Scheel has made very careful measurements of the ascending, the thoracic, and the abdominal aorta, and the pulmonary artery. He found that from birth to sixty years, the aorta became progressively wider and lost its elasticity. The pulmonary changed little, if at all, after thirty to forty years, and where before it was wider than the aorta, it now was found to be smaller. In chronic nephritis both were widened. The continuous increase of width and length of the aorta stands in reverse relationship to the elasticity of its walls.
Although the division of the lesions into nodular, diffuse, and senile has been the usual one, it is better to separate three groups into (1) nodular, (2) diffuse or senile, and (3) syphilitic. There is more known about the histology of the syphilitic form and the lesions which consist of puckerings and scars seen on opening an aorta just above the valves, and on the ascending portion of the arch are characteristic. A macroscopic examination suffices in most cases for a definite diagnosis.
In the nodular form the lesions are found on the aorta and large branches particularly at or near the orifices of branching vessels. These nodules may increase in size, forming rather large, slightly raised plaques of yellowish-white color. They are, as a rule, irregularly scattered throughout the aorta and branches and tend to be more numerous and larger in the abdominal aorta. The initial lesion is in the media, consisting of an actual dissolution of this coat with rupture of the elastic fibers and infiltration with small round cells. There is thus a weak spot in the artery. Hypertrophy of the intimal cells takes place, layer upon layer being added in an attempt to strengthen the vessel at the injured place. Coincidently with this, there is thickening by a connective tissue growth in the adventitia. The process begins, at least in syphilis, around the terminals of the vasa vasorum. It will be recalled that the blood supply of the inner portion of the media comes from within the vessel itself. As the intimal growth increases, the blood supply is cut off. The inevitable result is softening of the portion farthest from the lumen of the vessel. As a rule there has been a sufficient growth of connective tissue in the media and adventitia to repair the damage done to the media. This softening and dissolution gives rise to a granular debris composed of degenerated cells and fat. This is the so-called atheromatous abscess. There are no leucocytes as in ordinary pus. These "abscesses" are frequent and in rupturing leave open ulcers with smooth bases, the atheromatous ulcer. A further change which often takes place is calcification of the bases of the ulcers and calcification of the softened spots before rupture takes place. This only occurs in advanced cases. (See Fig. 3.)
Fig. 3.—Arteriosclerosis of the thoracic and abdominal aorta, showing irregular nodules, atheromatous plaques, denudation of the intima, thin plates of bone scattered throughout with spicules extending into the lumen of the vessel. Note the contraction of the openings of the large branches, the rough appearance of the aorta and the greater degree of sclerosis of the upper two-thirds, i. e., of the aorta above the diaphragm. This aorta in the recent state was much thickened and almost inelastic.
Fig. 4.—Arteriosclerosis of the arch of the aorta. Numerous calcified plaques, thickening and curling of the aortic valves, giving rise to insufficiency of the aortic valves. The aortic ring is rigid and not much dilated. (Milwaukee County Hospital.)