When Dr. O. W. Holmes was asked how to live to the age of seventy, he replied that a man should begin to pick his ancestors one hundred years before he was born. Our parents determine the character of the tissues with which we start in life, and this determines our general resistance. We might properly speak of congenital arteriosclerosis where the affected individual had poor arterial tissue with which to begin life, for that, in a sense, is a congenital defect, and arterial tissue that is poor in quality is prone to disease.
The author is more and more impressed with the part that heredity plays in the determination of arterial degeneration. Especially does syphilis in the parents or grandparents leave its stigma in the succeeding generations in the shape of poor arterial tissue which is prone to early degeneration. Recently W. W. Graves has called attention to a malformation of the vertebral border of the scapula which consists in a concavity instead of the normal convexity of the bone. To this malformation he has given the name, scaphoid scapula. He considers this to be but one manifestation of a general lack of development in the individual. He speaks of this maldevelopment as a blight and considers that syphilis in the ancestors is responsible for the condition in the offspring. He finds that even in children, the subjects of the scaphoid scapula, the arteries are very definitely thickened. While confirmation of his observations is lacking, there is no doubt that we must lay the blame for much of the arteriosclerosis in our patients to the poor quality of arterial tissue transmitted by ancestors who have acquired some constitutional disease. It may have been syphilis, it may have been the degeneration produced by alcohol or other drug. We can not ignore the part which heredity plays. The various factors to be considered in the production of the acquired form of arteriosclerosis appear to me to be but contributory factors to a very great extent, the essential and fundamental factor being the quality of arterial tissue with which the individual is endowed.
Arteriosclerosis may occur in infants. Cases have been reported of calcification of the arteries in infants and children. The arteriosclerosis may occur without nephritis or rise of blood pressure. Cerebral hemorrhage in a child of two years has been seen. Heredity in these cases plays a most important rôle. In many of the reported cases there was no question of congenital syphilis. Aneurysms, single or multiple, have been found in the arteries of children, and even the pulmonary artery may show sclerotic changes.
Acquired Form
As a rule the cases usually seen belong in this group because it seems as if a connection could be established almost always between one or more of the etiologic factors to be described and the disease. While this apparently is the case, we must never lose sight of the part which the quality of the tissue plays. When we leave this out of our calculations we undoubtedly make many false deductions. When two men of the same age who have been exposed to the same conditions as far as we can learn, are found to have quite different arteries, the one normal, the other thickened, we must postulate congenitally poor tissue on the part of the latter. Such tissue readily becomes diseased following conditions which would very likely have produced no noticeable effect on perfectly normal, healthy tissue.
Hypertension
Hypertension must still be reckoned with in the etiology of arteriosclerosis although the rôle that it was thought to play does not seem so important. Changes of blood pressure alone are not considered by many to be sufficient for the production of arteriosclerosis. This may play some part, but there are many other factors mostly unknown which determine in any case the production of arterial lesions.
With every systole of the heart, blood is forced out into the arterial system against a certain amount of resistance represented by the tonicity of the capillary area, and the amount of cohesion between the viscous blood and the walls of arterioles. When a dilatation of the capillaries over any large area takes place, the blood pressure falls, provided there is no compensatory contraction in other areas to make up for the decreased resistance in the dilated vessels. The viscosity of the blood, as such, probably has very little effect on the resistance to the flow. With the systole of the heart there is a sudden dilatation of the arch of the aorta, and a wave of expansion follows, which is transmitted to the periphery and is lost only in the capillaries.
The blood pressure is constantly changing. Physiologically there are relatively wide variations in the pressure in a perfectly normal individual. There are some persons who have hypotension, a blood pressure much below the normal. Such persons have usually small hearts, small aortas, and they seem to have but little resistance to disease. Many diseases, especially the prolonged fevers, diminish markedly the blood pressure. Whether the hypertension is the cause of the structural changes that are found in the walls of the vessels, or is the result of the diminished area of the arterial tree through which the same amount of blood has to be driven as before the vessel walls became narrowed, is still disputed. As has been stated, experimental evidence would tend to place the initial blame upon the poisons circulating in the blood, which first damage the vessel walls. The subsequent changes then produce thickening and inelasticity. Some think (Allbutt) that the hypertension is primary. There are cases seen clinically that lend support to this view and there is experimental evidence also (v. Chap. II). Not infrequently individuals in middle life begin to show increase of arterial blood pressure without discoverable cause. In such case it may be that there is slowly progressing chronic nephritis. The urine if examined only superficially in single specimens may not reveal any abnormalities. Careful functional examination by means of the newer tests may reveal functional deficiency. It must not be supposed that all cases of increasing hypertension are cases of chronic nephritis. The opinion has already been expressed (Chap. III) concerning this point. Experience has convinced me that the opinion expressed in former editions is not altogether correct.