This name designates inflammation of the muscular substance of the heart. Several forms are distinguished.

Parenchymatous myocarditis is a general inflammation of the proper muscular fibre of the heart. The term is applied chiefly to cases of aggravated parenchymatous degeneration, occurring in acute infective diseases. It is met with chiefly in septic and pyaemic conditions, and in diphtheria.

It must be said that this form of disease is somewhat indefinite, and, in any case, is secondary in its origin. There is reason to believe, however, that certain of the morbid poisons attack the heart more especially, and act directly on its muscular substance. This is true especially of diphtheria, and perhaps also small-pox.

Purulent myocarditis is also a secondary affection, occurring in consequence of the transportation of material containing infective microbes. It is frequently embolic, being part of the phenomena of Pyaemia or Ulcerative endocarditis. The infective matter is distributed by the coronary arteries, and gives rise to multiple softenings going on to the formation of Abscesses. Such localized suppurations soften the wall of the heart, and may lead to Aneurysm or Rupture. The abscesses do not readily burst into the cavities of the heart, but are liable to extend to the pericardium, where they give rise to a purulent pericarditis. A suppurative inflammation of the myocardium may also occur by extension from the endocardium in ulcerative endocarditis. The microbes on which this disease depends may propagate into the muscular substance, and so cause ulceration (acute ulcer of the heart), or may even lead to an abscess burrowing in the wall of the heart. This also may lead to aneurysm or rupture of the wall. It must be seldom that such abscesses as those will heal, but there are cases in which calcification either of the abscesses, or of portions of the heart's substance which had been softened by embolism, has been observed in pyaemia. A case observed by the author, and referred to under calcareous infiltration, was probably of this kind.

Interstitial myocarditis consists in an inflammatory increase of the interstitial connective tissue. There is no doubt that in the great majority of cases the cicatricial or tendinous patches met with in the heart are due to obstruction of the coronary artery, as already described,, and in all such cases these arteries should be examined. A more direct local inflammation may be due to other specific causes. Thus in pericarditis or in endocarditis, the inflammation may extend to the muscular substance, causing induration of the superficial layers on the one hand, or of the internal layers on the other. And again in chronic endocarditis affecting the mitral valve we often find, along with thickening of the chordae tendineae, a partial conversion of the musculi papillares into dense fibrous tissue, in fact, an interstitial inflammation with destruction of the muscular tissue.

A localized interstitial myocarditis may be the result of Syphilis, There is sometimes a definite gumma, around which a great new formation of connective tissue has occurred, but there may be a local cicatricial condition without any gumma being detected. In these cases-there has probably been a gumma at an earlier period. Syphilis may also, perhaps, produce fibrous transformation by causing syphilitic lesions in the coronary artery such as already described.

It is doubtful whether a general interstitial myocarditis occurs. Some have asserted its existence in dilated and hypertrophied hearts, and especially in the hypertrophy of the left ventricle in Bright's disease (see especially Turner). There is, no doubt, in the congested heart hypertrophy of the connective |tissue, but the author has failed to find evidence of a true inflammatory condition either here or in the hypertrophy of Bright's disease.