Progressive atherosclerosis is the most common underlying etiology of lower-extremity arterial occlusive disease. Although the exact mechanisms responsible for the atherosclerotic changes remain to be fully elucidated, it is clear that cholesterol plays a central role in plaque accumulation and disease progression. Elevated serum cholesterol levels initiate a process of endothelial cell activation. The cholesterol particles, retained in the vessel wall at areas of hemodynamic stress, are modified by the endothelial cells and become oxidized/activated. These modified lipids then cause the endothelial cells themselves to be activated, thereby initiating the adhesion of platelets and macrophages to these areas of “injury.” The adherent platelets and macrophages further activate the endothelial cells in the area, while the macrophages enter the vessel wall and actively scavenge the activated cholesterol particles. These cells, commonly referred to as “foam cells,” contain highly active lipid particles with oxidative potential. These activated cells within the vessel wall lead to further activation of the endothelium and adhesion of additional platelets and other inflammatory cells. The inflammatory process soon becomes self-sustaining with the adhesion/ activation of a range of inflammatory cells. These cells lead to tissue destruction and release of active oxygen and nitrogen species that cause breakdown of the intercellular matrix of the vessel wall. Destruction of the architecture of the normal vessel wall leads to vessel remodeling with luminal loss and instability. The affected vessels can have a significant reduction of the lumen from the deposition of more lipid within the wall or from hemorrhage within injured vessel walls (i.e., intraplaque hemorrhage). Additionally, these areas can rupture, leading to distal embolization and the exposure of the extremely thrombogenic material and further activation of the process. While cholesterol alone was initially thought to be the etiology of atherosclerosis, it has become increasingly clear that the inflammation within the vessel wall plays a major role in plaque formation.

Patients with lower-extremity arterial occlusive disease often present with symptoms related to a hemodynamically significant stenosis within the superficial femoral artery. The vessel is affected most often where it emerges from the adductor foramen or the region referred to as Hunter’s canal. The
mechanisms responsible for the development of atherosclerosis in this specific location remain unclear but may be related to the surrounding tendinous structures. Additionally, occlusive lesions both in the lower extremity and throughout the body frequently develop at the site of arterial bifurcations (e.g., common carotid bifurcation, common femoral artery bifurcation), presumably due to changes in shear stress within the vessel wall.

The risk factors for lower-extremity atherosclerosis are the same as those for the other vascular beds. These include family history, hypertension, hyperlipidemia, diabetes mellitus, smoking, and obesity. Controlling the modifiable risk factors can alter the progression of the disease but does not completely eliminate the associated risk. Before treating hemodynamically significant lesions, the physician must address the patient’s risk factors in an attempt to reduce the risk of disease progression and recurrence.

Patients with lower-extremity arterial occlusive disease will present with a spectrum of symptoms ranging from mild claudication to extensive tissue loss so severe that it may preclude limb salvage. Patients with claudication will typically describe activity-induced muscle pain, cramping, or fatigue. Depending upon the location of the stenosis, these symptoms can occur in the buttock, hip, calf, or foot. For those with disease below the inguinal ligament, the symptoms usually occur in the calf or foot. The extent of exercise necessary to induce these symptoms varies and depends upon the speed at which the individual is walking, the angle of ascent, and the patient’s general cardiovascular health. In some patients with severe claudication, the symptoms may develop at <100 feet. These patients are often unable to do any activity outside their own home without the onset of lower-extremity pain. The symptoms may be masked by the presence of a peripheral neuropathy in diabetics. The neuropathy makes it difficult for the patients to distinguish the usual symptoms of claudication, and the vascular insufficiency may contribute to further progression of the neuropathic changes. In addition, diabetics have impaired wound healing and are predisposed to developing soft tissue infections in the foot; both concerns merit an aggressive approach to revascularization.

Patients with more advanced disease may present with nonhealing ulceration or progressive tissue loss. These patients truly have limb-threatening ischemia and often require amputation without revascularization. In addition, a subset of these patients will present with nonhealing wounds after minor surgical procedures on their feet (e.g., ingrown toenail excision). These patients also require revascularization in order to avoid further tissue loss and amputation.

The indications for treatment have remained fairly stable and are dictated by the ischemic symptoms at presentation. Patients with limb-threatening ischemia have a significant risk of amputation without treatment and merit revascularization unless contraindicated. The indications for patients with claudication are less clear, but revascularization appears justified in patients with shortdistance claudication (<100 ft) or those with lifestyle/economically limiting symptoms.

The healthcare provider must weigh the relative risks and benefits of intervention for each patient with vascular disease similar to the decision algorithm for all medical treatments. As the risk of the procedure decreases, assuming similar benefits, the operative indications may change, because the risk:benefit ratio has been altered. Indeed, this appears to be the situation for the endovascular procedures in patients with limb-threatening ischemia and claudication. In the hands of an experienced endovascular surgeon, the risk and disability from percutaneous revascularization has significantly decreased, thereby justifying a more aggressive approach. This is particularly relevant for patients with poor overall health in whom the potential complications associated with open revascularization would be prohibitive.

The potential to decrease peri-operative morbidity, even in healthier patients, has encouraged the authors to explore all endovascular options. In our current approach, the diagnostic arteriograms are reviewed to determine whether percutaneous revascularization is an option, and revascularization is attempted at the same setting if feasible. Important factors in the decision-making process include the extent of the occlusive disease and the status of the outflow vessels. In cases where only one arterial segment (i.e., femoral, popliteal, tibial) is involved and the outflow is nondiseased, percutaneous therapy is a reasonable initial option. Predictably, the likelihood of success diminishes with the number of involved segments and is quite small when all three segments are involved. It is important to recognize that the complication rate associated with endovascular revascularization varies with the anatomic segment. For example, the risk of perforation and dissection is significantly higher in the popliteal segment when compared to that of the common femoral and superficial femoral arteries. These factors should be taken into consideration especially when planning revascularization in multiple segments.

It is important to stress that the revascularization plan should be tailored to the clinical scenario at hand, and the endovascular surgeon should be able to use different treatment modalities. With the advent of newer endovascular tools (e.g., atherectomy devices, cryoplasty balloon), the indications and potential application of endoluminal therapies will likely further expand. The following sections provide a straightforward approach to interventions in the infrainguinal arterial tree. The specific plan must take into account the clinical situation as well as the endovascular surgeon’s experience and level of comfort with the proposed procedure.

There are a number of basic techniques for percutaneous revascularization of the lower extremity. The most commonly used modalities include PTA, subintimal angioplasty, intravascular stenting, and atherectomy. In most situations, one of these modalities or a combination thereof can be used to achieve a successful result. These techniques will be addressed individually with the understanding that they may be used simultaneously as necessary to achieve the desired result. Indeed, it is important to be facile with these different techniques, because they may be required as a remedial or “bailout” procedure if the initial angioplasty is unsuccessful or complications arise.