Syphilis is one of the most important of the etiologic factors in the production of arteriosclerosis. It has been shown that in 85 per cent of cases of aortic insufficiency in persons, usually males, over forty-five years, who did not have chronic infective endocarditis, the Wassermann reaction was positive. Acute aortitis affecting the ascending and transverse portions of the arch of the aorta is very commonly seen, and the irregular, scattered, slightly raised, yellowish-white patches of sclerosis in the arch which are found years after the syphilitic lesion, are considered by some to be very characteristic of syphilis. Mesaortitis is the primary lesion and acts as a locus minoris resistentiæ where an aneurysm forms.
Hypertensive cardiovascular cases have been serologically studied, and a positive Wassermann reaction found in a large percentage of one series. In fifty cases, 90 per cent either gave a positive Wassermann reaction or luetin test, were known to have syphilis, or had children with hereditary syphilis. This suggests what might be called "familial cardiovascular syphilis."
Hypertensive disease is possibly one of the common so-called "late" manifestations of syphilis. That syphilis is responsible for the arterial disease in the vessels of the brain, resulting in apoplexy or sudden cardiac death in middle life, has long been known. In fact, it is claimed (Osler) that all aneurysms occurring in persons under thirty years of age are due to syphilitic aortitis. In the late stages of syphilis the arterial lesions may be of a diffuse character.
Chronic Drug Intoxications
Lead, tobacco, and according to some, tea and coffee, are to be classed as causal factors in the production of arteriosclerosis. Certain it is that all these substances have a tendency to raise the arterial pressure, but whether the drug itself causes first a degeneration, and later a hypertension results, or vice versa, is not yet positively known. We have just mentioned that lead particularly has a marked effect in producing arterial lesions. Other drugs as adrenalin, barium chloride, physostigmin, etc., while producing experimental arteriosclerosis, hardly could produce the disease in man. Alcohol has been blamed for much, and as an etiologic factor in the production of arteriosclerosis formerly was accorded a first place. More recently much doubt has been thrown on this supposition by the work of Cabot, who showed that the mere drinking of even large quantities of spirits had no effect in producing arterial disease.
This observation has been recently substantiated by Hultgen, who carefully studied clinically 460 cases of chronic alcoholism. He says, "There are no cardiovascular symptoms which might be termed characteristic of chronic alcoholism, unless it be the peculiar fetal qualities of the heart sounds which we know as embryocardia. I find this very frequent among drinkers, but I can offer only a tentative explanation for it, namely the following: Embryocardia can only occur with low tension blood pressure, and in the absence of renal insufficiency. Hence it might be considered as a useful condition of no pathologic significance at all. That alcohol is a sclerogenic pharmakon and productive of arteriosclerosis with its usual train of symptoms may be a fact, but its demonstration would be difficult and is really not shown by my tabulations. There were cardiovascular changes, such as myocarditis, aortitis, valvular heart disease and arteriosclerosis in chronic alcoholics in 54.3 per cent of 461 cases, but this by no means constitutes a proof of the causal relationship between these lesions and the abuse of liquors. I believe it, nevertheless, to be good reasoning to ascribe the bulk of cardiovascular symptoms to the sclerogenic action of alcohol, while abstaining from an interpretation of its pathogenesis." Just what rôle tobacco plays is difficult to say. My own opinion is, that of itself when used in moderation, it has no ill effects. However, as tobacco is a drug that may raise the blood pressure, excessive use must be held responsible for the production of arteriosclerosis. It is difficult to separate its effects from those produced by eating and drinking.
Overeating
There can be no doubt but that the constant overloading of the stomach with rich or difficultly digestible food is responsible for a large number of cases of arteriosclerosis. Every one must have noted the increase in force and volume of the heart beat after the ingestion of a large meal. The constant repetition of such processes conceivably can lead to damage to the vessel walls through hypertension.
In the metabolism of food in the intestines there are substances produced which are poisonous when absorbed directly into the circulation. Ordinarily these substances are rendered harmless either before absorption or are detoxicated in the liver to harmless substances. It is conceivable that a constant overproduction of such poisons would eventually damage the defensive mechanism of the body to such an extent that some of the poisons would circulate in the blood. An expression of a surplus of one, at least, of these decomposition products is the appearance of indican in the urine. It is not believed that indicanuria has the importance attached to it which some authors would have us believe. It is found too often and in too many varying conditions, nevertheless it undoubtedly does reveal the presence of perverted metabolism.
In how far the toxins absorbed from the intestinal tract are responsible for the production of arterial disease, it is not possible to say. Some observers lay great stress on this factor as a cause of arteriosclerosis. The author believes that the rôle played by the absorption of products of perverted intestinal metabolism is an important one. The primary change is an increased tension in the arterioles which later leads to thickening of the coats of the vessels and to the other consequences of arterial disease. A vicious circle is thus established which has a tendency to become progressively worse.