Aortoiliac Occlusive Disease

Updated: Aug 21, 2017
  • Author: Khanjan H Nagarsheth, MD, MBA; Chief Editor: Vincent Lopez Rowe, MD  more...
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Overview

Background

In patients with peripheral arterial disease (PAD), obstructing plaques caused by atherosclerotic occlusive disease commonly occur in the infrarenal aorta and iliac arteries. Atherosclerotic plaques may induce symptoms either by obstructing blood flow or by breaking apart and embolizing atherosclerotic and/or thrombotic debris to more distal blood vessels. If the plaques are large enough to impinge on the arterial lumen, reduction of blood flow to the extremities occurs.

Several risk factors exist for development of the arterial lesions, and recognition of these factors enables physicians to prescribe nonoperative treatment that may alleviate symptoms as well as prolong life.

Aortoiliac occlusive disease (AIOD) occurs commonly in patients with PAD. Significant lesions in the aortoiliac arterial segment are exposed easily by palpation of the femoral pulses. Any diminution of the palpable femoral pulse indicates that a more proximal obstruction exists.

Obstructive lesions may be present in the infrarenal aorta, common iliac artery, internal iliac (hypogastric) artery, external iliac artery, or combinations of any or all of these vessels. Occasionally, degenerated nonstenotic atheromatous disease exists in these vessels and may manifest by atheroembolism to the foot, the "blue toe" or "trash foot" syndrome. Generally, patients with aortoiliac PAD have a poorer general prognosis than those with more distal PAD. [1]

Before prosthetic grafts for aortic bypasses became available, the first direct surgical reconstructions on the aorta were performed using the technique of thromboendarterectomy (TEA), first described by Dos Santos of Lisbon in 1947. [2] The initial procedure was performed on a patient with superficial femoral artery (SFA) obstruction, and Dos Santos termed the procedure disobliteration. Wylie adapted this technique to the aortoiliac region and, in 1951, performed the first aortoiliac endarterectomy in the United States. [3]

With the discovery of suitable prosthetic graft materials for aortic replacement in the 1960s, surgical treatment of AIOD became available to even more patients.

In 1964, Dotter first performed percutaneous iliac angioplasty using a coaxial system of metal dilators. [4] This procedure proved to have limited application, because of the cumbersome nature of the device. However, Dotter's early work paved the way for Grüntzig, who, in 1974, developed a catheter with an inflatable polyvinyl chloride balloon that could be passed over a guide wire. [5] This device became the cornerstone for the percutaneous treatment of arterial occlusive lesions today.

In 1985, Palmaz introduced the first stent that helped to improve the results of angioplasty for arterial occlusive disease. [6] Since the advent of angioplasty and stenting, the technology has evolved at an astronomic rate. The design and quality of endovascular devices, as well as the ease and accuracy of performing the procedures, have improved. These improvements have led to improved patient outcomes following endovascular interventions for AIOD.

Surgical treatment of AIOD has been well standardized for many years, and the outcomes are quite good. However, the additional techniques of percutaneous transluminal angioplasty (PTA) and stenting have provided more alternatives to open surgery and make successful approaches available to patients who may have been considered at an unacceptably high risk for conventional open surgical repairs.

Catheter-based endovascular treatments for AIOD offer the advantages of less morbidity, faster recovery, and shorter hospital stays. In fact, most endovascular interventions today are simply performed as outpatient procedures.

This article reviews the risk factors for development of atherosclerotic occlusive disease of the aorta and iliac arteries and describes the natural history, diagnosis, and treatment of the disease.

For patient education resources, see the Cholesterol Center, as well as High Cholesterol and Cholesterol FAQs.

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Pathophysiology

Atherosclerosis is an extraordinarily complex degenerative disease with no known single cause. However, many variables are known to contribute to the development of atherosclerotic lesions. One popular theory emphasizes that atherosclerosis occurs as a response to arterial injury. Factors that are known to be injurious to the arterial wall include the following:

  • Mechanical factors, such as hypertension and low wall shear stress
  • Chemical factors, such as nicotine, hyperlipidemia, hyperglycemia, and homocysteine

Lipid accumulation begins in the smooth-muscle cells and macrophages that occur as an inflammatory response to endothelial injury, and the "fatty streak" begins to form in the arterial wall. The atheroma consists of differing compositions of cholesterol, cholesterol esters, and triglycerides. Some plaques are unstable, and fissures occur on the surface of the plaque that expose the circulating platelets to the inner elements of the atheroma.

Platelet aggregation then is stimulated. Platelets bind to fibrin through activation of the glycoprotein (GP) IIb/IIIa receptor on the platelets, and a fresh blood clot forms in the area of plaque breakdown. These unstable plaques are prone to atheromatous embolization and/or propagation of clot that eventually can occlude the arterial lumen.

If the atheroma enlarges enough to occupy at least 50% of the arterial lumen, the flow velocity of blood through that stenosis can significantly increase. The oxygen requirements of the lower extremity at rest are low enough that even with a moderate proximal stenosis, no increase in blood flow velocity occurs. During exercise, however, the oxygen debt that occurs in ischemic muscle cannot be relieved, because of the proximal obstruction of blood flow; this results in claudication symptoms.

