On chronic endocarditis regarded as a fibrosis of the valves of non-infective origin / by J. George Adami.
- John George Adami
- Date:
- 1911
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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![[Reprint from Interstate Medical 1911.] ON CHRONIC ENDOCARDITIS A FIBROSIS OF THE VALVES OF NON-INFECTIVE ORIGIN. By J. Georgia Adami, M. D., F. R. S., of Montreal. In these days when bacteriology is dominant, if not indeed rampant, it is difficult to rid ourselves of the idea that fundamentally underlying one or other morbid condition of the tissues there is some primary microbic factor. Or perhaps, more accurately, our first inclination is to search after and seize upon evidences of present or past microbic activity, and, if we can find indications which with greater or less plausibility can be regarded as suggesting the outcome of microbic growth within the tissues, then we are satisfied to believe that we have grasped the etiology of the condition. If, on the other hand, we find ourselves compelled to fall back upon physical or metabolic factors as causes of tissue change, we do this with a certain distrust or discontent. For example, we have nowadays to accept such conditions as myxedema, acromegaly, Addi- son’s disease, obesity, gout and acidosis as the resultants of disorders of the internal secretions or more broadly of cellular metabolism. But doing this, confessedly, it is difficult to form a mental picture of the succession of changes in the cells and tissues that lead to the anatomical manifestations of these different states. On the other hand, we have been drilled so thoroughly into an appreciation of the various stages which may result from an infective inflammation, and those stages, it may be added, are so many and so varied, that it is easy for us to imagine almost any morbid process as a resultant of some form of infection. Thus in the matter of valvular disorders^—of endocarditis—I think I make a correct statement in saying that our tendency is to regard the valve changes as outcomes, whether recent or late, of some infective process, and, whether voluntarily or involuntarily, we find ourselves sceptical as to explanations of any other order. Nevertheless, are we justified in considering chronic endocarditis as essentially of microbic origin? For myself, I must acknowledge that very early in my career a series of experiments by my old chief, the late Professor Roy, of Cambridge, published in our joint names, gave me food for thought. Among pathologists there has been no more brilliant mechanical genius than was Roy. His ability to devise instruments fitted to give records of one or other order was extraordinary. He devised and I noted. And incidentally in the course of our studies upon the effects of increased arterial pressure upon the volume and work of the dog’s heart we found, that increased aortic pressure, produced by narrow-](https://iiif.wellcomecollection.org/image/b22438889_0003.jp2/full/800%2C/0/default.jpg)
