On chronic endocarditis regarded as a fibrosis of the valves of non-infective origin / by J. George Adami.

  • Adami, J. George (John George), 1862-1926.
Date:
1911
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Licence: In copyright

Credit: On chronic endocarditis regarded as a fibrosis of the valves of non-infective origin / by J. George Adami. Source: Wellcome Collection.

Provider: This material has been provided by The Royal College of Surgeons of England. The original may be consulted at The Royal College of Surgeons of England.

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    ing the aorta was repeatedly followed by very definite changes in the aortic valves. Ihese, we found, were not mere inert mechanical mem- branes, hut reacted to their environment. The aortic cusps, it may he re- called, are normally devoid of vessels save near their bases. Their nourish- ment therefore is by means of blood plasma absorbed through or between the lining endothelial cells, or both, from the cardio-aortic blood. After extreme high pressure in the first part of the aorta we found that the cusps presented a series or chaplet of fine glistening bead-like elevations just below the line of their apposition. Evidently during diastole the high pressure acting upon their aortic aspect coupled with the low pres- sure on their ventricular aspect, and it may also he with expansion of the endothelial cells and increase in the intercellular spaces due to stretch- ing of the cusps under the increased pressure; all these had led an increased percolation of “lymph” into the valve substance with a collection of the same along the line of greatest strain or weakness of the cusps. And Roy and I then called attention to the possibility that the thickening of the aortic valves in cases characterized by high blood-pressure might be a later outcome of this same process. Now chronic endocarditis in elderly people is characteristically associated with the presence of nodose arteriosclerosis, and the two pro- cesses are, I would point out, of identical type. Both conditions involve intimal structures, (for the heart valves are but infoldings of the cardiac intima), and, histologically, they are of the same order, with overgrowth of the subendothelial connective tissue, the most recent layers being near- est tbe surface, the deeper layers exhibiting a series of degenerative changes which culminate in the development of calcareous plaques. I freely admit that in one order of arteriosclerotic changes a proliferation and swelling of the cells of the musculo-elastic layer immediately to the inner side of the internal elastic lamina is a prominent feature. In the cases that I here refer to these changes while they may be present are not dominant. What is especially significant is this laying down in an orderly manner of layer after layer of connective tissue parallel to the surface, whether of aorta or of aortic cusp. There are here none of the cardinal signs of inflammation or its after results; no accumulation of leucocytes or plasma cells, no entry and no formation of new vessels, such as we see, for instance, after the chronic inflammation of other non-vascular regions, as the cornea. As my old colleague, Professor Klotz, has demonstrated (although he does not see eye to eye with me in the explanation of these changes) a similar uniform connective-tissue hypertrophy with accompany- ing overgrowth of the musculo-elastic layei can be produced in the rabbit by purely mechanical means, namely, by periodical raising of the blood-pressure for a few minutes every day extending over several months. In the absence, therefore, of adequate evidence of in- fective origin in these cases, in the absence of signs of ordinary inflam- mation and from tbe bistological features of the new tissue, it is neces-