34% of PAD patients, such as those with severe coronary artery disease or neurologic and musculoskeletal impairment. Second, PAD patients are usually poorly compliant with exercise programs, which are furthermore not widely available. Finally, and even worse, these exercise programs are not reimbursed by most insurance companies even though they are proven to be cost-effective compared to surgical or endovascular vascular procedures.10,11 Structured exercise programs are therefore not widely prescribed.

Many pharmacologic agents have been studied for the relief of symptoms of IC. Only a few, however, have shown any evidence of clinical utility, and they do not provide the same level of symptom relief as a successful revascularization.12 The first U.S. Food and Drug Administration (FDA) agent approved for claudication was pentoxifylline, a methylxanthine derivative thought to increase red blood cell membrane deformability and decrease fibrinogen activity and platelet adhesion, with the overall effect of reduced blood viscosity. Multiple trials have failed to show other than mild clinical benefit, so this drug is probably beneficial only to those who cannot tolerate cilostazol,13 a better claudication drug. Cilostazol is a phosphodiesterase-III inhibitor with some antiplatelet and vasodilatation activity. As such it should not be prescribed to patients with congestive heart failure (CHF), owing to decreased survival compared to placebo in patients with class III-IV CHF. Cilostazol increases maximal and pain-free walking distances by half and two thirds, respectively, after 3 to 6 months of therapy,14 but its side effects of diarrhea, headaches, and dizziness present a compliance issue, with up to 60% of patients stopping the drug within 3 years.15

Use of antiplatelet agents, specifically aspirin, is an important topic and deserves more attention. Aspirin use has been associated with a 25% odds reduction in subsequent cardiovascular events in patients with cardiovascular disease.16 Although an initial meta-analysis by the Antithrombotic Trialists’ Collaboration concluded aspirin use in patients without any evidence of vascular disease does not statistically reduce cardiovascular events,17 more recent studies combining data from trials using not only aspirin but also other antiplatelet agents showed a significant reduction in ischemic events in patients with PAD. The American College of Cardiology and American Heart Association (ACC/AHA) recommend aspirin or clopidogrel daily for cardiovascular risk reduction in patients with PAD, and studies do indicate a relative risk reduction in all cardiovascular events for patients receiving such agents, especially clopidogrel.18 Other agents such as naftidrofuryl, propionyl-l-carnitine, and some lipid-lowering agents have also shown promise in improving walking distance in patients with IC.

Other critical elements of treatment include adequate pain control and treatment of infections if present. Care of ulcerations will require specialized treatment and should be done in conjunction with specialists in foot and wound care. Primary major amputation may become necessary if anatomic or comorbid medical conditions do not allow for a successful revascularization. Frequently, minor amputations are done after a revascularization procedure for limb salvage.

Surgical Revascularization Procedures

Bypass surgery has been the traditional treatment modality in the majority of patients in need of lower extremity revascularization, but the less invasive nature of endovascular approaches and better outcomes data are shifting this paradigm. The change was reflected in the 2007 TransAtlantic Inter-Society Consensus (TASC II) document that expanded recommendations for endovascular therapies.2 TASC II classification of diseases of the FPS is shown in Table 36-2. Although TASC class A and B lesions in symptomatic patients are best treated endovascularly, the recommended treatment for class D patients is surgical bypass in suitable candidates. Class C patients represent the “gray area” where endovascular techniques are applicable in selected patients not suitable or agreeable to surgical bypass. These recommendations are based on the consensus of a panel of experts after reviewing the current literature. For comparison purposes, the surgical gold standard for treating the diseased FPS is femoral-to–above knee popliteal venous bypass with 6-month, 1-, 2-, 3-, and 4-year primary patency rates of 87%, 81%, 77%, 71%, and 70%, respectively, with these numbers slightly decreasing when prosthetic material is used as the bypass conduit (85%, 77%, 66%, 59%, and 51% at the same time intervals).19

The remainder of this chapter describes current endovascular approaches to femoropopliteal occlusive disease. Table 36-3 lists patency rates, complications, and the lesion types and locations suitable for various techniques as described in the recent literature. These data are best compared and contrasted with the results from best medical therapy, surgical bypass, and balloon angioplasty (also included, where possible, in Table 36-3). Even the most modern endovascular devices marketed for the FPS (and there have been many) struggle to achieve results comparable to balloon angioplasty, and most remain woefully inferior to surgical bypass. We will briefly describe those devices falling short of expectations, then conclude with a discussion of the best currently available techniques to reliably open diseased femoropopliteal arteries—namely nitinol stents and stent-grafts.

TABLE 36-3

Comparison of Current Treatment Methods for Superficial Femoral Artery Occlusive Disease

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Dec 23, 2015 | Posted by in INTERVENTIONAL RADIOLOGY | Comments Off on Endovascular Management of Chronic Femoropopliteal Disease
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Treatment Initial Success (%) Primary Patency (%) Secondary Patency (%) Adjunct Use of Stents or Angioplasty (%) Restenosis on Ultrasound (%)
6 mo 1 yr Longer (time) 6 mo 1 yr Longer (time)
Venous above-knee femoropopliteal bypass   87 81 77 (3 yr)          
Prosthetic above-knee femoropopliteal bypass   85 77 66 (3 yr)          
Balloon angioplasty 95 63 58 55-68 (3 yr)          
Atherectomy (SilverHawk)     62 52 (18 mo) 80.3 75 (18 mo)   35  
Atherectomy (Pathway) 99 73           50 30 (6 mo) 40 (1 yr)
Laser (Spectranetics) 90.5   59 54   75   88 41 (6 mo) 46 (1 yr)
Cryoplasty 94 63 55   91 91