Abstract
This study examines the hypothesis that progressive intimal thickening and atherosclerosis in the larger pulsatile arteries arise from failure to maintain, subjacent to the endothelial cells, a substantial elastin membrane, a component which has been shown to be of special structural significance. The internal thoracic arteries of 293 subjects of all ages up to 60 years were compared histologically with the anterior descending coronary arteries of the same individuals by light- and electronmicroscopy and immunoperoxidase staining for macromolecules. The internal thoracic arteries usually developed a new robust reduplicated internal elastic lamina at an early age, no further intimal thickening, and no significant entry of lipid or cells to the intima. The coronary arteries showed areas of rapid intimal thickening with poor and incomplete reduplicated internal elastic laminae, entry of lipid, macrophages, and other cells to the intima. The reduplicated internal elastic laminae appeared to be formed primarily by the endothelial cells themselves. An elastin membrane subjacent to the endothelial cells appears to be essential. It provides a secure attachment for the cells and a barrier to the entry of macromolecules and cells to the intima. Its absence is associated with progressive intimal thickening and atherosclerosis.
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