In more advanced cases, critical tissue ischemia occurs, and neuropathic rest pain or tissue loss ensues. However, critical limb ischemia (CLI) is seldom, if ever, caused by AIOD alone. Commonly, in patients with CLI, multiple arterial segments are involved in the occlusive atherosclerotic process.

Three distinct arterial segments distal to the visceral bearing portion of the abdominal aorta may become diseased by atherosclerosis, as follows:

  • Type I atherosclerosis involves the infrarenal aorta and the common iliac arteries only; the vessels distal to the common iliac arteries usually are normal or only minimally diseased; this pattern of atherosclerosis is present in about 5-10% of patients with PAD and occurs more commonly in women
  • Type II atherosclerosis involves the infrarenal aorta and the common and external iliac arteries and may extend into the common femoral arteries; this pattern is observed in 35% of patients with PAD
  • Type III atherosclerosis is the most severe form and, unfortunately, also the most common; this pattern of atherosclerosis involves the infrarenal aorta and the iliac, femoral, popliteal, and tibial arteries

Diabetes mellitus is a risk factor that results in a characteristic pattern of atherosclerotic lesions in patients with PAD. The proximal inflow vessels (aorta, iliac arteries) tend be normal. However, the femoropopliteal segment (including the deep femoral artery), and especially the proximal tibial arteries, are usually severely diseased. Fortunately, the distal tibial and plantar vessels may be normal, enabling successful arterial reconstruction for limb-threatening ischemia.

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Etiology

Atherosclerosis is the most common cause of occlusive plaques in the aorta and iliac arteries. Several risk factors exist for the development of atherosclerotic plaques in the aortoiliac arterial segment. Cigarette smoking and hypercholesterolemia are observed more commonly in patients with AIOD than in those with infrainguinal occlusive disease. In addition, patients with AIOD tend to be younger and less likely to have diabetes.

An uncommon cause of aortic obstruction is Takayasu disease, a nonspecific arteritis that may cause obstruction of the abdominal aorta and its branches. The etiology of Takayasu disease is not known. For the purposes of this article, only occlusive lesions caused by atherosclerosis are considered.

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Epidemiology

At least 50% of patients with PAD have no symptoms, and therefore, the exact incidence and prevalence of the condition is unknown. However, the incidence of PAD is known to increase with advancing age, so that by age 70 years, as much as 25% of the US population is affected. Occlusive disease involving the aortoiliac arterial segment occurs commonly in patients with PAD and is second only to occlusive disease of the SFA in frequency.

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Prognosis

Outcomes after aortic operations for AIOD are measured in terms of operative mortality and patency of the arterial reconstruction over time. These outcomes are similar for aortoiliac TEA and aortofemoral bypass (AFB). The 30-day operative mortality is 2-3%. Long-term patency is excellent too: 85-90% at 5 years after AFB or TEA. If patients continue to smoke, however, these excellent patency rates are reduced by half.

Outcomes for extra-anatomic (axillofemoral or femorofemoral) bypasses are clearly not as good as those for either AFB or aortoiliac TEA. Operative mortality might be expected to be better for extra-anatomic bypass than for AFB because of the extracavitary nature of these procedures and the absence of the requirement for aortic occlusion during the operation. However, the operative mortality (0-4% for femorofemoral bypass; 2-11% for axillobifemoral bypass) reflects the selected patients in whom these procedures are performed. The 5-year primary patency rate with extra-anatomic bypass for AIOD is 19-50% for axillobifemoral bypass and 44-85% for femorofemoral bypass.

In a study of 92 patients with AIOD who underwent AFB (n=72), aortioiliac bypass (n=15), or both (n=5), Lee et al reported overall primary patency rates of 86.2% at 5 years and 77.6% at 10 years, [7] as well as a 10-year limb salvage rate of 97.7% and an overall survival rate of 91.7%.

Endovascular techniques (ie, PTA and stent placement) offer alternatives to conventional surgical repair. Therefore, understanding the outcomes offered with such interventions is important.

Although isolated stenosis of the infrarenal aorta or common iliac artery is uncommon, this lesion is suited ideally to PTA, stent placement, or both. For localized segmental occlusive disease in the aorta, PTA can achieve initial technical success rates of 95%, with 5-year patency rates of 80-87%. For iliac lesions, PTA yields initial success rates of 93-97%, with 5-year patency rates of 54-85%. These results seem to be improved when arterial stents are used either primarily or as an adjunct to PTA for the treatment of iliac artery stenosis.

One study investigating the effects of heavy calcification in stent-implanted iliac arteries showed that iliac stents in heavily calcified lesions presented significant residual stenosis; however, even in cases with incomplete expansion of the stent, further blockage was not found, and all stents remained anatomically patent. [8]

In a systematic review and meta-analysis designed to examine the clinical outcomes of endovascular and open bypass treatment for AIOD, Indes et al found that endovascular treatment was associated with shorter hospital stays, lower complication rates, and reduced 30-day mortality, whereas open bypass was associated with higher primary and secondary patency rates at 1, 3, and 5 years. [9]

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