MYOCARDITIS - RHEUMATISM.
When considering the question of the action of the rheumatic poison on the various structures involved in acute rheumatism, we saw good reason to believe that the voluntary muscles were directly affected by it, and that the excess of lactic acid characteristic of the disease was a consequence of increased muscle metabolism. If the voluntary muscles are thus affected, there is no reason why the car diac muscles should escape, for they are similar in structure and func tion. Indeed in their case there is distinct and direct evidence that they do thus suffer during the course of rheumatic fever, for many cases have been recorded in which the cardiac walls have been found after death to be the seat of inflammatory softening or induration. With this evidence of myocarditis there have usually been associated the ordinary post-mortem signs of endocarditis, of pericarditis, or of both. The existence of this association, and the rarity of post-mortem evidence of myocarditis except in combination with inflammation of the membranes, have not unnaturally led to the belief that inflamma tion of the muscular substance is secondary to that of the membranes, and results from the direct extension to it of an already existing in flammation of one or both of these.
Myocarditis occurring independently of endo-pericarditis is de scribed by Walshe as "an affection, to say the least, of extreme rarity." Peacock says that myocarditis "is rather interesting in a patho logical point of view than practically important. It probably always occurs in connection with one or both the other forms of disease," i.e., endocarditis or pericarditis.
" Inflammation of the heart substance is frequently set up in the layers contiguous to an inflamed endocardium or pericardium" (Roberts).
"Inflammation of the muscular substance of the heart rarely occurs except in connection with peri- or endo-carditis. In pericar ditis a greater or less thickness of the muscular walls in contact with the inflamed serous membrane is often distinctly implicated; and there is no doubt that their inner aspect may be similarly involved during the course of an attack of endocarditis" (Bristowe).
But when we come to examine the grounds on which this opinion is based, we find that they are scarcely adequate to its support, and that especially the view that myocarditis is secondary to and depen dent on prior inflammation of the endocarclium is one which can hardly be maintained. The lining membrane of the heart is a non vascular structure in which inflammation cannot, and as a matter of fact does not, spread. The morbid change which takes place in it during the course of acute rheumatism is secondary to change in the subjacent fibrous tissue, and, is limited entirely to that part of the membrane which is reflected over the fibrous valves. It never extends to the much more extensive portion which lines and is in contact with the muscular substance, and from which alone it could extend to that substance. Limited as the morbid process thus is, showing no ten dency to spread, and never affecting the part of the membrane which is in contact with the muscular walls, it is simply impossible that in flammation should extend from the endocardium to the muscular sub stance of the heart. Endocarditis and myocarditis may coexist, but myocarditis cannot be secondary to and consequent on endocarditis.
It is different with the pericardium: it is a very vascular mem brane in which inflammation rapidly spreads; the whole membrane may suffer, and its inflamed part be in direct contact with the mus cular walls. It is quite possible, therefore, that inflammation may extend from it to them; it is equally possible that the process may occasionally be reversed and that inflammation may extend from the muscular walls to the pericardium. But more probable than either is it that when pericarditis and myocarditis coexist, each occurs independently of the other—both being part of a general carditis.