Atherosclerotic plaque-like lesions are prevalent in synthetic arteriovenous shunts created to provide vascular access for hemodialysis. Similarities to atherosclerotic plaques in native arteries include eccentric location, immunoreactivity for smooth muscle actin, dystrophic calcifications, superimposed thrombi, and foam cells. Fatty streaks were not grossly identified on Sudan IV staining. Because of the similarities to atherosclerosis in native vessels, these findings may have several implications for atherogenesis. The development of raised, fibrous lesions does not require decades. The presence of smooth muscle in atherosclerotic plaque-like lesions does not require a source from tunica media. A precursor fatty streak may not be required for the development of raised, fibrous lesions. Finally, development of atherosclerotic plaque-like lesions does not require putative inflammatory effects from cholesterol or LDL accumulation, or even a native vessel that can respond to injury. The atherosclerotic plaque-like lesions in this study probably developed from organization of mural thrombi.

Fifty-seven sections of human vessels, collected in the Pathobiological Determinants of Atherosclerosis in Youth study from individuals aged 25-34, were stained with two monoclonal antibodies to oxidatively-modified lysine. Intensity and extent of immunoreactivity were graded by three pathologists. Aorta from a Watanabe heritable hyperlipidemic (WHHL) rabbit was stained as a positive control. Intimal immunoreactivity in the rabbit was predominantly localized to lesions. Although immunoreactivity in humans was somewhat more intense in atherosclerotic plaques, substantial staining was present in intima with diffuse intimal thickening and coronary veins. Localization of oxidatively-modified lysine in humans did not correlate with localization or severity of atherosclerosis. Localization of immunoreactivity for oxidatively-modified lysine to intimal lesions in the WHHL rabbit may be due to absence of diffuse intimal thickening, which prevents retention of epitopes throughout the intima.

Coronary heart disease is the most common cause of death in the US. Studies have demonstrated that smoking is a major risk factor for coronary heart disease and that a positive relationship occurs between smoking and aortic and coronary atherosclerosis in adults. In 1985, a multicenter cooperative study, Pathobiological Determinants of Atherosclerosis in Youth (PDAY), was organized to study atherosclerosis in trauma victims 15–34 years of age. Reports from this study have demonstrated that smoking is strongly associated with the prevalence and extent of grossly visible raised lesions in the abdominal aorta but only weakly associated with similar lesions in the right coronary artery. Coronary arteries from 50 smokers and 50 non-smokers were classified microscopically using a system developed by the American Heart Association in order to determine the stage at which smoking affects atherosclerosis. Smokers had over twice as many advanced lesions, types IV and V, as non-smokers (32 vs 14%) and fewer early lesions, types I, II, III, as non-smokers (38 vs 62%). The prevalence of advanced or types IV and V lesions (32%) was over twice that of intermediate or type III lesions (14%) in smokers. The opposite relationship was observed in non-smokers (14 vs 26%). This observation suggest that intermediate lesions progress rapidly into advanced lesions in smokers and that intima formerly having early lesions is replaced by intima with raised lesions.