Syphilitic Aortitis
Fig. 7.—Syphilitic aortitis of long standing. The aortic valves are curled and thickened, the heart is enlarged and the cavity of the left ventricle is dilated. (Milwaukee County Hospital.)
The seat of election of the syphilitic poison is in the aorta just above the aortic valves, Fig. 7, and in the ascending portion of the arch. There are semitranslucent, hyaline-like plaques which have a tendency to form into groups and, instead of undergoing an atheromatous change as in the ordinary nodular form of arteriosclerosis, they are prone to scar formation with puckering, so that macroscopically the nature of the process may, as a rule, be readily diagnosed. Microscopically the process is found to be a subacute inflammation of the media, which has been called a mesaortitis. There is marked small celled infiltration around some of the branches of the vasa vasorum and there appears to be actual absorption of the tissue elements of the middle coat. This is accompanied by hypertrophy of the intimal tissue. There follows degeneration in the deeper portions of this new tissue and new capillaries are formed which have their origin in the inflammatory area in the media. As is everywhere the case throughout the body, granulation tissue in the process of healing contracts and forms scars. This explains the scar formation in the aorta. When the process is more acute, instead of there being a reparative attempt on the part of the intima, there is actual stretching of the wall at the weakened spot and there results an aneurysmal dilatation. Spirochetæ pallidæ have been found in the degenerated media and in small gummata which were situated beneath the intima. Within the past years it has been found that a large percentage of patients with cardiovascular disease give the Wassermann reaction. In cases of aortic insufficiency, the reaction is present in almost every case. This is in marked contrast to the cases of diffuse endocarditis where the reaction is rarely present.
According to Adami the effects of syphilis upon the aorta are the following: (1) the primary disturbance is a granulomatous, inflammatory degeneration of the media; (2) this leads to a local giving way of the aorta; (3) if this be moderate it results in a strain hypertrophy of the intima and of the adventitia, with the development of a nodose intimal sclerosis; (4) if it be extreme, there results, on the contrary, an overstrain atrophy of the intima and aneurysm formation; (5) the intimal nodosities are here not of an inflammatory type and are nonvascular, although, with the progressive laying down of layer upon layer of connective tissue on the more intimal aspect of the intima, the earlier and deeper-placed layers of new tissue gain less and less nourishment, and so are liable to exhibit fatty degeneration and necrosis; (6) these products of necrosis exert a chemotactic influence upon the nearby vessels of the medial granulation tissue, with, as a result, (a) a secondary and late entrance of new vessels into the early and deeply-placed atheromatous area, (b) absorption of the necrotic products, (c) replacement by granulation tissue, (d) contraction of the granulation tissue, and (e) depression and scarring of the sclerotic nodules so characteristic of syphilitic sclerosis.
In the smaller arteries and arterioles the arteriosclerotic process appears on superficial examination to be a different process from that in the aorta and large arteries, but the difference is only apparent. It will be recalled that there is relatively much more muscle tissue in the arterioles than in the large arteries. The size, of course, is much less. Large nodular plaques are not possible. The atheromatous degeneration is not marked. In the smaller muscular arteries is seen the intimal proliferation, the stretching of the Moenckeberg type, and the calcification of the media rather than the intima. The media is thinned beneath the marked intimal proliferation so that the artery exhibits translucent areas when held to the light. Again, there is seen degeneration of the muscle and replacement by connective tissue with or without hypertrophy of the intima. In the arterioles three kinds of changes occur: a muscular hypertrophy; a fibrosis of all the coats; or a marked proliferation of the intimal endothelium. The last two are probably the same process, the connective tissue having its origin in the proliferated endothelial cells. Such a deposition of layer upon layer of cells in an arteriole and the resulting fibrosis leads to the condition of disappearance of the lumen of the vessel, endarteritis obliterans. This obliterating endarteritis is not, of course, due alone to syphilis. Syphilis is only a type of poison which produces such changes as have been described above. It is in the organs such as the kidney, liver, spleen, and intestines that one sees the most perfect examples of this obliterating endarteritis. Endarteritis deformans is a term applied to the condition of the arteries as a result of irregular thickenings and deposits of lime salts in the walls. These changes give rise to marked tortuosity of the vessels.
Occasionally such an obliterating process takes place in a larger artery. A thrombus forms and by a process of central softening, new channels permeate the thrombus, thus restoring to some extent the function of the vessel.
That the same process leads at one time to thinning and at another time to thickening of the arterial walls has been noted above. Prof. Adami holds that the regular development of layer upon layer of new connective tissue is non-inflammatory. He calls it a "strain hypertrophy." It is analogous to the localized hypertrophy of bone where the muscle tendons are attached, as is so frequently seen in athletes. The increased tension on connective tissue, provided that it is not overstrained, leads to its overgrowth, but only when there is sufficient nourishment. Such conditions are adequately fulfilled in the arteries. When a local giving way under pressure occurs in the media, the intima is put on the stretch (see Fig. 8), and there results a hypertrophy of the intima until the volume of the new tissue and the resistance which this affords to the mean distending force, balances the loss sustained by the weakened media. When the balance is struck, the hypertrophy is arrested. The youngest tissue is thus found directly beneath the endothelium. Now should this local weakening of the media have an acute origin, instead of a stimulus to growth there is overstrain, and there is, in consequence, not hypertrophy but atrophy. The beginning process is here a mesaortitis, but the acuteness of the poison, and the pressure from within the artery so stretches the artery that there is no compensatory hypertrophy, but a thinning, and the ground is prepared for aneurysmal dilatation or pouching.