Arteriosclerosis in the african elephant Part 1. Intimal atherosclerosis and its possible causes

Abstract

The occurrence, nature and severity of atherosclerosis have been investigated in 463 elephants randomly culled from free-living populations in East Africa. Atherosclerotic lesions were of two types: intimal atherosclerosis and medial calcific sclerosis. This paper describes the first of these conditions. Atherosclerotic plaques were found throughout the aorta, and in the coronary, carotid, renal and iliac arteries. They were typically fibrous thickenings in which degenerative changes such as necrosis, hyalinisation, softening, lipid accumulation, lymphocytic infiltration and calcification were common. Evidence of mural thrombosis or plaque haemorrhage was not observed. 78% of mature plaques showed areas of histologically demonstrable lipid. Most of the cells in the plaques were typical fibroblasts. Modified smooth muscle cells were seen occasionally but were not common. The extent of atherosclerotic involvement in the aorta was dependent on age, and there was no significant difference in the severity of atherosclerosis between males and females. The severity of the disease in the coronary arteries was found to be considerably less than, and uncorrelated with, the severity of atherosclerosis in the aorta. The mean concentrations of serum free and esterified cholesterol, phospholipid and triglyceride were less than half their mean concentrations in human serum. No relationship was found between individual serum lipid levels and the severity of atherosclerosis. Neither was the amount of circulating low-density lipoprotein higher in those animals severely affected by atherosclerosis than in similar animals showing only mild lesions. The lipid content of the normal elephant aortic intima did not increase with age and neither did the cholesterol/phospholipid ratio. The lipid content of atherosclerotic plaques was higher than that of normal intima and the fatty acid composition of the cholesterol esters resembled that of plasma triglycerides. The intimal lipids did not appear to play an important part in stimulating the growth of atherosclerotic plaques. Rather, the lesions appeared to arise in response to repeated trauma of the arterial endothelium.