Atherosclerosis occurs spontaneously in swine and is easily induced by proatherogenic diets. It occurs in distributions similar to that observed in humans, and the common circulatory mechanisms and large caliber of porcine arteries facilitates their analysis. The pathogenesis and histology of lesions in swine closely parallels that observed in humans: focal intimal thickening, fatty streaks, inflammatory cell infiltration, lipid deposits, and fibrous plaque formation are all observed in lesions in pigs (see Figure 72.1).

In spite of these features, swine have been used only infrequently for pharmacologic studies of atherosclerosis. Pigs are extremely expensive and require special handling, and their dietary requirements can be formidable. Because pigs grow quickly, changes in weight can make pharma-cologic dosing studies nontrivial. Miniature swine, such as the Yucatan, have been developed to circumvent some of these issues, but microswine remain expensive to purchase and maintain. The recent development of a pig model with features of metabolic syndrome (Nichols et al., 1992) may reinvigorate the use of this model to study cardiovascular disease, given the increasing appreciation of a tight link between this syndrome and atherosclerosis in humans.

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