Fig. 8.—I, media weakened at M' with overgrowth of intima filling in the depression. II, with postmortem rigor and contraction of the muscles of the media and removal of the blood pressure from within, the stretched media at M'' contracts; the intimal thickening thus projects into the arterial lumen. (After Adami.)
Again, one not infrequently encounters intimal nodosities when the underlying media appears of normal thickness. The explanation of this apparent exception is that the media in the living aorta is actually thinned, but the layers of subintimal tissue deposited over the weak spot due to strain hypertrophy become bulged inward when the pressure is relieved, as at postmortem. The media has not lost all of its elasticity (see Fig. 9), hence it contracts and there is the appearance of a nodule on the intima beneath which is a media equal in thickness to that of the healthy surrounding media.
Fig. 9.—Schematic representation of the increased strain brought to bear upon the cells of the intima, Int., when the media, Med., undergoes a localized expansion through relative weakness. (After Adami.)
The essential lesion in arteriosclerosis of the aorta and large arteries is a degeneration in the middle coat. This may be brought about by a variety of poisons circulating in the body. In syphilis, for example, the initial lesion has been shown to be a mesaortitis. The media seems to be dissolved, the artery is consequently thinned, there is actual depression along the level of the vessel. The elastic fibers disappear and small-celled infiltration takes its place. The intima hypertrophies, layer upon layer being added in an attempt to restore the strength of the vessel. There is also, as a rule, rather pronounced hypertrophy of the adventitia.