Mental Strain
More and more does one become impressed with the fact that patients with arteriosclerosis are very often those who take life too seriously and either from ambition or from an exalted sense of duty lead especially strenuous lives. Not always are these persons addicted to drug or liquor habit. Many are rather abstemious in their habits. It is not so often that we see as a victim of arteriosclerosis, the carefree person who laughs his way through life without worrying about the morrow. He is not so prone to arteriosclerosis. Worry is a far more potent cause of breakdown than actual manual work. It is the rule to find thickened arteries among neurasthenics. This may be only part of a generalized degeneration of all tissue in the body. The blood pressure in such persons is usually low. So many men of our better class live under a continuous mental strain in the business world. The increase in arteriosclerosis cases is real, not apparent. The intense mental strain seems to cause a marked increase in blood pressure (for short periods of mental effort this has been proved) over a period of time sufficient to cause permanent changes in the vessel walls. The same sequence of events repeats itself; high tension, arterial strain, compensatory thickening, hypertrophied heart, etc.
Certainly the character of the arterial tissue has much to do with the determination of degenerative changes which may result from the action of one or more of the etiologic factors.
Muscular Overwork
Muscular overwork is to be reckoned with as an etiologic factor. One sees it especially among the laboring class in both whites and negroes. Possibly other factors, as alcohol and coarse heavy food, contribute to the early arterial degeneration. Hypertrophy of the heart occurs in athletes, and statistics gathered among the oarsmen especially, show a relatively high mortality at the different decades traceable to the high tension produced while in training. This question deserves more consideration than has been accorded it.
Renal Disease
Chronic disease of the kidneys (contracted red kidney) is one of the most certain producers of hypertension; in fact, some maintain that high tension, even without demonstrable kidney lesions, as revealed by careful urine examinations, is a valuable sign pointing to chronic nephritis. This is doubted by others, myself among them. Just what causes the increase in blood pressure sometimes to over 270 mm. of Hg, is not definitely known. It seems most probable that it is some poison elaborated by the diseased kidneys and absorbed into the general circulation. There it acts primarily on the musculature of the arterioles causing tonic contraction and an increase of work on the part of the heart to force the blood through narrowed channels. One fact is certain. We see patients in coma due to renal disease with blood pressure much over 200 mm of Hg. As these cases clear up, the pressure may fall, and should they seemingly recover, the recovery is accompanied with a marked decrease in blood pressure, finally reaching the normal for the individual. Moreover, in the course of a severe acute or subacute nephritis, hypertension is associated with headache, partial or total blindness, and drowsiness. When the pressure is reduced, all these symptoms disappear.
There is also the chronically shrunken and scarred kidney known pathologically as the arteriosclerotic kidney. It is probable that there are two groups of cases which we may designate: (1) primary; (2) secondary. In the primary group the kidney disease antedates the sclerosis of the arteries, and the sclerosis is most probably dependent on the constant high tension. We know that prolonged hypertension will produce severe forms of arteriosclerosis. The arterial disease in this group is caused by the renal disease.
In the second group the kidney changes are apparently due to the general arteriosclerosis which, affecting the kidney vessels, causes changes leading to atrophy and subsequent fibrous tissue ingrowth of scattered areas. These cases are not necessarily associated with hypertension; on the contrary there is more apt to be hypotension. Where the first group occurs for the most part in young and active middle-aged people, the second group is the result of involutionary processes which accompany advanced age.
However careful a urinalysis may be, there is no assurance that one can predict the pathologic state of the kidney. Often so-called normal urine will be secreted by a badly diseased kidney, whereas a urine which contains considerable albumin and many casts may be secreted by a kidney which is only temporarily the seat of inflammation. What matters after all is not the state of the kidney which the pathologist describes, but the actual functional response of the kidney in the body to the various tests now well known.