Aim: Current theories fail to explain the localisation of atheromatous lesions or their variable incidence in different arteries of the same subject. The objective of this study was to compare by scanning electron microscopy (SEM) the endothelial surface and the subjacent elastic lamina of human coronary arteries at the location of areas showing infiltration by lipid and cells, with the same components of internal thoracic arteries of the same subjects.
Methods: The endothelial surface and the subjacent elastic lamina of localised atheromatous areas of 146 anterior descending coronary arteries were compared with the same structural components of the internal thoracic arteries of the same subjects, using SEM, transverse paraffin sections and freeze-fracture.
Background: The localization of atheromatous lesions in vulnerable arteries and their relatively rare occurrence in other arteries of the same subject cannot be explained by current theories of the aetiology of atherosclerosis.
Objective: To determine whether abnormal diffusion of gamma globulin into the arterial wall from the lumen will identify defects of barrier function allowing localized entry of lipid and cells in atherosclerosis.
Methods: Paraffin sections of left anterior descending coronary arteries and corresponding internal thoracic arteries from 80 human subjects aged 1-65 years were stained for gamma globulin by the immunoperoxidase technique.
To obtain more detailed information about the relationship of intimal thickening to defects in the elastin structure of the arterial wall, the internal elastic lamina and subsequent elastin formation in the intima was studied by very oblique sectioning of paraffin sections of the arterial wall, and by scanning electron microscopy of formic acid digested preparations. Comparison was made in the same subject between the internal thoracic artery (a vessel showing only slight intimal thickening) and the anterior descending coronary (which usually develops advanced intimal thickening). There was no evidence of penetration of the normal fenestrations of the internal elastic lamina by medial smooth muscle cells.
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