Aortoiliac Occlusive Disease 

In patients with peripheral arterial disease, 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.

Surgical treatment of aortoiliac occlusive disease (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 offered more alternatives to open surgery and offer successful techniques to patients who may have been considered at an unacceptably high risk for conventional open surgical repairs. Catheter-based endovascular treatments for aortoiliac occlusive disease (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 chapter 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.

An image depicting atherosclerosis can be seen below.

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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.^[1] The initial procedure was performed on a patient with superficial femoral artery (SFA) obstruction, and Dos Santos termed the procedure disobliteration. Edwin J. Wylie, MD, adapted this technique to the aortoiliac region and, in 1951, performed the first aortoiliac endarterectomy in the United States.^[2] With the discovery of suitable prosthetic graft materials for aortic replacement in the 1960s, surgical treatment of aortoiliac occlusive disease (AIOD) became available to even more patients.

In 1964, Dotter first performed percutaneous iliac angioplasty using a coaxial system of metal dilators.^[3] This procedure proved to have limited application due to 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 guidewire.^[4] This device became the cornerstone for the percutaneous treatment of arterial occlusive lesions today. In 1985, Julio Palmaz introduced the first stent that helped to improve the results of angioplasty for arterial occlusive disease.^[5] Since the advent of angioplasty and stenting, the technology has evolved at an astronomical 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 aortoiliac occlusive disease (AIOD).

Aortoiliac occlusive disease (AIOD) occurs commonly in patients with peripheral arterial disease (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, internal iliac (hypogastric), external iliac, 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.

Aboyans et al found that patients with aortoiliac peripheral arterial disease (PAD) have a poorer general prognosis than those with more distal PAD. Their review of 400 patients with PAD showed that after adjustment for age, sex, cardiovascular disease history and risk factors, critical leg ischemia status, and treatments, proximal PAD was significantly associated with a worse prognosis (hazard ratio [HR] for death, nonfatal myocardial infarction or stroke, and coronary or carotid revascularization: 3.28; HR for death ratio: 3.18, p < 0.002 vs. distal PAD).^[6]

Frequency

At least half of patients with peripheral arterial disease (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 many as 25% of the US population is affected. Occlusive disease involving the aortoiliac arterial segment occurs commonly in patients with peripheral arterial disease (PAD) and is second only to occlusive disease of the SFA in frequency.

Atherosclerosis is the most common etiology 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 aortoiliac occlusive disease (AIOD) as compared with infrainguinal occlusive disease. In addition, patients with aortoiliac occlusive disease (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 purpose of this chapter, only occlusive lesions caused by atherosclerosis are considered.

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 mechanical factors such as hypertension and low wall shear stress, as well as 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 is seldom, if ever, caused by aortoiliac occlusive disease (AIOD) alone. Commonly, in patients with critical limb ischemia, multiple arterial segments are involved in the occlusive atherosclerotic process.

The most common symptom of patients with hemodynamically significant aortoiliac disease is claudication. The word claudication stems from the Latin word claudicatio, to limp. The symptom complex of claudication is defined as muscle cramps in the leg(s) that occur following exercise and are relieved by resting. In any individual patient, the exercise distance at which claudication occurs is quite constant. Claudication usually occurs first in the calf muscles, although thigh, hip, and buttocks muscles also can be affected when more extensive proximal lesions are present. Location of the muscle pain (ie, calf vs thigh) does not necessarily correlate with the level of arterial obstruction. However, more proximal symptoms (ie, buttocks or thigh claudication) are generally associated with severe aortoiliac occlusive disease.

Symptoms of buttock claudication can occur in association with erectile dysfunction in patients with absent femoral pulses. This constellation of symptoms is termed Leriche syndrome, named for the surgeon who described the condition in 1923. Leriche syndrome occurs when either preocclusive stenosis or complete occlusion of the infrarenal aorta is present due to severe aortic atherosclerosis. Due to the chronic nature of the occlusive process leading to development of rich collateral vessels that supply the lower extremity, limb-threatening ischemia seldom occurs.

Treatment of patients with peripheral arterial disease (PAD) has 2 goals. The first and foremost goal is to reduce the risk of vascular events (myocardial infarction, stroke, vascular death) that occur at an alarmingly high rate in patients with PAD. About 30% of patients with peripheral arterial disease (PAD) die within 5 years, and death is usually due to an ischemic coronary event.

The second goal of treatment is to improve symptoms in those patients with claudication and prevent amputation in patients with critical limb ischemia. Critical limb ischemia is present when patients have symptoms of ischemic rest pain, nonhealing foot ulcers, or gangrene, and its presence mandates urgent evaluation with aortography and endovascular and/or surgical revascularization to prevent limb loss.

At least half of patients with peripheral arterial disease (PAD) are asymptomatic and are diagnosed only by physical examination and/or measurement of the ankle/brachial index (ABI). An ABI less than 0.9 clearly is abnormal and confirms the diagnosis of peripheral arterial disease (PAD). An abnormal ABI should alert the clinician to the fact that this group of patients is at risk for early mortality from cardiovascular causes, ie, myocardial infarction, stroke, other vascular death. The goal for treatment of asymptomatic patients is to reduce the risk of subsequent vascular events.

Three distinct arterial segments distal to the visceral bearing portion of the abdominal aorta may become diseased by atherosclerosis. Type I atherosclerosis involves the infrarenal aorta and common iliac arteries only. This pattern of atherosclerosis is present in about 5-10% of patients with peripheral arterial disease (PAD) and occurs more commonly in women. The vessels distal to the common iliac arteries usually are generally normal or only minimally diseased. Type II atherosclerosis involves the infrarenal aorta, common and external iliac arteries, and may extend into the common femoral arteries. This pattern is observed in 35% of patients with peripheral arterial disease (PAD). Type III atherosclerosis is the most severe form and, unfortunately, also the most common. This pattern of atherosclerosis involves the infrarenal aorta, iliac, femoral, popliteal, and tibial arteries.

Diabetes mellitus is a risk factor that results in a characteristic pattern of atherosclerotic lesions in patients with peripheral arterial disease (PAD). The proximal inflow (aorta, iliac) arteries tend be normal. However, the femoropopliteal segment (including the profunda femoris 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.

At least 50% of patients with peripheral arterial disease (PAD) may be asymptomatic. Because natural history data are poor for iliac stenosis, surgical and/or endovascular intervention should not be considered if patients truly are asymptomatic. Surgical intervention for limb-threatening ischemia is accepted universally, unless the limb is deemed nonviable. Determining whether or not to intervene in a patient with mild claudication may not be as straightforward.

An important role exists for conservative therapy in patients with aortoiliac occlusive disease (AIOD). Although surgical therapy usually alleviates symptoms, the patient must be apprised of the operative risk of mortality (2-3%) as well as anticipated outcomes over time. Since the advent of catheter-based treatments for aortoiliac occlusive disease (AIOD), asymptomatic patients are often treated prophylactically with either angioplasty or stenting of iliac arterial lesions that are discovered during coronary angiography. This practice of drive-by angioplasty should not be recommended.