The authors surveyed arterial diseases in 405 mammals and birds representing 162 species from the Oklahoma City Zoo. Typical atherosclerotic plaques were common in the birds, being found in the aortas of 24% of 72 individuals. The prevalence of aortic atherosclerosis in birds could not be correlated with the type of diet consumed in captivity or in nature. Fish eating birds had as much atherosclerosis as meat eating, grain eating, and insect eating birds. Predominant epicardial coronary and intracranial cerebral artery atherosclerosis was found in 2 chimpanzees. These lesions were analogous to those which occur in young Western males dying with myocardial infarction. The spontaneous lesions in the chimpanzees were not associated with a high fat diet but were possibly associated with neurotic behavior. Fatty streaks and fibrous plaques were quite common in many species of mammals and birds. In seals and sea lions, aortic fibrous plaques were plentiful. These fibrous plaques contained no stainable lipid, indicating that some mechanism other than lipid insudation was responsible for the proliferation of intimal smooth muscle cells. The hoofed mammals were another group in which lipids appeared to play little part in the pathogenesis of elevated fibrous plaques. Fatty streaks were common in young hoofed mammals, but were localized to the thoracic aortas. Fibrous plaques were common on older hoofed mammals, but were localized to the abdominal aortas. The cumulative evidence seems to show that factors other than lipid insudation may be important in the production of elevated fibrous plaques. An important question in human atherosclerosis involves the pathogenesis of central plaque necrosis. In the atherosclerotic plaques of giant anteaters and aardvarks, central plaque necrosis appeared to precede lipid accumulation. Moreover, frequent areas of focal plaque necrosis, apparently involving smooth muscle cells, were found within fibrous plaques in a number of species. These areas of focal necrosis were also present within fibrous plaques of some of the pigs receiving chronic electric shock. Virtually no mural thrombi were seen, even though the aortas of several of the birds had 60 to 80% of their surfaces covered by lipid containing lesions. This remarkable lack of mural thrombi probably explains why ischemic complications are seldom seen in animals, despite occasional examples of extensive atherosclerosis, and conversely, why ischemic complications are so common in man, sometimes in the presence of only moderate atherosclerosis.
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