Arteriosclerosis is essentially a disease of middle life and old age. It is not unusual, however, to find evidences of the disease in persons in the third decade and even in the second decade. Hereditary influences play a most important rÔle, syphilis and the abuse of alcohol in the family history are particularly momentous. The recognition of the early changes in the arteries among young persons depends largely upon how carefully these changes are looked for. The difference in the point of view of one man who finds many cases in the comparatively young, and another man who rarely finds such changes early in life, at times, depends upon the acuity of perception and observation and not upon the fact that one man has had a series of unusually young arteriosclerotic subjects. The diagnosis of arteriosclerosis may be so easily made that the tyro could not fail to make it. It is, however, the purpose of this volume to lay stress on the earliest possible diagnosis and, if possible, to point out how the diagnosis may be arrived at. It is obviously much to the advantage of the patient to know that certain changes are beginning in his arteries, which, if allowed to go on, will inevitably lead to one or more of the symptom groups described in the preceding chapters.

The combination of (1) hypertrophied heart, (2) increased blood pressure, (3) palpable arteries, and (4) ringing, accentuated second sound at the aortic cartilage is, in reality, the picture of advanced arteriosclerosis. If the individual is in good condition much may be done by judicious advice and treatment to ward off complications and prolong life with a considerable degree of comfort. But we should not wait until such signs are found before making a diagnosis and instituting treatment. As in all forms of chronic disease the early diagnosis is all important.

The history of the case is the first essential. Often a careful inquiry into the personal habits of a patient, with the record of all the preceding infectious diseases will give us valuable information and may be the means of directing the attention at once to the possible true condition. Particularly must we inquire into the family history of gout and rheumatism. An individual who comes of gouty stock is certainly more prone to arterial degeneration than one who can show a healthy heredity. Alcoholism in the family also is of importance because of the fact that the children of alcoholics start in life with a poor quality of tissue, and conditions that would not affect a man from healthy stock might cause early degeneration of arterial tissue in one of bad ancestry.

What infectious diseases has the patient had? Even the exanthemata may cause degenerations in the arteries, but, as has been shown, such lesions probably heal completely with no resulting damage to the vessel. Should the patient have passed through a long siege of typhoid fever the problem is quite different. Here (vide supra) (Thayer), the palpable arteries do appear to be sclerosed permanently. Probably the length of time that the toxin has had a chance to act determines the permanent damage to the vessel wall. More potent than all other diseases to cause early arteriosclerosis is syphilis, and hence very careful inquiry should be made in regard to the possibility of infection with this virus. Not only the fact of actual infection but the duration and thoroughness of treatment are important matters for the physician to know.

What is the patient's occupation? Has he been an athlete, particularly an oarsman? Has he been under any severe, prolonged, mental strain? Is he a laborer? If so, in what form of manual labor is he engaged? Such questions as these should never be overlooked, as they form the foundation stones of an accurate diagnosis, and early, accurate diagnosis, we repeat, is essential to successful therapy.

We have called attention to the factor of sustained high pressure in the production of arteriosclerosis. Constant overstretching of the vessels leads to efforts of the body to increase the strength of the part or parts. The material which is used to strengthen the weakened walls has a higher elastic resistance than muscle and elastic tissue, but a lower limit of elasticity, and is none other than the familiar connective tissue. In athletes, laborers, brain workers who are under constant mental strain, and in those whose calling brings them into contact with such poisons as lead, there is every factor necessary for the production of high tension and consequently of arteriosclerosis.

Another question in regard to personal habits is how much tobacco does the patient use and in what form does he use it? Our experience is that the cigar smoker is more prone to present the symptoms of arteriosclerosis than the cigarette smoker, the pipe smoker, or the one who chews the tobacco. A very irritable heart results not infrequently from cigarette smoking but such is almost always found in young men in whom the lesions of arteriosclerosis are exceedingly rare. The probabilities are that the arteriosclerosis in cigar smoking results from the slowly acting poison which causes a rapid heart rate with an increase of pressure.

Last but not least, and perhaps the most important question is, has the patient been a heavy eater? This I believe to be a potent cause of splanchnic arteriosclerosis with the resulting indigestion, cramp-like attacks, high blood pressure, etc. In a joking manner we are accustomed to remark, "Overeating is the curse of the American people." There is, however, much truth in that sentence. Osler, than whom there is no keener observer, states that he is more and more impressed with the fact that overloading the stomach with rich or heavy or spiced foods is today one of the first causes of arterial degeneration. It stands to reason that this is true. We know that organs exposed constantly to hard work undergo hypertrophy, and that the blood tension in those organs is high. Blood tension is, after all, dependent on capillary resistance, and if the capillaries are distended with blood, the resistance is great. The digestive organs can be no exception to this rule. Increased work means an increase of blood. This inevitably causes distension of the capillaries with stretching of the arteries and consequent damage to the walls. Once arteriosclerosis is present a vicious circle is established.

