Heart.—Some difference of opinion exists as to the condition of the heart; Parkes Weber[158] says that the only true senile change is diminution in size and weight; this as it is worded is no doubt correct; but pure atrophy is less rare in the heart than in most parts of the senile body. Charcot[159] indeed stated that it does not atrophy in old age, but preserves the dimensions of middle life. The heart may even hypertrophy in old people; this is pathological; Councilman[160] found it in 248, or 43 per cent, of 580 persons over 60 years of age, and could not refer it to aortic or renal arteriosclerosis or to the diminished capillary area in the skin; but the average blood pressure 158 systolic/88 diastolic of the cases with cardiac hypertrophy was higher than that 130/78 of the others.
Fatty degeneration of the myocardium is very frequent; Charcot stated that at the Salpêtrière it was almost constant in old women, but according to Councilman there is no clear evidence that it produces permanent injury or functional insufficiency; he noted some fibrosis in 15 per cent of his cases. Atrophy of the epicardial fat—serous atrophy—is common, and increase of the so-called lipochrome pigment in the muscular fibres which become smaller and fewer—brown atrophy—is frequent as it is in the other organs in old age.
Chronic valvulitis and subendocardial fibrosis are, like arteriosclerosis, common morbid changes.
Arteriosclerosis, contrary to what has been stated by Huchard and others, is not constant in a considerable degree in old people, and therefore cannot, as Demange and others considered, be regarded as the cause of the atrophic changes seen in old age. Arteriosclerosis is due to several factors, namely, infection and intoxication of various kinds and to damage caused by long-continued high arterial blood pressure. The primary changes are degeneration and weakness, however brought about, in the middle coat. Ophülz[161] has recently discussed the question whether the degeneration is entirely or largely a senile change; if it were so, the curve of the incidence of arterial sclerosis would begin gradually about the age of 40 years, so as to include premature cases, and rise slowly until the age of 55 years, when there would be a sudden increase to 80 or 90 per cent, and at the age of 70 it would be improbable that any one would be free from well-marked arteriosclerosis. He found that the curve of incidence was very different from this; beginning much earlier its rise is gradual all the way without any sudden increase, and indeed seems, if anything, to be retarded by old age. Old persons may have practically healthy arteries, so, although arteriosclerosis may undoubtedly produce atrophy and senile changes in the tissues and organs by diminishing the blood supply, for example in the case of the red granular kidney, it cannot be regarded as the causal factor in healthy old age.
The primary calcification of the middle coat, sometimes called Mönckeberg’s sclerosis, which leads to the formation of regular rings in the degenerated muscular media and the “pipe-stem” arteries associated with senile gangrene, may be independent of, or combined with, endarterial sclerosis. It follows fatty degeneration of the media, which is the commonest form of medial degeneration in the aged, and specially picks out the elastic fibres.[162] The femoral, tibial, radial arteries and the aorta are most often affected. It is difficult to estimate its incidence, but that it is not very common, at any rate in a high degree, seems probable from the comparative infrequency of its detection in x-ray examinations of the lower limbs in old people. It would be natural to associate its occurrence with the rarefaction of bone that goes on in advanced life, and so to consider it as in some respects different from the secondary calcification in endarteritic sclerosis; in answer to an enquiry Professor W. T. Councilman of Harvard kindly wrote to me that he did not regard calcification as characteristic of any particular type of arterial disease, lime salts being in certain cases more easily deposited in any pre-existing lesions. Klotz describes fatty and calcareous change in the middle third of the media of the aorta as quite characteristic of senescence.
Cazalis’s famous aphorism “man is as old as his arteries” is true in so far that the state of the arteries is a good index of the general condition, for they are extremely prone to suffer as the result of infection, toxaemia, and strain; strictly speaking, therefore, the state of the arteries is not so much an index of the individual’s age as of his adventures.
Phlebosclerosis, analogous to arteriosclerosis, is common, and dilatation, often due to stagnation and lack of the normal vis a tergo, of the veins is a familiar change in the aged.
The capillary area is diminished in the skin and elsewhere, but not uncommonly there are dilated venules or angiomas on the skin; the latter, commoner on the trunk and upper limbs and in men, were formerly known as “de Morgan’s spots” and were thought to accompany cancer, but the association is only due to a rough correspondence of their age incidence.
The blood of healthy octogenarians may not show any departure from that of the earlier periods of life as regards the number of the reds and the amount of haemoglobin (Hansen[163]), though some have described a secondary anaemia. Thus in a female centenarian Macnaughton[164] found slight secondary anaemia with a normal number of leucocytes, the differential count showing a relative lymphocytosis. The red bone marrow diminishes, its place being taken by fat cells.
The lymphoid tissues undergo atrophy all over the body including the leucoblastic bone marrow, but though it does not appear that the blood shows any definite change in the leucocyte count it is tempting to correlate the diminution of resistance to acute infections, such as pneumonia and erysipelas, with the atrophy of the lymphoid tissue. The alimentary canal often shows lymphoid atrophy in a high degree, but two normal Peyer’s patches were present in a man reputed to be 106 years old (G. Rolleston[165]).