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Although atherosclerotic obstructive peripheral arterial disease (PAD) has a prevalence of only 3% in patients of age 40–59 years, this rises to 15% in the age group older than 65 years. This translates into approximately 9 million cases in the United States in 2005, and this number is expected to increase along with the aging demographics of our population.1,2 PAD is often unrecognized clinically and more than one-half of all patients are asymptomatic. Gender predisposition shows preponderance in males, although the incidence in females rises rapidly after menopause. Anatomically, superficial femoral artery disease predominates, with development of symptoms typically in the seventh decade. Interestingly, symptoms from aortoiliac disease usually present a decade earlier.
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Etiology and Pathogenesis
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Atherosclerotic risk factors are similar to those identified for coronary artery disease and include diabetes mellitus, hypertension, hyperlipidemia, smoking, family history of vascular disease, and obesity. Among these, diabetes mellitus and smoking are the most significant and are associated with a fourfold and doubling of relative risk, respectively. Patients with diabetes mellitus develop the disease at an earlier age than nondiabetics and have more severe and progressive disease. The anatomic distribution of obstruction differs from nondiabetics with less aortoiliac involvement and more extensive disease of the runoff vessels below the knees; however, superficial femoral artery disease is similar in both populations. Approximately 50% of patients have hyperlipidemia. PAD is also more commonly encountered in patients with hypertension.
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The pathologic findings in atherosclerosis occur in large- and medium-sized arteries, and are morphologically diverse, with focal accumulation of lipids and lipoproteins, mucopolysaccharides and collagen, smooth muscle cells and macrophages, and calcium deposits in variable quantities. Localized areas of intimal thickening secondary to smooth muscle cell proliferation and lipid-laden macrophages are seen in early stages with disruption of the internal elastic lamina. The media is often atrophic with thin strands of smooth muscle, lipid pools, collagen tissue, and calcium deposits. Enlarging plaques encroach on the lumen despite dilation of the artery, and the plaques may ulcerate. Hemorrhages occur in the arterial wall. Thrombi may form and occlude the narrowed arterial lumen.
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The etiology of atherosclerosis is complex and multifactorial, but progressive buildup of plaque narrows the vessel lumen, and complete occlusion may develop acutely secondary to thrombosis. Because disease progression ...