The opinion that arteriosclerosis is due in large part to poisoning by end products or by-products of protein digestion is now receiving much support. Experiments on dogs and rabbits have lent some confirmation to chemical observations. It has been shown that dogs fed for a long time on putrefied meat developed inflammation and degeneration of the adventitia and media, with hyperplasia and calcification of the intima of many arteries. In the pulmonary and carotid arteries, in the vena cavas and myocardium, there were extensive necroses and hyaline degeneration. Moreover, injections of sodium urate and ergot caused necroses in the muscularis and elastica of the aorta, pulmonary artery, vena cavas inferior and heart muscle, but there was no calcification. Guinea pigs which were fed indol in small doses by the mouth over a long period showed atheromatous degeneration of the aorta.
Infectious Diseases
As more study has been given to the arteries in persons who have died of the acute infectious diseases, more has come to light concerning the effects of the toxins of these diseases on the vessel walls. In the arteries of children who have died of measles, scarlet fever, diphtheria, cerebrospinal meningitis, etc., degenerative changes in the arteries occur, modified only by the length of time that the toxins have acted.
Thayer has shown that the arteries of those who have passed through an attack of moderately severe or severe typhoid fever are as a rule more readily palpable than are the vessels of persons of corresponding years who have never had the disease. Clinically the typhoid toxin appears to cause the early production of arteriosclerosis. The changes in the arteries occur for the most part, and always earlier, in the peripheral arteries, and the media is chiefly affected. Minute yellowish patches are found on the aorta, carotids, and coronaries. In persons who have passed through an attack of one of the fevers, and have later died from some other cause, regenerative changes are sometimes found to have taken place in the arteries, consisting of an ingrowth of elastic fibers from the intact adventitia to the diseased media.
That there are some other factors than the infectious disease which are concerned in the production of arterial changes seems evident from a study[14] made recently among a group of almshouse inmates ranging in age from 38 to 90 years. The study included 500 persons of both sexes. Careful histories were taken to determine the presence of antecedent infectious disease. The radial artery was palpated to determine the presence of sclerosis. Among the cases giving a history of one infectious disease the following table gives the results:
| DISEASE | NO. | + | ++ | +++ | POSITIVE | NEGATIVE |
| Measles | 47 | 10 | 6 | 12 | 28 | 19 |
| Infectious arthritis | 38 | 9 | 6 | 4 | 19 | 19 |
| Pneumonia | 30 | 5 | 8 | 5 | 18 | 12 |
| Typhoid | 27 | 6 | 8 | 3 | 17 | 10 |
| Scarlet fever | 10 | 0 | 0 | 4 | 4 | 6 |
| Smallpox | 14 | 1 | 4 | 0 | 5 | 9 |
| Miscellaneous | 12 | 2 | 5 | 2 | 9 | 3 |
| 178 | 33 | 37 | 30 | 100 | 78 |
A summary of the cases showed: 252 cases without sclerosis; 248 with sclerosis; 147 cases with infections but no sclerosis; 180 cases with infections and sclerosis.
This study failed to throw any positive light on the question. Infectious diseases undoubtedly play a certain rôle, particularly those continuing a long time and certain particular infectious diseases, as measles.