A man about forty-five consults us and says that he has noticed recently that he gets out of breath easily; in tying his shoes he experiences some dizziness. He finds that he has palpitation of the heart and possibly pain over the precordial region now and then. He notices also that he is irritable, that is, his family tell him he is, and he notices that things that formerly did not annoy him, now are almost hateful to him. On examination, one finds a palpable radial, a somewhat hypertrophied heart and slightly accentuated second aortic sound. The blood pressure may be high. The urine may or may not reveal any abnormalities. Not infrequently, although no albumin may be found, there are hyaline casts. Such a case of arteriosclerosis is evidently not to be regarded as early. Then the question arises, How are we to recognize early arteriosclerosis? I do not believe that the solution of this problem lies entirely in the hands of the physician. Some men are fortunate enough to come up for an examination for life insurance before an observant doctor who recognizes the palpable artery, makes out the beginning heart hypertrophy and the slightly accentuated second aortic sound. The patient will tell you that he never felt better in his life. He gets up at seven, works all day, plays golf, drinks his three to six whiskies, and is proud of his physical development. But the great mass of people are not fortunate from this standpoint. They do not seek the advice of the physician until they are stretched out in bed. They boast of the fact that for twenty years they have never had a doctor. One may well say that it is a problem how to reach such persons. It seems to me that there can be but one way to do this. The people must be taught that the duty of a physician is just as much to keep them in health as it is to bring them back to health when they are ill. To that end people should be taught that at least twice a year they should be carefully examined. I do not mean that the patient should present himself to the doctor and, after a few questions the doctor say cheerfully, "You are all right." The patient should be systematically examined. That means a removal of the clothing and examination on the bare skin. Such cooperation on the part of patient and doctor would save the patient years of active life and make of the doctor, what his position entitles him to be, the benefactor to the community. Too often careless work on the physician's part lulls the patient into a false sense of security and he wakes up too late to find that he has wasted months or years of life. Early diagnosis of arteriosclerosis is only possible in exceptional cases unless people present themselves to the physician with the thought in mind that he is the guardian of health as well as the healer.

There are patients who go to the ophthalmologist for failing vision. Physically they feel quite well. They have been heavy eaters, hard workers, men and women who have been under great mental strain. On examination of the fundus of the eye there is found slight tortuosity of the vessels with possibly areas of degeneration in the retina. A careful physical examination will usually reveal the signs of arteriosclerosis elsewhere. We have mentioned frequently high tension as an early sign. This must be taken with somewhat of a reservation, for this reason: not infrequently a persistent high tension is the earliest sign of chronic nephritis. The arteries may be pipe stem in character and the heart small and flabby. However, if one watches for the palpably thickened superficial arteries (always bearing in mind the normal palpability as age advances) and the high tension, he can not go far wrong in his treatment whether the case is one of chronic nephritis or of arteriosclerosis.

There is also this to bear in mind. Arteriosclerosis may be marked in some vessels and so slight in the peripheral vessels that it can not with certainty be made out. But when the radials are sclerosed, it is usually the case that similar changes exist in other parts. Then too, there may be marked changes at the root of the aorta leading to sclerosis of the coronary vessels alone, and the first intimation that the patient or any one else has that there is disease, may be an attack of angina pectoris. Except for symptoms on the part of the heart there is no way to make the diagnosis of sclerosis of the coronary arteries.

Differential Diagnosis

In arriving at a diagnosis, when the question is whether or not arteriosclerosis is the main etiologic factor, the most important fact to know is the age of the patient. Other points that have been dwelt on fully must of necessity also be borne in mind.

Possibly the chief conditions that may be confused with some of the results of arteriosclerosis are pseudo angina pectoris which may be mistaken for true angina pectoris, and ulcer of the stomach, appendicitis (?) or other inflammatory abdominal condition which may be mistaken for angina abdominalis.

Differential tables are sometimes of value in fixing the chief points of difference graphically.

In differentiating between ulcer of the stomach and angina abdominalis the following points may be of service:

Diseases in Which Arteriosclerosis Is Commonly Found

There are certain more or less chronic diseases in which arteriosclerosis is found either as a separate disease or as a result of the chronic disease itself, or the sclerosis may be the cause of the disease. As examples of the first class are diabetes mellitus and cirrhosis of the liver. As examples of the second class are chronic nephritis, gout, syphilis, and lead poisoning. Examples of the third class have already been fully described. Then certain rare diseases that have been briefly described in this chapter, viz.: Raynaud's disease and erythromelalgia are frequently associated with demonstrable arteriosclerosis.