This is a disease most commonly seen in the arch of the aorta, or at a little distance posterior to that point.

The early stages of the disease are marked by the appearance of small greyish-white spots and patches which are noticed scattered over the interior of the vessel, slightly raised above the surface, and somewhat irregular in size and in form.

The inner surface of the aorta is perfectly smooth, but somewhat irregular over the seat of the patches. The endothelium lining the vessel remains for the present quite intact, but the inflammatory new growth situated beneath it raises the endothelium in the direction of the interior of the vessel.

In the second stage the cell proliferation, or growth, to which the patches are due, undergoes a process of fatty change or degeneration, and becomes soft, yellow, and cheese-like, or assumes what is known as an atheromatous condition (Atheroma Endarteritis Deformans 30073 = meal).

The degenerative process may extend to the cells lining the vessel, when they break down, and expose the underlying pasty matter.

Should this occur, the blood in its course backwards washes up the degenerated inflammatory product and carries it away, leaving the middle and external coat exposed.

In the third stage of the disease the pasty mass, instead of being thus removed, becomes more or less calcified, in which case small bone-like spicules are seen ramifying through the structure of the vessel wall, in some instances completely surrounding it and giving it the appearance of a bony tube (see Aneurism, fig. 196).

The effect of this disease on the wall of the vessel is seriously to spoil its elastic reaction, and so interfere with the circulation.

When the inflammatory products have undergone the softening process, and become exposed to the blood current, the vessel yields to the pressure from within, causing it to dilate still further, and in consequence an aneurism is formed, or the blood may insinuate itself between the coats of the vessel and cause them to separate, when a dissecting aneurism is the result.

When the vessel becomes thin, as is sometimes the case in this form of the disease, its walls may rupture, and death take place more or less suddenly, or the fibrine of the blood coagulated on the diseased surface may fill up the vessel and form a thrombus.

If in the second stage of the disease the pasty mass or some adhering clot of fibrine becomes exposed to the current of the blood, and carried away, some portion of it may be arrested in a distant small vessel, establishing the condition of embolism.

If this should occur in the lungs, or the brain, or the kidneys, organs specially predisposed to embolism, further, and perhaps fatal, mischief may be the result.