[Human aorta: endothelium and atheroma (author's transl)]

An electron microscopic study of aortic endothelium obtained from necropsy and biopsy material shows pathological changes corresponding the severity of the atheromatous state, but unrelated to age. All stage I aortas show the same type of endothelial changes. So do stage II aortas. The pathological structural changes in the endothelial cells corresponding to aortas of stage I, II-III involve the microfilaments, vesicles, intercellular junctions and basement membrane. The microfilaments are more numerous and better defined in atheromatous aortas. Also rare bundles of microfilaments with electron-dense centers are seen. The intra-cytoplasmic vesicles increase presently deeper invaginations (pseudo-channels) in the stages II and III aortas. In these stages the intercellular junctions are open involving all or part of the junctions. All three described ultra-structural changes increase the permeability of the endothelium to lipids and plasma glycoproteins. The thickening of the sub-endothelial basement membrane résults from the increase of type IV collagen synthesized by the endothelial cells. Lysis of endothelial cells and platelet agregation are related to the stage of atheromatosis. The number of Weibel Palade bodies increase in stade II and III aortas. These organelles play a role in blood coagulation and accelerate atheromatosis. In conclusion, the aortic endothelium constitutes an active barrier. The pathological atheromatosis process involves the endothelium. The endothelial cells play a normal role in the passage of molecules from blood plasma into the aortic wall. That explains intimal formation and intimal fibrosis. The endothelium also participates in the initial pathogenic mechanism of atheroma formation (fatty dot and streak, gray gelatinous elevation and mural thrombus).